Inflammation, a requisite process in the pathogenesis of several disorders, is coupled with the enhanced gene expression of the immune regulators . Nuclear factor κ-light-chain-enhancer of activated B cells (NF-κB), a prominent pleiotropic transcription factor, organizes a broad range of genes required for the distinct processes of the inflammatory and immune responses by displaying critical roles in the development of autoimmunity . The NF-κB family in mammals consists of five Rel homology domain-containing proteins in mammals, namely, p50/p105, p65/RelA, p52/p100, RelB, and c-Rel, present in a homo- or heterodimerized formation. The most commonly observed heterodimer forms of NF-κB are the p50 and the p65 (also known as RelA), encoded by NFKB1 and NFKB2, respectively. NFKB1—having 24 exons, spanning 156 kb, and being strongly associated with inflammation and immunity—encodes the genes for the p50 and p105 NF-κB isoforms, which are always-ready transcription regulators remarkable for their association with the pathological states of many diseases [2, 3]. NFKBIA (NF-κB inhibitor, α), having 6 exons and located on chromosome 14q13, instead, encodes the alpha subunit of the inhibitor of κB (IκBα), a typical form of the IκB family that naturally sequesters the NF-κB proteins within the cytoplasm .
The variations present in the genes responsible for the synthesis of the NF-κB (NFKB1) and IκB proteins (NFKB1A) are thus considered to exist in inflammatory disorders and cancer pathogenesis. So far, the U.S. National Center for Biotechnology Information (NCBI) database has 25,820 single-nucleotide polymorphisms (SNPs) reports on NFKB1 (accessed March 25, 2020). The most studied variation rs28362491 (−94 ins/del ATTG) is present within the promoter region of NFKB1 (Figure 1). Owing to its presence between two essential promoter regulatory elements, only this variation (of the 6 variations is known to have a likely functional behavior modulating nuclear protein binding to the NFKB1 promoter site .
IκBα, conversely, includes a number of polymorphisms. NFKBIA −881 A/G, −519 C/T, and −826 C/T variations, respectively located at putative binding sites for transcription factors retinoic acid-related orphan receptor α, CCAAT/enhancer-binding protein, and GATA binding protein 2, may regulate expression of the genes for IκBα and indirectly NF-κB activation [5, 6]. Another well-studied variant, namely, rs696 (3′ untranslated region [UTR] A→G polymorphism; Figure 1), alters NF-κB activity . There is a general agreement on the involvement of an imbalance of IκB and NF-κB in a wide variety of diseases, yet, the mechanisms behind how functional changes within numerous genes are associated with disease development remain to be elucidated. We consider that evaluation of studies of NFKB1 and NFKB1A polymorphisms may open a beneficial window to establish the connection between these two genes, if any, in inflammation-related diseases.
The present narrative review is based mainly on a comparative discussion of our findings with other literature regarding variations of NFKB1 and NFKB1A and their association with susceptibility to widespread inflammatory disorders (such as atherosclerosis [AT, morbid obesity, Behçet syndrome, Graves disease, Hashimoto disease) and common cancers (such as gliomas).
NFKB1 and NFKB1A variants and their relation to inflammatory disorders
As a widespread transcription factor in every mammalian cell dominating the gene expression of many acute-phase proteins such as cell adhesion molecules, chemokines, growth factors, and cytokines [8, 9], NF-κB manages the gene products required for both adaptive and innate immune responses. NF-κB is activated after intra- or extracellular stimuli, such as viral products, cytokines, and ultraviolet irradiation [10, 11]. In an unstimulated phase, NF-κB proteins are present within the cytoplasm in their sequestered homo- or heterodimer formation and interact with IκB inhibitors .
NF-κB signaling is critically involved in both cancer development and inflammation pathways first by enhancing antiapoptosis, proliferation, and angiogenesis and, second, by repressing immune responses. NF-κB performs its unique roles using two distinct signaling pathways, i.e., noncanonical and canonical pathways. The noncanonical pathway has a completely different signaling process, such as involving variable signaling molecules and leading to p52/RelB dimer activation [2, 13]. By contrast, in the canonical pathway, the phosphorylation of two N-terminal serines of IκBα by IκB kinase (IKK) is followed by its ubiquitination and proteasomal degradation, finally leading to the nuclear translocation of dimerized p50/c-Rel and p50/RelA of NF-κB complexes. After activation, the NF-κB/RelA unit induces the transcription of several proinflammatory genes, displaying its prominent role through inflammation.
Although the purpose of this chapter is to review NFKB1 and NFKB1A variants and their relation to specific inflammatory disorders, before proceeding, it is useful to mention the general relationship of NFKB1 with some other diseases. In neurodegenerative diseases such as vascular cognitive impairment, NF-κB contribution may lead to demyelination, axonal loss, and memory impairment of astrocytes . By contrast, in healing processes, elevated NF-κB activation through NFKB1 deletion enriches aggregation of both myofibroblasts and macrophages, leading to enhanced collagen deposition . This finding is in agreement with Stone's findings in a mouse model of multiple sclerosis, which showed NF-κB-associated protection of oligodendrocytes against inflammation .
Being described as immune activation within the arterial wall in the presence of inflammatory mediators, atherosclerosis (AT) is believed to be a chronic immunoinflammatory disease. As NF-κB is accepted as regulating the expression of a wide range of genes cooperating with the distinct aspects of atherosclerotic pathogenesis , NFKB1 may be an appropriate candidate for investigating arterial wall inflammation-related disorders such as atherosclerosis and coronary artery disease (CAD) . Özbilüm et al.  draw our attention to alveolar epithelial cells as a piece of evidence for the mechanism of the IκBα–NF-κB-dependent anti-inflammatory effect. Our results differed from those of Özbilüm et al.: we reported that rs28362491 polymorphism has no association with AT; however, the AA genotype of the rs696 polymorphism of NFKB1A gene was considerably elevated in atherosclerotic patients in a Turkish population. Moreover, the combined genotype association of rs28362491 and rs696 polymorphisms with atherosclerosis was not statistically significant, suggesting that these two polymorphisms together play no role in the pathogenesis of atherosclerosis . Although the findings represent NFKB1A rs696 polymorphism as a novel marker of susceptibility to atherosclerosis, the results from such analyses should be treated with caution because of the limited sample size.
NFKB1A −826 C/T promoter polymorphism was reported as a risk factor for susceptibility to CAD, but NFKB1A −297C/T and −881A/G polymorphisms had no associations, in a Turkish population , whereas Lai et al.  found that rs28362491 polymorphism had a critical role and was related to functional interleukin (IL)-6 expression in a Chinese Uygur population. In an Iranian subpopulation, rs28362491 polymorphism, but not NFKB1A −826C/T polymorphism, was found to be significantly associated with the development and severity of CAD as an independent risk factor . In research into an NFKB1 promoter variant in coronary heart diseases (CHDs) of people of European ancestry, Vogel et al.  reported that a variant previously found to lead to partial depletion of NF-κB p50 is associated with CHD. The participation of rs28362491 polymorphism in CAD in Korean and Chinese populations was reported more recently [24, 25]. There is general agreement that inflammation occupies a pivotal role in both initiation and progression of coronary atherosclerosis is the necessarily condition for CHD. Jin et al.  concluded that the del/del genotype of rs28362491 is associated with the risk and the severity of the disease.
NF-κB is a good illustration of two sides of the same coin. While a majority of authors mention that NF-κB activation is associated with normal conditioning, Peterson et al. , using a murine model of Duchenne muscular dystrophy, report the importance of NF-κB blocking in normal cardiac function.
MicroRNAs (miRNAs) are noncoding, single-stranded RNAs around 20–22 nucleotides in length, which organize gene expression through posttranscriptional repression  and are members of a large array of remodification processes, such as cellular differentiation, proliferation, development, immunity, apoptosis, and angiogenesis [28,29,30], but these are linked to several chronic and acute diseases, such as heart diseases, cancer, acute organ injury, autoimmunity, and ischemic stroke, when they are dysregulated [31,32,33,34]. In a major advance for understanding inflammatory diseases, Taganov et al.  noted that an NF-κB-targeting actor, namely, mir-146a, enhances the inflammatory response by being used as a feedback inhibitor of NF-κB activation. Generally, the expression level of mature miRNA-146a may be regulated by SNPs of pre-miR-146a. An SNP located in the stem region, namely, rs2910164, may modify the transcription of genes involved putatively in the pathogenesis of inflammation-related diseases, such as cardiovascular diseases, reducing the total amount of mature miRNA [36, 37].
