NFKBIA


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NFKBIA

A gene on chromosome 14q132 that encodes an I-kappa-B protein that inhibits the multimeric NFKB complex by trapping it in the cytoplasm. Kinases IKBKA or IKBKB phosphorylate NFKBIA’s serine residues, marking them for destruction via the ubiquination pathway, allowing activation of the NFKB complex which, once activated, translocates to the nucleus, binds DNA and activates transcription.
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To test our hypothesis, we conducted a case-control study to investigate the association of NFKB1 -94 ins/del ATTG polymorphism and NFKBIA -826C>T and -881A>G polymorphisms with the risk of lung cancer in a Chinese population.
Association of NFKB1 and NFKBIA polymorphisms with lung cancer risk: The association between NFKB1 and NFKBIA polymorphisms and lung cancer risk is shown in Table-I.
Table-I: Association between NFKB1 -94 ins/del ATTG polymorphism, NFKBIA -826C>Tpolymorphism and NFKBIA -881A>G polymorphism and lung cancer risk.
Table-II: Association between combinations of NFKB1 -94 ins/del ATTG polymorphism and NFKBIA -826C>T polymorphism and lung cancer risk.
Table-III: Association between combinations of NFKB1 -94 ins/del ATTG polymorphism and NFKBIA -881A>G polymorphism and lung cancer risk.
Combinations of polymorphisms and lung cancer risk: The association of combinations of NFKB1 -94 ins/del ATTG polymorphism and NFKBIA -826C>T polymorphism with lung cancer risk is shown in Table-II.
Table-IV: Association between combinations of NFKBIA -826C>T polymorphism and NFKBIA -881A>G polymorphism and lung cancer risk.
The combinations of NFKBIA -826C>T polymorphism and NFKBIA -881A>G polymorphism and their association with lung cancer risk is shown in Table-IV.
Analysis of NFKBIA -826C>T risk association by gender and smoking status: The association between NFKBIA -826C>T polymorphism and lung cancer risk according to sex and smoking status is shown in Table-VI..
Polymorphisms in NF-B pathway genes and their association with risk of lung cancer in the Chinese population
The defects on NFKBIA and EGFR have a similar effect on an important molecule called NF-kappa-B, a "transcription factor" found in all cells, but they do this by different mechanisms.
Most common adult brain cancer associated with gene deletion
In our study, UFPs altered the expression of many of the genes in these processes, including FOS (1.6-fold), JUN (1.3-fold), NFKBIA (1.3-fold), and early growth response-1 (EGR-1, Unigene accession no.
Gene symbol Gene name change 517617 MAFF v-maf musculoaponeurotic fibrosarcoma oncogene homolog F 1.7 25292 JUNB jun B proto-oncogene 1.7 590958 FOSB FBJ murine osteosarcoma viral 1.5 oncogene homolog B 132225 PIK3R1 phosphoinositide-3-kinase, 1.5 regulatory subunit 1 155396 NRF2 nuclear factor (erythroid-derived 1.3 2)-like 2 534313 EGR3 early growth response 3 1.3 81328 NFKBIA nuclear factor of kappa light 1.3 polypeptide gene enhancer in B-cells inhibitor, alpha 252229 MAFG v-maf musculoaponeurotic 1.2 fibrosarcoma oncogene homolog G (avian) 326035 EGR1 early growth response 1 1.2 Gene annotations are from Unigene (http://www.ncbi.nlm.nih.gov/entrez/ query.fcgi?db=unigene).
Up-regulation of tissue factor in human pulmonary artery endothelial cells after ultrafine particle exposure

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