m6A Target Gene Information

General Information of the m6A Target Gene (ID: M6ATAR00683)
Target Name NF-kappa-B inhibitor alpha (Nfkbia)
Synonyms
I-kappa-B-alpha; IkB-alpha; IkappaBalpha; Major histocompatibility complex enhancer-binding protein MAD3
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Gene Name Nfkbia
Chromosomal Location 14q13.2
Family NF-kappa-B inhibitor family
Function
Inhibits the activity of dimeric NF-kappa-B/REL complexes by trapping REL dimers in the cytoplasm through masking of their nuclear localization signals. On cellular stimulation by immune and pro-inflammatory responses, becomes phosphorylated promoting ubiquitination and degradation, enabling the dimeric RELA to translocate to the nucleus and activate transcription.
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Gene ID 4792
Uniprot ID
IKBA_HUMAN
HGNC ID
HGNC:7797
KEGG ID
hsa:4792
Full List of m6A Methylation Regulator of This Target Gene and Corresponding Disease/Drug Response(s)
Nfkbia can be regulated by the following regulator(s), and cause disease/drug response(s). You can browse detail information of regulator(s) or disease/drug response(s).
Browse Regulator
Browse Disease
Methyltransferase-like 14 (METTL14) [WRITER]
 Regulator Info 
Representative RNA-seq result indicating the expression of this target gene regulated by METTL14
Cell Line mouse embryonic stem cells Mus musculus
Treatment: METTL14-/- ESCs
Control: Wild type ESCs
 GSE145309
Regulation
logFC: 1.05E+00
p-value: 4.32E-28
More Results Click to View More RNA-seq Results
In total 1 item(s) under this regulator
Experiment 1 Reporting the m6A Methylation Regulator of This Target Gene [1]
Response Summary Colonic mucosal barrier dysfunction is one of the major causes of inflammatory bowel disease (IBD). Mettl14 restricted colonic epithelial cell death by regulating the stability of NF-kappa-B inhibitor alpha (Nfkbia) mRNA and modulating the NF-Kappa-B pathway,suggesting that m6A modification could be a potential therapeutic target for IBD.
Target Regulation Down regulation
Responsed Disease Inflammatory bowel disease ICD-11: DD7Z
 Disease Info 
Pathway Response NF-kappa B signaling pathway hsa04064
Cell Process Cell apoptosis
In-vivo Model Mettl14f/f mice were generated as previously described with CRISPR-Cas9 technology by insertion of two loxp sites into Mettl14 genome loci. Mettl14f/f mice without Villin-Cre were used as WT controls (Mettl14 WT) for Mettl14 KO mice. Mettl14f/f mice were crossed with Lgr5-eGFP-IRES-creERT2 (Lgr5-Cre) mice to generate Mettl14 depletion in Lgr5+ stem cells.
Inflammatory bowel disease [ICD-11: DD7Z]
 Disease Info 
In total 1 item(s) under this disease
Experiment 1 Reporting the m6A-centered Disease Response [1]
Response Summary Colonic mucosal barrier dysfunction is one of the major causes of inflammatory bowel disease (IBD). Mettl14 restricted colonic epithelial cell death by regulating the stability of NF-kappa-B inhibitor alpha (Nfkbia) mRNA and modulating the NF-Kappa-B pathway,suggesting that m6A modification could be a potential therapeutic target for IBD.
Responsed Disease Inflammatory bowel disease [ICD-11: DD7Z]
Target Regulator Methyltransferase-like 14 (METTL14) WRITER
 Regulator Info 
Target Regulation Down regulation
Pathway Response NF-kappa B signaling pathway hsa04064
Cell Process Cell apoptosis
In-vivo Model Mettl14f/f mice were generated as previously described with CRISPR-Cas9 technology by insertion of two loxp sites into Mettl14 genome loci. Mettl14f/f mice without Villin-Cre were used as WT controls (Mettl14 WT) for Mettl14 KO mice. Mettl14f/f mice were crossed with Lgr5-eGFP-IRES-creERT2 (Lgr5-Cre) mice to generate Mettl14 depletion in Lgr5+ stem cells.
References
Ref 1 m(6)A mRNA modification maintains colonic epithelial cell homeostasis via NF-KappaB-mediated antiapoptotic pathway. Sci Adv. 2022 Mar 25;8(12):eabl5723. doi: 10.1126/sciadv.abl5723. Epub 2022 Mar 25.
Ref 2 The role of carbonyl reducing enzymes in oxcarbazepine in vitro metabolism in man. Chem Biol Interact. 2014 Sep 5;220:241-7. doi: 10.1016/j.cbi.2014.07.005. Epub 2014 Jul 22.