More recently, literature has emerged that describes consistent findings for mir-146a SNP. Xiong et al.  reported that a G-to-C substitution in the precursor of mir-146a seems to lead to the enhanced expression of mature mir-146a. This is in agreement with findings by Guo et al.  that the function of TH-1 cells, which is necessary for the progression of acute coronary syndrome, is stimulated by increased mature mir-146a expression levels.
The following findings also seem to be consistent with this research, which found significant differences within atherosclerotic patients compared with control subjects, concerning pre-miR-146a rs2910164 polymorphism. The G allele and GG genotype were associated with an elevated risk for atherosclerosis thus pre-miR-146a rs2910164 is assumed to play a role as a novel marker for possible atherosclerosis susceptibility .
The link between obesity and obesity-related disorders can be explained by inflammation, which is noticed as an elevation in circulating levels of C-reactive protein (CRP) with low-grade inflammation [40, 41]. The debate about the association of NFKB1 with obesity has gained fresh prominence, with many arguing that NF-κB is weakly initiated in a nonobese murine model of type 1 diabetes , whereas NF-κB is directly correlated with pancreatic β-cell failure within diabetes . However, we previously concluded that the ins allele of NFKB1 rs28362491 and/or ins/ins genotype is related to morbid obesity in a Turkish population . These findings are in contrast to those of Stegger et al. , who found no substantial interaction between rs28362491 and gluteofemoral, abdominal, and general obesity in a Danish population.
Morbid obesity is correlated with elevated circulating systemic acute-phase proteins, namely, CRP, and the expression of CRP is regulated by the p50 homodimer of NFKB1. We found that the rs28362491 deletion variant tends to decrease the p50 subunit level and that increased serum CRP levels are correlated with NFKB1 rs28362491 polymorphism . By modulating serum levels of CRP, this polymorphism may be correlated with morbid obesity.
There is good evidence for an association among toll-like receptor (TLR) polymorphisms, hepatic fat accumulation, and chronic inflammation, and the NF-κB gene appears to play a key role. We reported that TLR2 variants, such as rs5743708 (G/G), and high levels of liver enzymes, such as alanine transaminase, alkaline phosphatase, aspartate transaminase, and γ-glutamyl transpeptidase, are associated with high levels of CRP . These results are important for 2 main reasons. First, detecting the ins allele of rs28362491 and Arg753Gln allele of rs5743708, combined with a high level of CRP, may offer better treatments in the future. Second, NFKB1 may be useful to monitor both the course and severity of liver disease, suggesting new trends of therapies for these conditions.
Male infertility accounts for approximately 50% of infertility cases, even though 60% of whole infertility cases are idiopathic . Severe oligozoospermia or azoospermia is responsible for most idiopathic male infertility. The interaction between the egg and the sperm is a key point, but the molecular mechanisms of egg–sperm membrane protein binding and fusion reactions are not fully clarified.
NFKB1 is a candidate gene in spermatogenesis, whose failure may lead to male infertility [48, 49]. The relationship of the variants of the promoter sites of NFKB1 with numerous diseases has been studied widely. Ranganathan et al.  have associated decreased NFKB1 expression with poor sperm production.
The E-cadherin short interfering RNA (siRNA) is known to trigger the stimulation of NF-κB transcriptional activity . α-Catenin and E-cadherin are validated to be good indices of infertility . Hernandez Gifford et al.  proposed anti-catenin/anti-cadherin antibodies for male contraception, and Purohit et al.  reported the absence of E-cadherin on the head domain of spermatozoa from oligospermic individuals; however, as yet, the precise mechanisms of both recognition and fusion processes remain to be elucidated. We found increased risk of development of male infertility associated with the presence of the ins allele of NFKB1. Moreover, in the context of low E-cadherin expression, NFKB1 rs28362491 ins/ins and del/del genotypes are likely to display an essential role in the case of susceptibility to oligospermic male infertility . In other works, we were not able to find any correlation of rs28362491 within NFKB1 or the rs696 polymorphisms within NFKB1A in cases of elevated apoptosis in oligospermia. However, we concluded that the rs28362491 heterozygosity is likely to play a protective role by altering oligospermia susceptibility . Consistent with these findings, in the context of E-cadherin and fibronectin levels, we found that the insertion allele within the promoter region of NFKB1 is presumably a key function in the susceptibility to normospermic male infertility .
There is other evidence to suggest that the NF-κB also contributes to female infertility. In a murine model, Wang et al. confirmed the idea that intrauterine adhesion results in impaired pregnancy and concluded that NF-κB activation is notably increased within the endometrial tissues of patients with Asherman syndrome .
Hashimoto disease is a common chronic inflammation-based disorder present in the thyroid gland influenced by the interplay between various cytokines, and the potential risk factors for Hashimoto disease have been studied widely for decades .
As NF-κB is at the center of all autoimmune diseases, and since inflammation is inevitable, we have previously analyzed the associations of polymorphisms of rs28362491 within NFKB1 and rs696 within NFKBIA with susceptibility to Hashimoto disease. There was no significant association between the frequency of the alleles of these two variants and the genotypes. In a combined genotype analysis of NFKB1 and NFKBIA polymorphisms, instead, the ins/ins/AG combined genotype was negatively associated with Hashimoto disease, which predominantly depends on the G allele of rs696 in the Turkish population. In the presence of at least one G allele, the IL-6 levels were also higher in patients with the del/del genotype . Elevated serum IL-6 levels were correlated with the del allele of rs2836249. Therefore, polymorphism of the functional NFKB1 rs28362491 promoter was significantly associated with modulated IL-6 levels in the population with Hashimoto disease .
Graves disease is classified as a distinctive organ-specific inflammatory and autoimmunity-based disease of the thyroid, defined by dermopathy, hyperthyroidism, an ocular disorder, and especially diffuse goiter. At least 79% of genetic factors are involved in this disorder; cooperation between several inflammation-related genes, such as NFKB1 and NFKBIA, and cytokines, may have an impact on the development of Graves disease. An association study within a Turkish population found that the rs28362491 del/ins genotype is a possible candidate variation for the development of Graves disease, whereas the ins/ins genotype is likely to play a protective role in this disorder. By contrast, in the case of rs696, there were no statistical differences between the groups . The levels of cytokines IL-1β, IL-6, and tumor necrosis factor (TNF)-α showed remarkable associations with variations in NFKB1 rs28362491. Kurylowicz et al.  found that susceptibility to Graves disease is associated with NFKB1 rs28362491 polymorphism within a Polish population.
Behçet syndrome is both a systemic autoimmune disorder and a chronic inflammatory disease defined by ocular inflammation, recurrent vasculitis, oral and genital ulcers, and skin lesions . Although there is some evidence for the involvement of both environmental and genetic factors, Behçet syndrome remains classified as a disease of unknown origin. NFKB1 and its inhibitor, NFKBIA, are important actors in the inflammatory cascade of Behçet syndrome.
The promoter region polymorphisms of NFKB1 in Behçet syndrome could lead to modified NFKB1 expression, which then promotes altered inflammatory cytokine transcription and might clarify the elevated expression and serum concentrations of these cytokines. In an association study in a Turkish population, the association of NFKB1 rs28362491 polymorphism with the ins allele and ins/ins genotype of rs28362491 is found to increase susceptibility to Behçet syndrome by 1.8- and 2.5-fold, respectively  (Tables 1 and 2). There appears to be no doubt that NF-κB inhibition is caused by binding of an inhibitor (IKBα) that is encoded by NFKBIA, and any instability of this binding may lead to progression of inflammatory diseases. Hung et al. , in their study of Behçet syndrome, found an association with NFKBIA promoter polymorphisms, including −826 T/T, −826 C/T, 519C/T, and −881A/G, and −550A/T, and reported a correlation with the −826 T/T genotype and characteristic skin lesions. Consistent with these studies, we observed an rs696 AA genotype within NFKBIA as a factor that leads to a 2.5-times-increased risk for development of Behçet syndrome . By contrast, assuming them as variations, Kaustio et al.  associated NFKB1 mutations, such as I553M and H67R, with Behçet syndrome-like phenotypes.
Genotype assessment of SNPs rs28362491 within NFKB1A and rs696 within NFKB1 in inflammatory disorders and glioma in the Turkish population
SNP, single-nucleotide polymorphism; WW, wild homozygote (ins-ins for rs28362491, AA for rs696); WD, heterozygote (ins-del for rs28362491, AG for rs696); DD, mutant homozygote (del-del for rs28362491, GG for rs696).
Assessment of SNP alleles rs28362491 within NFKB1A and rs696 within NFKB1 in inflammatory disorders and glioma in the Turkish population
Elevated NF-κB activation has also been related to cancer progression . In cancer, the process that controls gene expression in response to inflammatory stimuli combines its survival with both its phenotype and function with the rest of the tissue . This is generally apparent in strictly compromised regulation of NF-κB activity, which enables abnormal cohorts of the NF-κB target gene expression in cancer cells . The conclusion is not only that the cells of surrounding tissue change their function and fail to support the organism exclusively, but also that the cancer cells function abnormally. Instability of NF-κB and IκB interactions have been observed generally in several diseases; however, the mechanisms behind the association between certain variations within different genes and cancer development remain elusive.
Glioblastoma (glioblastoma multiforme), accounting for less than 2% of all human cancers, is the most malignant primary brain tumor in the adult nervous system [72, 73]. Although the origin of glioblastoma development is still unknown, some genetic modifications that lead to aberrant activity of pathways, such as proliferation, apoptosis, and cell cycle regulation, are considered to contribute to their pathogenesis [74, 75].
Deregulated NF-κB activity has become a central issue in the development of most human cancers [76, 77]. NF-κB organizes cancer aggressiveness and development by increasing angiogenesis, antiapoptosis, and tumor proliferation and by reducing the immune response and thus managing pathogenetic regulation .
Numerous studies advocate the idea that several malignant tumor types, including glioblastomas, have strong connections with NF-κB cascades [5, 79]. We have evaluated 120 glioma samples and 225 controls. There are significant associations between insertion allele carriers and elevated risk of gliomas  (Tables 1 and 2). Previous studies reported conflicting results. Meta-analyses such as those conducted by Sun et al.  and Yu et al. , for instance, concluded that the deletion allele is both a risk and a protection against cancer susceptibility in populations with European or Asian ancestry. The rs28362491 del/del genotype appears related to bladder, prostate, oral, and ovarian cancers but not with hepatocellular carcinoma . Concetti and Wilson reviewed the status of this polymorphism and concluded that rs28362491 polymorphism is disadvantageous for colorectal, gastric, liver, bladder, and thyroid cancers but advantageous for prostate, ovarian, and cervical cancers . Similarly, rs28362491 polymorphism was found to be associated with decreased cancer risk , as well as the development of head and neck cancer , and rs696 polymorphism was found to be associated with colorectal cancer risk .
Various NFKB1 variations in specific pathways are associated with cancer progression, but blocking a signaling pathway in multifactorial diseases such as cancer may not be appropriate because the polymorphisms can be advantageous for the individual.
NF-κB as a therapeutic target for inflammatory diseases and cancer
Abnormal activation of NF-κB is commonly noticed in several inflammatory diseases and cancers. Thus, to advance therapeutic applications in cancer and inflammatory diseases, there has been increased interest in inhibiting NF-κB signaling. Many natural products used for their alleged anti-inflammatory and cancer-preventing activities have been found to inhibit NF-κB; therefore, dysregulations in NF-κB signaling may potentially be connected to certain cancers and inflammatory diseases [87, 88]. Characterization of these natural products is warranted.
In lymphoid, colon, breast, skin, and prostate cancers, prior persistent activation of NF-κB signaling is found; hence, the therapeutic inhibition of NF-κB signaling in malignant cells may provide a strategy for anticancer drug development.
Miller et al. screened approximately 2,800 clinically approved drugs to identify small molecule inhibitors of NF-κB signaling. Drugs such as bithionol, emetine, tribromsalan, metformin, lestaurtinib, sunitinib malate, and narasin were observed to inhibit NF-κB signaling through inhibition of IκBα phosphorylation, whereas bortezomib, chromomycin A3, and ecteinascidin 743 act through other mechanisms . According to these findings, many currently approved pharmaceuticals have unpredictable impacts on the NF-κB signaling cascade; therefore, more detailed characterization of approved drugs might broaden the horizon of knowledge of their molecular mechanisms. Yamamoto et al.  highlighted a type of drug utilized in the treatment of inflammatory disease, which has an impact on NF-κB activity, which, in turn, leads to numerous therapeutic strategies aimed at blocking NF-κB activity.
According to a survey conducted by Tak and Firestein , the mode of action of corticosteroids, preferred in the treatment of psoriasis, asthma, rheumatoid arthritis, and inflammatory bowel disease, for instance, is presumably modulated by inhibiting NF-κB activation. Similarly, nonsteroidal anti-inflammatory drugs, such as leflunomide and sulfasalazine, inhibit nuclear translocation of NF-κB by inhibiting IκBα degradation . The most preferable NF-κB-related inhibitors are selective IκB kinase inhibitors that block the catalytic activity of IκB kinase; and hence the IκBα phosphorylation; proteasome inhibitors; inhibitors that prevent nuclear translocation of NF-κB subunits; and drugs that block the DNA-binding activity of NF-κB. Kiliccioglu et al. , e.g., reported the importance of NF-κB and Hsp-27 inhibition, along with therapies for inhibition of androgen receptor variant-7. However, because of the lack of specificity of these drugs, relatively high concentrations were required to achieve strong inhibition of NF-κB.
We concluded in an in vitro study that metformin serves as a potential agent for breast cancer treatment in a dose-dependent manner. We observed that metformin blocked NF-κB through the prevention of the latter's nuclear translocation and reduced the expression of proteins such as matrix metalloproteinase (MMP)-2 and MMP-9, which are required for the invasion in breast cancer . Metformin might have a protective function against breast cancer by regulating NF-κB.
There are differences between mechanisms of regulating NFKB1 and NFKB1A and the autoimmune diseases discussed. We sought to supply a general update on the association of NFKB1 and NFKB1A variations with their inhibitory effects on inflammatory diseases, as blocking NF-κB activation may open a path to new therapies. Despite its exploratory nature, the analysis of these polymorphisms undertaken here offers some insight into new therapies for, and has extended our knowledge of, the genetic variation in inflammation-related disorders.
Coussens LM, Werb Z. Inflammation and cancer. Nature. 2002; 420:860–7.CoussensLMWerbZInflammation and cancer2002420860710.1038/nature01322Search in Google Scholar
Oeckinghaus A, Ghosh S. The NF-κB family of transcription factors and its regulation. Cold Spring Harb Perspect Biol. 2009; 1:a000034. doi: 10.1101/cshperspect.a000034OeckinghausAGhoshSThe NF-κB family of transcription factors and its regulation20091a00003410.1101/cshperspect.a000034DOI öffnenSearch in Google Scholar
Héron E, Deloukas P, van Loon APGM. The complete exon-intron structure of the 156-kb human gene NFKB1, which encodes the p105 and p50 proteins of transcription factors NF-κB and IκB-γ: implications for NF-κB-mediated signal transduction. Genomics. 1995; 30:493–505.HéronEDeloukasPvan LoonAPGMThe complete exon-intron structure of the 156-kb human gene NFKB1, which encodes the p105 and p50 proteins of transcription factors NF-κB and IκB-γ: implications for NF-κB-mediated signal transduction19953049350510.1006/geno.1995.1270Search in Google Scholar
Le Beau MM, Ito C, Cogswell P, Espinosa R 3rd, Fernald AA, Baldwin AS Jr. Chromosomal localization of the genes encoding the p50/p105 subunits of NF-κB (NFKB2) and the IκB/MAD-3 (NFKBI) inhibitor of NF-κB to 4q24 and 14q13, respectively. Genomics. 1992; 14:529–31.Le BeauMMItoCCogswellPEspinosaR3rdFernaldAABaldwinASJrChromosomal localization of the genes encoding the p50/p105 subunits of NF-κB (NFKB2) and the IκB/MAD-3 (NFKBI) inhibitor of NF-κB to 4q24 and 14q13, respectively1992145293110.1016/S0888-7543(05)80261-7Search in Google Scholar
Karban AS, Okazaki T, Panhuysen CI, Gallegos T, Potter JJ, Bailey-Wilson JE, et al. Functional annotation of a novel NFKB1 promoter polymorphism that increases risk for ulcerative colitis. Hum Mol Genet. 2004; 13:35–45.KarbanASOkazakiTPanhuysenCIGallegosTPotterJJBailey-WilsonJEFunctional annotation of a novel NFKB1 promoter polymorphism that increases risk for ulcerative colitis200413354510.1093/hmg/ddh00814613970Search in Google Scholar
Zhou Y, Eppenberger-Castori S, Marx C, Yau C, Scott GK, Eppenberger U, Benz CC. Activation of nuclear factor-κB (NFκB) identifies a high-risk subset of hormone-dependent breast cancers. Int J Biochem Cell Biol. 2005; 37:1130–44.ZhouYEppenberger-CastoriSMarxCYauCScottGKEppenbergerUBenzCCActivation of nuclear factor-κB (NFκB) identifies a high-risk subset of hormone-dependent breast cancers20053711304410.1016/j.biocel.2004.09.00615743683Search in Google Scholar
Li R-N, Hung Y-H, Lin C-H, Chen Y-H, Yen J-H. Inhibitor IκBα promoter functional polymorphisms in patients with rheumatoid arthritis. J Clin Immunol. 2010; 30:676–80.LiR-NHungY-HLinC-HChenY-HYenJ-HInhibitor IκBα promoter functional polymorphisms in patients with rheumatoid arthritis2010306768010.1007/s10875-010-9439-920563630Search in Google Scholar
Chen F, Castranova V, Shi X, Demers LM. New insights into the role of nuclear factor-κB, a ubiquitous transcription factor in the initiation of diseases. Clin Chem. 1999; 45:7–17.ChenFCastranovaVShiXDemersLMNew insights into the role of nuclear factor-κB, a ubiquitous transcription factor in the initiation of diseases19994571710.1093/clinchem/45.1.7Search in Google Scholar
Dong QG, Sclabas GM, Fujioka S, Schmidt C, Peng B, Wu T, et al. The function of multiple IκB: NF-κB complexes in the resistance of cancer cells to Taxol-induced apoptosis. Oncogene. 2002; 21:6510–19.DongQGSclabasGMFujiokaSSchmidtCPengBWuTThe function of multiple IκB: NF-κB complexes in the resistance of cancer cells to Taxol-induced apoptosis20022165101910.1038/sj.onc.120584812226754Search in Google Scholar
Hayden MS, Ghosh S. Shared principles in NF-κB signaling. Cell. 2008; 132:344–62.HaydenMSGhoshSShared principles in NF-κB signaling20081323446210.1016/j.cell.2008.01.02018267068Search in Google Scholar
Karin M. NF-κB as a critical link between inflammation and cancer. Cold Spring Harb Perspect Biol. 2009; 1:a000141. doi: 10.1101/cshperspect.a000141KarinMNF-κB as a critical link between inflammation and cancer20091a00014110.1101/cshperspect.a000141277364920066113DOI öffnenSearch in Google Scholar
Madrid LV, Mayo MW, Reuther JY, Baldwin AS Jr. Akt stimulates the transactivation potential of the RelA/p65 Subunit of NF-κB through utilization of the IκB kinase and activation of the mitogen-activated protein kinase p38. J Biol Chem. 2001; 276:18934–40.MadridLVMayoMWReutherJYBaldwinASJrAkt stimulates the transactivation potential of the RelA/p65 Subunit of NF-κB through utilization of the IκB kinase and activation of the mitogen-activated protein kinase p382001276189344010.1074/jbc.M10110320011259436Search in Google Scholar
Gupta SC, Sundaram C, Reuter S, Aggarwal BB. Inhibiting NF-κB activation by small molecules as a therapeutic strategy. Biochim Biophys Acta. 2010; 1799:775–87.GuptaSCSundaramCReuterSAggarwalBBInhibiting NF-κB activation by small molecules as a therapeutic strategy201017997758710.1016/j.bbagrm.2010.05.004295598720493977Search in Google Scholar
Saggu R, Schumacher T, Gerich F, Rakers C, Tai K, Delekate A, Petzold GC. Astroglial NF-kB contributes to white matter damage and cognitive impairment in a mouse model of vascular dementia. Acta Neuropathol Commun. 2016; 4:76. doi: 10.1186/s40478-016-0350-3SagguRSchumacherTGerichFRakersCTaiKDelekateAPetzoldGCAstroglial NF-kB contributes to white matter damage and cognitive impairment in a mouse model of vascular dementia201647610.1186/s40478-016-0350-3497306127487766DOI öffnenSearch in Google Scholar
Best KT, Lee FK, Knapp E, Awad HA, Loiselle AE. Deletion of NFKB1 enhances canonical NF-κB signaling and increases macrophage and myofibroblast content during tendon healing. Sci Rep. 2019; 9:10926. doi: 10.1038/s41598-019-47461-5BestKTLeeFKKnappEAwadHALoiselleAEDeletion of NFKB1 enhances canonical NF-κB signaling and increases macrophage and myofibroblast content during tendon healing201991092610.1038/s41598-019-47461-5666278931358843DOI öffnenSearch in Google Scholar
Stone S, Jamison S, Yue Y, Durose W, Schmidt-Ullrich R, Lin W. NF-κB activation protects oligodendrocytes against inflammation. J Neurosci. 2017; 20;37:9332–44.StoneSJamisonSYueYDuroseWSchmidt-UllrichRLinWNF-κB activation protects oligodendrocytes against inflammation2017203793324410.1523/JNEUROSCI.1608-17.2017560747228842413Search in Google Scholar
Gareus R, Kotsaki E, Xanthoulea S, van der Made I, Gijbels MJ, Kardakaris R, et al. Endothelial cell-specific NF-κB inhibition protects mice from atherosclerosis. Cell Metab. 2008; 8:372–83.GareusRKotsakiEXanthouleaSvan der MadeIGijbelsMJKardakarisREndothelial cell-specific NF-κB inhibition protects mice from atherosclerosis200883728310.1016/j.cmet.2008.08.01619046569Search in Google Scholar
Fontaine-Bisson B, Wolever TM, Connelly PW, Corey PN, El-Sohemy A. NF-κB–94Ins/Del ATTG polymorphism modifies the association between dietary polyunsaturated fatty acids and HDL-cholesterol in two distinct populations. Atherosclerosis. 2009; 204:465–70.Fontaine-BissonBWoleverTMConnellyPWCoreyPNEl-SohemyANF-κB–94Ins/Del ATTG polymorphism modifies the association between dietary polyunsaturated fatty acids and HDL-cholesterol in two distinct populations20092044657010.1016/j.atherosclerosis.2008.10.03719070859Search in Google Scholar
Özbilüm N, Arslan S, Berkan Ö, Yanartaş M, Aydemir EI. The role of NF-κB1A promoter polymorphisms on coronary artery disease risk. Basic Clin Pharmacol Toxicol. 2013; 113:187–92.ÖzbilümNArslanSBerkanÖYanartaşMAydemirEIThe role of NF-κB1A promoter polymorphisms on coronary artery disease risk20131131879210.1111/bcpt.1208523692311Search in Google Scholar
Oner T, Arslan C, Yenmis G, Arapi B, Tel C, Aydemir B, Sultuybek GK. Association of NFKB1A and microRNAs variations and the susceptibility to atherosclerosis. J Genet. 2017; 96:251–9.OnerTArslanCYenmisGArapiBTelCAydemirBSultuybekGKAssociation of NFKB1A and microRNAs variations and the susceptibility to atherosclerosis201796251910.1007/s12041-017-0768-928674224Search in Google Scholar
Lai H-M, Li X-M, Yang Y-N, Ma Y-T, Xu R, Pan S, et al. Genetic variation in NFKB1 and NFKBIA and susceptibility to coronary artery disease in a Chinese Uygur population. PLoS One. 2015; 10:e0129144. doi: 10.1371/journal.pone.0129144LaiH-MLiX-MYangY-NMaY-TXuRPanSGenetic variation in NFKB1 and NFKBIA and susceptibility to coronary artery disease in a Chinese Uygur population201510e012914410.1371/journal.pone.0129144DOI öffnenSearch in Google Scholar
Seidi A, Mirzaahmadi S, Mahmoodi K, Soleiman-Soltanpour M. The association between NFKB1 -94ATTG ins/del and NFKB1A 826C/T genetic variations and coronary artery disease risk. Mol Biol Res Commun. 2018; 7:17–24.SeidiAMirzaahmadiSMahmoodiKSoleiman-SoltanpourMThe association between NFKB1 -94ATTG ins/del and NFKB1A 826C/T genetic variations and coronary artery disease risk201871724Search in Google Scholar
Vogel U, Jensen MK, Due KM, Rimm EB, Wallin H, Nielsen MR, et al. The NFKB1 ATTG ins/del polymorphism and risk of coronary heart disease in three independent populations. Atherosclerosis. 2011; 219:200–4.VogelUJensenMKDueKMRimmEBWallinHNielsenMRThe NFKB1 ATTG ins/del polymorphism and risk of coronary heart disease in three independent populations2011219200410.1016/j.atherosclerosis.2011.06.018Search in Google Scholar
Kim SK, Jang HM, Kim D-Y. The promoter polymorphism of NFKB1 gene contributes to susceptibility of ischemic stroke in Korean population. J Exerc Rehabil. 2018;14:1096–1100.KimSKJangHMKimD-YThe promoter polymorphism of NFKB1 gene contributes to susceptibility of ischemic stroke in Korean population2018141096110010.12965/jer.1836592.296Search in Google Scholar
Jin S-Y, Luo J-Y, Li X-M, Liu F, Ma Y-T, Gao X-M, Yang Y-N. NFKB1 gene rs28362491 polymorphism is associated with the susceptibility of acute coronary syndrome. Biosci Rep. 2019; 39:BSR20182292. doi: 10.1042/BSR20182292JinS-YLuoJ-YLiX-MLiuFMaY-TGaoX-MYangY-NNFKB1 gene rs28362491 polymorphism is associated with the susceptibility of acute coronary syndrome201939BSR20182292.10.1042/BSR20182292DOI öffnenSearch in Google Scholar
Peterson JM, Wang DJ, Shettigar V, Roof SR, Canan BD, Bakkar N, et al. NF-κB inhibition rescues cardiac function by remodeling calcium genes in a Duchenne muscular dystrophy model. Nat Commun. 2018; 9:3431. doi: 10.1038/s41467-018-05910-1.PetersonJMWangDJShettigarVRoofSRCananBDBakkarNNF-κB inhibition rescues cardiac function by remodeling calcium genes in a Duchenne muscular dystrophy model20189343110.1038/s41467-018-05910-1DOI öffnenSearch in Google Scholar
Bartel DP. MicroRNAs: genomics, biogenesis, mechanism, and function. Cell. 2004; 116:281–97.BartelDPMicroRNAs: genomics, biogenesis, mechanism, and function20041162819710.1016/S0092-8674(04)00045-5Search in Google Scholar
Chen Y, Fu LL, Wen X, Liu B, Huang J, Wang JH, et al. Oncogenic and tumor suppressive roles of microRNAs in apoptosis and autophagy. Apoptosis. 2014; 19:1177–89.ChenYFuLLWenXLiuBHuangJWangJHOncogenic and tumor suppressive roles of microRNAs in apoptosis and autophagy20141911778910.1007/s10495-014-0999-724850099Search in Google Scholar
O’Neill LA, Sheedy FJ, McCoy CE. MicroRNAs: the fine-tuners of Toll-like receptor signalling. Nat Rev Immunol. 2011; 11:163–75.O’NeillLASheedyFJMcCoyCEMicroRNAs: the fine-tuners of Toll-like receptor signalling2011111637510.1038/nri295721331081Search in Google Scholar
Winter J, Jukng S, Keller S, Gregory RI, Diederich S. Many roads to maturity: microRNA biogenesis pathways and their regulation. Nat Cell Biol. 2009; 11:228–34.WinterJJukngSKellerSGregoryRIDiederichSMany roads to maturity: microRNA biogenesis pathways and their regulation2009112283410.1038/ncb0309-22819255566Search in Google Scholar
Ma Y, Wang J, Wang Y, Yang G-Y. The biphasic function of microglia in ischemic stroke. Prog Neurobiol. 2017; 157:247–72.MaYWangJWangYYangG-YThe biphasic function of microglia in ischemic stroke20171572477210.1016/j.pneurobio.2016.01.00526851161Search in Google Scholar
Bhalala OG, Srikanth M, Kessler JA. The emerging roles of microRNAs in CNS injuries. Nat Rev Neurol. 2013; 9:328–39.BhalalaOGSrikanthMKesslerJAThe emerging roles of microRNAs in CNS injuries201393283910.1038/nrneurol.2013.67375589523588363Search in Google Scholar
Zhang L, Huang J, Yang N, Greshock J, Megraw MS, Giannakakis A, et al. MicroRNAs exhibit high frequency genomic alterations in human cancer. Proc Natl Acad Sci USA. 2006; 103:9136–41.ZhangLHuangJYangNGreshockJMegrawMSGiannakakisAMicroRNAs exhibit high frequency genomic alterations in human cancer200610391364110.1073/pnas.0508889103147400816754881Search in Google Scholar
Davidson-Moncada J, Papavasiliou FN, Tam W. MicroRNAs of the immune system. Roles in inflammation and cancer. Ann N Y Acad Sci. 2010; 1183:183–94.Davidson-MoncadaJPapavasiliouFNTamWMicroRNAs of the immune system. Roles in inflammation and cancer201011831839410.1111/j.1749-6632.2009.05121.x287671220146715Search in Google Scholar
Taganov KD, Boldin MP, Chang K-J, Baltimore D. NF-κB-dependent induction of microRNA miR-146, an inhibitor targeted to signaling proteins of innate immune responses. Proc Natl Acad Sci USA. 2006; 103:12481–86.TaganovKDBoldinMPChangK-JBaltimoreDNF-κB-dependent induction of microRNA miR-146, an inhibitor targeted to signaling proteins of innate immune responses2006103124818610.1073/pnas.0605298103156790416885212Search in Google Scholar
Hashemi M, Eskandari-Nasab E, Zakeri Z, Atabaki M, Bahari G, et al. Association of premiRNA-146a rs2910164 and pre-miRNA-499 rs3746444 polymorphisms and susceptibility to rheumatoid arthritis. Mol Med Rep. 2013; 7:287–91.HashemiMEskandari-NasabEZakeriZAtabakiMBahariGAssociation of premiRNA-146a rs2910164 and pre-miRNA-499 rs3746444 polymorphisms and susceptibility to rheumatoid arthritis201372879110.3892/mmr.2012.117623138379Search in Google Scholar
Jazdzewski K, Murray EL, Franssila K, Jarzab B, Schoenberg DR, de la Chapelle A. Common SNP in premiR-146a decreases mature miR expression and predisposes to papillary thyroid carcinoma. Proc Natl Acad Sci USA. 2008; 105:7269–74.JazdzewskiKMurrayELFranssilaKJarzabBSchoenbergDRde la ChapelleACommon SNP in premiR-146a decreases mature miR expression and predisposes to papillary thyroid carcinoma200810572697410.1073/pnas.0802682105243823918474871Search in Google Scholar
Xiong XD, Cho M, Cai XP, Cheng J, Jing X, Cen JM, et al. A common variant in pre-miR-146 is associated with coronary artery disease risk and its mature miRNA expression. Mutat Res Fund Mol. 2014; 761:15–20.XiongXDChoMCaiXPChengJJingXCenJMA common variant in pre-miR-146 is associated with coronary artery disease risk and its mature miRNA expression2014761152010.1016/j.mrfmmm.2014.01.00124447667Search in Google Scholar
Guo M, Mao X, Ji Q, Lang M, Li S, Peng Y, et al. miR146a in PBMCs modulates Th1 function in patients with acute coronary syndrome. Immunol Cell Biol. 2010; 88:555–64.GuoMMaoXJiQLangMLiSPengYmiR146a in PBMCs modulates Th1 function in patients with acute coronary syndrome2010885556410.1038/icb.2010.1620195282Search in Google Scholar
Dalmas E, Rouault C, Abdennour M, Rovere C, Rizkalla S, Bar-Hen A, et al. Variations in circulating inflammatory factors are related to changes in calorie and carbohydrate intakes early in the course of surgery-induced weight reduction. Am J Clin Nutr. 2011; 94:450–8.DalmasERouaultCAbdennourMRovereCRizkallaSBar-HenAVariations in circulating inflammatory factors are related to changes in calorie and carbohydrate intakes early in the course of surgery-induced weight reduction201194450810.3945/ajcn.111.01377121677057Search in Google Scholar
Paepegaey AC, Genser L, Bouillot J-L, Oppert J-M, Clément K, Poitou C. High levels of CRP in morbid obesity: the central role of adipose tissue and lessons for clinical practice before and after bariatric surgery. Surg Obes Relat Dis. 2015; 11:148–54.PaepegaeyACGenserLBouillotJ-LOppertJ-MClémentKPoitouCHigh levels of CRP in morbid obesity: the central role of adipose tissue and lessons for clinical practice before and after bariatric surgery2015111485410.1016/j.soard.2014.06.01025393045Search in Google Scholar
Irvin AE, Jhala G, Zhao Y, Blackwell TS, Krishnamurthy B, Thomas HE, Kay TWH. NF-κB is weakly activated in the NOD mouse model of type 1 diabetes. Sci Rep. 2018; 8:4217. doi: 10.1038/s41598-018-22738-3IrvinAEJhalaGZhaoYBlackwellTSKrishnamurthyBThomasHEKayTWHNF-κB is weakly activated in the NOD mouse model of type 1 diabetes20188421710.1038/s41598-018-22738-3DOI öffnenSearch in Google Scholar
Meyerovich K, Ortis F, Cardozo AK. The non-canonical NF-κB pathway and its contribution to β-cell failure in diabetes. J Mol Endocrinol. 2018; 61:F1–6.MeyerovichKOrtisFCardozoAKThe non-canonical NF-κB pathway and its contribution to β-cell failure in diabetes201861F1610.1530/JME-16-0183Search in Google Scholar
Yenmis G, Soydas T, Arkan H, Tasan E, Kanigur Sultuybek G. Genetic variation in NFKB1 gene influences liver enzyme levels in morbidly obese women. Arch Iran Med. 2018; 21:13–18.YenmisGSoydasTArkanHTasanEKanigur SultuybekGGenetic variation in NFKB1 gene influences liver enzyme levels in morbidly obese women2018211318Search in Google Scholar
Stegger JG, Schmidt EB, Berentzen TL, Tjønneland A, Vogel U, Rimm E, et al. Interaction between obesity and the NFKB1 – 94ins/delATTG promoter polymorphism in relation to incident acute coronary syndrome: a follow up study in three independent cohorts. PLoS One. 2013; 8:1–8.SteggerJGSchmidtEBBerentzenTLTjønnelandAVogelURimmEInteraction between obesity and the NFKB1 – 94ins/delATTG promoter polymorphism in relation to incident acute coronary syndrome: a follow up study in three independent cohorts201381810.1371/journal.pone.0063004Search in Google Scholar
Soydas T, Karaman O, Arkan H, Yenmis G, Ilhan MM, Tombulturk K, et al. The correlation of increased CRP levels with NFKB1 and TLR2 polymorphisms in the case of morbid obesity. Scand J Immunol. 2016; 84:278–3.SoydasTKaramanOArkanHYenmisGIlhanMMTombulturkKThe correlation of increased CRP levels with NFKB1 and TLR2 polymorphisms in the case of morbid obesity201684278310.1111/sji.12471Search in Google Scholar
Guzick DS, Overstreet JW, Factor-Litvak P, Brazil CK, Nakajima ST, Coutifaris C, et al. Sperm morphology, motility, and concentration in fertile and infertile men. N Engl J Med. 2001; 345:1388–93.GuzickDSOverstreetJWFactor-LitvakPBrazilCKNakajimaSTCoutifarisCSperm morphology, motility, and concentration in fertile and infertile men200134513889310.1056/NEJMoa003005Search in Google Scholar
Carlsen H, Alexander G, Austenaa LMI, Ebihara K, Blomhoff R. Molecular imaging of the transcription factor NF-kB, a primary regulator of stress response. Mutat Res. 2004; 551:199–211.CarlsenHAlexanderGAustenaaLMIEbiharaKBlomhoffRMolecular imaging of the transcription factor NF-kB, a primary regulator of stress response200455119921110.1016/j.mrfmmm.2004.02.024Search in Google Scholar
Yamamoto Y, Gaynor RB. IκB kinases: key regulators of the NF-κB pathway. Trends Biochem Sci 2004; 29:72–9.YamamotoYGaynorRBIκB kinases: key regulators of the NF-κB pathway20042972910.1016/j.tibs.2003.12.003Search in Google Scholar
Ranganathan P, Kattal N, Moustafa MH, Sharma RK, Thomas AJ Jr, Agarwal A. Correlation of nuclear factor kappa B (NFKB) with sperm quality and clinical diagnoses in infertile men. Fertil Steril. 2002; 78:S95 [abstract]RanganathanPKattalNMoustafaMHSharmaRKThomasAJJrAgarwalACorrelation of nuclear factor kappa B (NFKB) with sperm quality and clinical diagnoses in infertile men200278S95[abstract]10.1016/S0015-0282(02)03631-2Search in Google Scholar
Solanas G, Porta-de-la-Riva M, Agustí C, Casagolda D, Sánchez-Aguilera F, Larriba MJ, et al. E-Cadherin controls β-catenin and NF-κB transcriptional activity in mesenchymal gene expression. J Cell Sci. 2008; 121:2224–34.SolanasGPorta-de-la-RivaMAgustíCCasagoldaDSánchez-AguileraFLarribaMJE-Cadherin controls β-catenin and NF-κB transcriptional activity in mesenchymal gene expression200812122243410.1242/jcs.021667Search in Google Scholar
Aberle H, Schwartz H, Kemler R. Cadherin-catenin complex: protein interactions and their implications for cadherin function. J Cell Biochem. 1996; 61:514–23.AberleHSchwartzHKemlerRCadherin-catenin complex: protein interactions and their implications for cadherin function1996615142310.1002/(SICI)1097-4644(19960616)61:4<514::AID-JCB4>3.0.CO;2-RSearch in Google Scholar
Hernandez Gifford JA, Hunzicker-Dunn ME, Nilson JH. Conditional deletion of beta-catenin mediated by Amhr2cre in mice causes female infertility. Biol Reprod. 2009; 80:1282–92.Hernandez GiffordJAHunzicker-DunnMENilsonJHConditional deletion of beta-catenin mediated by Amhr2cre in mice causes female infertility20098012829210.1095/biolreprod.108.072280280480519176883Search in Google Scholar
Purohit S, Brahmaraju M, Palta A, Shukla S, Laloraya M, Kumar PG. Impaired E-Cadherin expression in human spermatozoa in a male factor infertility subset signifies e-cadherin-mediated adhesion mechanisms operative in sperm–oolemma interactions. Biochem Biophys Res Commun. 2004; 316:903–9.PurohitSBrahmarajuMPaltaAShuklaSLalorayaMKumarPGImpaired E-Cadherin expression in human spermatozoa in a male factor infertility subset signifies e-cadherin-mediated adhesion mechanisms operative in sperm–oolemma interactions2004316903910.1016/j.bbrc.2004.02.13315033487Search in Google Scholar
Tunçdemir M, Yenmiş G, Tombultürk K, Arkan H, Soydaş T, Tek RB, et al. NFKB1 rs28362491 and pre-miRNA-146a rs2910164 SNPs on E-Cadherin expression in case of idiopathic oligospermia: a case-control study. Int J Reprod BioMed (Yazd). 2018; 16:247–54.TunçdemirMYenmişGTombultürkKArkanHSoydaşTTekRBNFKB1 rs28362491 and pre-miRNA-146a rs2910164 SNPs on E-Cadherin expression in case of idiopathic oligospermia: a case-control study2018162475410.29252/ijrm.16.4.247Search in Google Scholar
Tek B, Elçin P, Tunçdemir M, Onaran İ, Özkara H, Kanıgür Sultuybek G. A role for heterozygosity of NF-κB1 rs28362491 polymorphism in patients with idiopathic oligospermia. Arch Iran Med. 2016; 19:275–81.TekBElçinPTunçdemirMOnaranİÖzkaraHKanıgür SultuybekGA role for heterozygosity of NF-κB1 rs28362491 polymorphism in patients with idiopathic oligospermia20161927581Search in Google Scholar
Elcin P, Burak Tek R, Koc A, Arkan H, Ozkara H, Kanigur-Sultuybek G. Effects of SNPs in nuclear factor kappa-B1, poly (ADP-ribose) polymerase-1 genes on E-Cadherin and fibronectin levels in case of male infertility. Androl Gynecol Curr Res. 2015;3:1–7.ElcinPBurak TekRKocAArkanHOzkaraHKanigur-SultuybekGEffects of SNPs in nuclear factor kappa-B1, poly (ADP-ribose) polymerase-1 genes on E-Cadherin and fibronectin levels in case of male infertility2015317Search in Google Scholar
Wang X, Ma N, Sun Q, Huang C, Liu Y, Luo X. Elevated NF-κB signaling in Asherman syndrome patients and animal models. Oncotarget. 2017; 8:15399–406.WangXMaNSunQHuangCLiuYLuoXElevated NF-κB signaling in Asherman syndrome patients and animal models201781539940610.18632/oncotarget.14853536249428148903Search in Google Scholar
Chistiakov DA. Immunogenetics of Hashimoto's thyroiditis. J Autoimmune Dis. 2005; 2:1. doi: 10.1186/1740-2557-2-1ChistiakovDAImmunogenetics of Hashimoto's thyroiditis20052110.1186/1740-2557-2-155585015762980DOI öffnenSearch in Google Scholar
Koc A, Aydin Sayitoglu M, Karakurt F, Batar B, Niyazoglu M, Celik O, et al. Association of three SNPs in the PARP-1 gene with Hashimoto's thyroiditis. Hum Genome Var. 2014; 1:14016. doi: 10.1038/hgv.2014.16KocAAydin SayitogluMKarakurtFBatarBNiyazogluMCelikOAssociation of three SNPs in the PARP-1 gene with Hashimoto's thyroiditis201411401610.1038/hgv.2014.16478552227081507DOI öffnenSearch in Google Scholar
Koc A, Batar B, Celik O, Onaran I, Tasan E, Sultuybek GK. Polymorphism of the NFKB1 affects the serum inflammatory levels of IL-6 in Hashimoto thyroiditis in a Turkish population. Immunobiology. 2014; 219:531–6.KocABatarBCelikOOnaranITasanESultuybekGKPolymorphism of the NFKB1 affects the serum inflammatory levels of IL-6 in Hashimoto thyroiditis in a Turkish population2014219531610.1016/j.imbio.2014.03.00924703107Search in Google Scholar
Niyazoglu M, Baykara O, Koc A, Aydoğdu P, Onaran I, Dellal FD, et al. Association of PARP-1, NF-κB, NF-κBIA and IL-6, IL-1β and TNF-α with Graves disease and Graves ophthalmopathy. Gene. 2014; 547:226–32.NiyazogluMBaykaraOKocAAydoğduPOnaranIDellalFDAssociation of PARP-1, NF-κB, NF-κBIA and IL-6, IL-1β and TNF-α with Graves disease and Graves ophthalmopathy20145472263210.1016/j.gene.2014.06.03824956560Search in Google Scholar
Kurylowicz A, Miśkiewicz P, Bar-Andziak E, Nauman J, Bednarczuk T. Association of polymorphism in genes encoding κB inhibitors (IκB) with susceptibility to and phenotype of Graves’ disease: a case-control study. Thyroid Res. 2009; 2:10. doi: 10.1186/1756-6614-2-10KurylowiczAMiśkiewiczPBar-AndziakENaumanJBednarczukTAssociation of polymorphism in genes encoding κB inhibitors (IκB) with susceptibility to and phenotype of Graves’ disease: a case-control study200921010.1186/1756-6614-2-10277784419886988DOI öffnenSearch in Google Scholar
Kaya Tİ. Genetics of Behçet's disease. Patholog Res Int. 2012; 2012:912589. doi: 10.1155/2012/912589KayaTİGenetics of Behçet's disease20122012912589.10.1155/2012/912589319543622013548DOI öffnenSearch in Google Scholar
Yenmis G, Oner T, Cam C, Koc A, Kucuk OS, Yakicier MC, et al. Association of NFKB1 and NFKBIA polymorphisms in relation to susceptibility of Behçet's disease. Scand J Immunol. 2014; 81:81–6.YenmisGOnerTCamCKocAKucukOSYakicierMCAssociation of NFKB1 and NFKBIA polymorphisms in relation to susceptibility of Behçet's disease20148181610.1111/sji.1225125367031Search in Google Scholar
Kına I, Kanigur Sultuybek G, Soydas T, Yenmis G, Biceroglu H, Dirican A, et al. Variations in Toll-like receptor and nuclear factor-kappa B genes and the risk of glioma. Br J Neurosurg. 2019; 33:165–70.KınaIKanigur SultuybekGSoydasTYenmisGBicerogluHDiricanAVariations in Toll-like receptor and nuclear factor-kappa B genes and the risk of glioma2019331657010.1080/02688697.2018.154076430450997Search in Google Scholar
Hung Y-H, Wu C-C, Ou T-T, Lin C-H, Li R-N, Lin Y-C, et al. IκBα promoter polymorphisms in patients with Behçet's disease. Dis Markers. 2010; 28:55–62.HungY-HWuC-COuT-TLinC-HLiR-NLinY-CIκBα promoter polymorphisms in patients with Behçet's disease201028556210.1155/2010/305953Search in Google Scholar
Kaustio M, Haapaniemi E, Göös H, Hautala T, Park G, Syrjänen J, et al. Damaging heterozygous mutations in NFKB1 lead to diverse immunologic phenotypes. J Allergy Clin Immunol. 2017; 140:782–96.KaustioMHaapaniemiEGöösHHautalaTParkGSyrjänenJDamaging heterozygous mutations in NFKB1 lead to diverse immunologic phenotypes20171407829610.1016/j.jaci.2016.10.05428115215Search in Google Scholar
Terzić J, Grivennikov S, Karin E, Karin M. Inflammation and colon cancer. Gastroenterology. 2010; 138:2101–14.e5.TerzićJGrivennikovSKarinEKarinMInflammation and colon cancer2010138210114.e510.1053/j.gastro.2010.01.05820420949Search in Google Scholar
Vlahopoulos SA, Cen O, Hengen N, Agan J, Moschovi M, Critselis E, et al. Dynamic aberrant NF-κB spurs tumorigenesis: a new model encompassing the microenvironment. Cytokine Growth Factor Rev. 2015; 26:389–403.VlahopoulosSACenOHengenNAganJMoschoviMCritselisEDynamic aberrant NF-κB spurs tumorigenesis: a new model encompassing the microenvironment20152638940310.1016/j.cytogfr.2015.06.001452634026119834Search in Google Scholar
Grivennikov S, Karin M. Dangerous liaisons: STAT3 and NF-κB collaboration and crosstalk in cancer. Cytokine Growth Factor Rev. 2010; 21:11–19.GrivennikovSKarinMDangerous liaisons: STAT3 and NF-κB collaboration and crosstalk in cancer201021111910.1016/j.cytogfr.2009.11.005283486420018552Search in Google Scholar
Reardon DA, Wen PY. Therapeutic advances in the treatment of glioblastoma: rationale and potential role of targeted agents. Oncologist. 2006; 11:152–64.ReardonDAWenPYTherapeutic advances in the treatment of glioblastoma: rationale and potential role of targeted agents2006111526410.1634/theoncologist.11-2-15216476836Search in Google Scholar
Maes W, Van Gool SW. Experimental immuno-therapy for malignant glioma: lessons from two decades of research in the GL261 model. Cancer Immunol Immunother. 2011; 60:153–60.MaesWVan GoolSWExperimental immuno-therapy for malignant glioma: lessons from two decades of research in the GL261 model2011601536010.1007/s00262-010-0946-621120655Search in Google Scholar
Furnari FB, Fenton T, Bachoo RM, Mukasa A, Stommel JM, Stegh A, et al. Malignant astrocytic glioma: genetics, biology, and paths to treatment. Genes Dev. 2007; 21:2683–710.FurnariFBFentonTBachooRMMukasaAStommelJMSteghAMalignant astrocytic glioma: genetics, biology, and paths to treatment200721268371010.1101/gad.159670717974913Search in Google Scholar
Cancer Genome Atlas Research Network. Comprehensive genomic characterization defines human glioblastoma genes and core pathways. Nature 2008; 455:1061–8.Cancer Genome Atlas Research NetworkComprehensive genomic characterization defines human glioblastoma genes and core pathways20084551061810.1038/nature07385267164218772890Search in Google Scholar
Szajnik M, Szczepanski MJ, Czystowska M, Elishaev E, Mandapathil M, Nowak-Markwitz E, et al. TLR4 signaling induced by lipopolysaccharide or paclitaxel regulates tumour survival and chemoresistance in ovarian cancer. Oncogene 2009; 28:4353–63.SzajnikMSzczepanskiMJCzystowskaMElishaevEMandapathilMNowak-MarkwitzETLR4 signaling induced by lipopolysaccharide or paclitaxel regulates tumour survival and chemoresistance in ovarian cancer20092843536310.1038/onc.2009.289279499619826413Search in Google Scholar
Kim S, Karin M. Role of TLR2-dependent inflammation in metastatic progression. Ann N Y Acad Sci. 2011; 1217:191–206.KimSKarinMRole of TLR2-dependent inflammation in metastatic progression2011121719120610.1111/j.1749-6632.2010.05882.x438309421276007Search in Google Scholar
Wang H, Cho CH. Effect of NF-κB signaling on apoptosis in chronic inflammation-associated carcinogenesis. Curr Cancer Drug Targets. 2010; 10:593–9.WangHChoCHEffect of NF-κB signaling on apoptosis in chronic inflammation-associated carcinogenesis201010593910.2174/15680091079185942520482486Search in Google Scholar
Hegazy DM, O’Reilly DA, Yang BM, Hodgkinson AD, Millward BA, Demaine AG. NFκB polymorphisms and susceptibility to type 1 diabetes. Genes Immun. 2001; 2:304–8.HegazyDMO’ReillyDAYangBMHodgkinsonADMillwardBADemaineAGNFκB polymorphisms and susceptibility to type 1 diabetes20012304810.1038/sj.gene.636377611607785Search in Google Scholar
Sun XF, Zhang H. NFKB and NFKBI polymorphisms in relation to susceptibility of tumour and other diseases. Histol Histopathol. 2007; 22:1387–98.SunXFZhangHNFKB and NFKBI polymorphisms in relation to susceptibility of tumour and other diseases200722138798Search in Google Scholar
Yu Y, Wan Y, Huang C. The biological functions of NF-kB1 (p50) and its potential as an anti-cancer target. Curr Cancer Drug Targ. 2009; 9:566–71.YuYWanYHuangCThe biological functions of NF-kB1 (p50) and its potential as an anti-cancer target200995667110.2174/156800909788486759374782019519322Search in Google Scholar
Yang X, Li P, Tao J, Qin C, Cao Q, Gu J, et al. Association between NFKB1 –94ins/del ATTG promoter polymorphism and cancer susceptibility: an updated meta-analysis. Int J Genomics. 2014; 2014:612972. doi: 10.1155/2014/612972YangXLiPTaoJQinCCaoQGuJAssociation between NFKB1 –94ins/del ATTG promoter polymorphism and cancer susceptibility: an updated meta-analysis2014201461297210.1155/2014/612972403354724895544DOI öffnenSearch in Google Scholar
Concetti J, Wilson CL. NFKB1 and cancer: friend or foe? Cells. 2018; 7:133. doi: 10.3390/cells7090133ConcettiJWilsonCLNFKB1 and cancer: friend or foe?2018713310.3390/cells7090133616271130205516DOI öffnenSearch in Google Scholar
Fu W, Zhuo Z-J, Chen Y-C, Zhu J, Zhao Z, Jia W, et al. NFKB1 -94insertion/deletion ATTG polymorphism and cancer risk: evidence from 50 case-control studies. Oncotarget. 2017; 8: 9806–22.FuWZhuoZ-JChenY-CZhuJZhaoZJiaWNFKB1 -94insertion/deletion ATTG polymorphism and cancer risk: evidence from 50 case-control studies2017898062210.18632/oncotarget.14190535477228039461Search in Google Scholar
Li L, Zhang ZT. Genetic association between NFKBIA and NFKB1 gene polymorphisms and the susceptibility to head and neck cancer: a meta-analysis. Dis Markers. 2019; 2019:6523837. doi: 10.1155/2019/6523837LiLZhangZTGenetic association between NFKBIA and NFKB1 gene polymorphisms and the susceptibility to head and neck cancer: a meta-analysis201920196523837.10.1155/2019/6523837675724531612070DOI öffnenSearch in Google Scholar
Simonian M, Mosallayi M, Miraghajani M, Feizi A, Khosravi S, Salehi AR, et al. Single nucleotide polymorphism rs696 in miR449a binding site of NFKBIA gene is correlated with risk of colorectal cancer. Gastroenterol Hepatol Bed Bench. 2018; 11:48–53.SimonianMMosallayiMMiraghajaniMFeiziAKhosraviSSalehiARSingle nucleotide polymorphism rs696 in miR449a binding site of NFKBIA gene is correlated with risk of colorectal cancer2018114853Search in Google Scholar
Westbrook AM, Szakmary A, Schiestl RH. Mechanisms of intestinal inflammation and development of associated cancers: lessons learned from mouse models. Mutat. Res. 2010; 705:40–59.WestbrookAMSzakmaryASchiestlRHMechanisms of intestinal inflammation and development of associated cancers: lessons learned from mouse models2010705405910.1016/j.mrrev.2010.03.001287886720298806Search in Google Scholar
Kanigur Sultuybek G, Soydas T, Yenmis G. NF-κB as the mediator of metformin's effect on ageing and ageing-related diseases. Clin Exp Pharmacol Physiol. 2019; 46:413–22.Kanigur SultuybekGSoydasTYenmisGNF-κB as the mediator of metformin's effect on ageing and ageing-related diseases2019464132210.1111/1440-1681.1307330754072Search in Google Scholar
Miller SC, Huang R, Sakamuru S, Shukla SJ, Attene-Ramos MS, Shinn P, et al. Identification of known drugs that act as inhibitors of NF-κB signaling and their mechanism of action. Biochem Pharmacol. 2010; 79:1272–80.MillerSCHuangRSakamuruSShuklaSJAttene-RamosMSShinnPIdentification of known drugs that act as inhibitors of NF-κB signaling and their mechanism of action20107912728010.1016/j.bcp.2009.12.021283487820067776Search in Google Scholar
Yamamoto M, Horie R, Takeiri M, Kozawa I, Umezawa K. Inactivation of NF-κB components by covalent binding of (–)-dehydroxymethylepoxyquinomicin to specific cysteine residues. J Med Chem. 2008; 51:5780–8.YamamotoMHorieRTakeiriMKozawaIUmezawaKInactivation of NF-κB components by covalent binding of (–)-dehydroxymethylepoxyquinomicin to specific cysteine residues2008515780810.1021/jm800624518729348Search in Google Scholar
Tak PP, Firestein GS. NF-κB: a key role in inflammatory diseases. J Clin Invest. 2001; 107:7–11.TakPPFiresteinGSNF-κB: a key role in inflammatory diseases200110771110.1172/JCI1183019855211134171Search in Google Scholar
Kiliccioglu I, Konac E, Dikmen AU, Sozen S, Bilen CY. Hsp-27 and NF-κB pathway is associated with AR/AR-V7 expression in prostate cancer cells. Gene. 2019; 697:138–43.KilicciogluIKonacEDikmenAUSozenSBilenCYHsp-27 and NF-κB pathway is associated with AR/AR-V7 expression in prostate cancer cells20196971384310.1016/j.gene.2019.02.05530807779Search in Google Scholar
Yenmis G. Investigation of the molecular mechanisms of the effect of metformin on aging and cancer [PhD dissertation]. Istanbul, Turkey: University of Istanbul; 2019. Thesis No. 541930. [in Turkish, English abstract]. Available from: https://tez.yok.gov.tr/UlusalTez-Merkezi/tezSorguSonucYeni.jspYenmisGIstanbul, TurkeyUniversity of Istanbul2019Thesis No. 541930. [in Turkish, English abstract]. Available from: https://tez.yok.gov.tr/UlusalTez-Merkezi/tezSorguSonucYeni.jspSearch in Google Scholar