Publication for NFKBIA and CCL20

Species	Symbol	Function*	Entrez Gene ID*	Other ID	Gene coexpression	CoexViewer
hsa	NFKBIA	NFKB inhibitor alpha	4792			[link]
hsa	CCL20	C-C motif chemokine ligand 20	6364

Pubmed ID	Priority	Text
23118497	0.97	CCL20 expression was dependent on Akt- and ERK1/2-mediated phosphorylation of IkappaBalpha on Ser32/36 and of p65 on Ser276, whereas p38 MAPK appeared to be dispensable.
	0.94	CCL20 in dendritic cells also differed from that in a transformed T-cell line, where Akt inhibition resulted in reduced phosphorylation of p65 on Ser536, whereas the IkappaBalpha phosphorylation remained unaffected.
	0.93	CCL20 is known to contain an NF-kappaB consensus sequence indicating that the expression of CCL20 might be regulated by NF-kappaB. In addition, it has been previously shown that NF-kappaB can be activated by Akt-dependent IkappaBalpha kinase phosphorylation, and Akt mediates an IL-17A-induced expression of CCL20 in human airway epithelial cells.
27564404	0.97	IkappaBalpha and beta-actin (control) expression in the cell lysates of cultured macrophages simulated with IL-27B (EBI3) or CCL20 for the indicated times.
	0.89	IkBalpha, which reflects NF-kB activation, was not influenced by either recombinant CCL20 or IL-27B (EBI3), whereas slight activation of Stat3 was induced by IL-27B (EBI3) (Fig. 4c).
31701553	0.97	CCL20, NFKBIA) in trans.
28629746	0.96	CCL20, ICAM1 and VCAM1 mRNA in unstimulated and LPS+anti-LTbetaR mAb stimulated fibroblasts from healthy controls (n=3) and patients with IkappaBalpha truncation (n=2) and point mutations (n=3).
	0.94	CCL20, ICAM1 and VCAM1 mRNA levels was significantly impaired in patients with IkappaBalpha point mutations (n=3) compared to healthy controls (n=3), confirming the RNA-Seq results.
	0.93	CCL20, ICAM1 and VCAM1 was abolished in patients with IkappaBalpha point mutations.
	0.89	CCL20, ICAM1 and VCAM1 mRNA in LPS+anti-LTbetaR mAb stimulated fibroblasts from patients with IkappaBalpha truncation mutations (n=2) were reduced compared to healthy controls (n=3) but the difference was not significant.
	0.88	CCL20, ICAM1 and VCAM1 mRNA in unstimulated and LPS+anti-LTbetaR mAb stimulated fibroblasts from healthy controls (n=3) and patients with IkappaBalpha truncation (n=2) and point mutations (n=2).
25882704	0.94	CCL20 gene through IkappaKbeta, IkappaBalpha and p65
	0.87	CCL20 expression, we expressed a mutant form of IkappaBalpha (IkappaBalphaSR; SR= super-repressor) containing S32A/S36A amino acid substitutions that render the protein resistant to phosphorylation-induced degradation.
20805562	0.92	NFKBIA, TNFAIP3, and CCL20 promoters, to which RelA was similarly inhibited (Fig. S4 B) This also occurred at the IL6 kappaB site (albeit with later kinetics of recruitment; Fig. S4 C).
21994190	0.89	CCL20, IL8), regulators of NF-kappaB (e.g. TNFAIP3, LY96, NFKBIA), genes involved in interferon-induced defense against pathogen invasion (e.g. IFIT1, ISG15) and genes involved in cell adhesion and/or migration (e.g. CD44, TMOD1).
29970882	0.86	CCL20, ERK, NFKBIA genes expression, while adding siRNA-CCL20 greatly inhibits the expression of CCL20, CCR6 and ERK.
	0.52	CCL20, ERK, NFKBIA genes expression, while adding siRNA-CCL20 greatly inhibits the expression of CCL20, CCR6, and ERK (Fig. 6g).
31781116	0.82	NF-kBIA (NF-kB inhibitor alpha) upregulation that was probably due to its continuous nucleocytoplasmic shuttling to counteract the islet damage induced by NF-kB. The release of four chemokines, namely IL-8, CXCL6, CXCL1, and CCL20, known to be regulated by NF-kB activation was partly confirmed using ELISA.
21961038	0.56	CCL20 mRNA by CORM-2 could be mediated by the reduction in NF-kappaB transcriptional activity which would be dependent on the inhibition of IkappaBalpha phosphorylation leading to a lower rate of nuclear translocation of this transcription factor.
22432004	0.55	nuclear factor of kappa light polypeptide gene enhancer in B-cells inhibitor alpha (NFKBIA), tumor necrosis factor alpha-induced protein 3 (TNFAIP3), chemokine C-C motif ligand 2 (CCL2), interferon regulatory factor 1 (IRF1), prostaglandin-endoperoxide synthase 2 (PTGS2), chemokine C-C motif ligand 20 (CCL20), dual specificity phosphatase 1 (DUSP1), eukaryotic translation initiation factor 2-alpha kinase 2 (EIF2AK2), TNF receptor superfamily member 6 (FAS), suppressor of cytokine signaling 1 (SOCS1), TNF receptor-associated factor 1 (TRAF1), and ubiquitin-conjugating enzyme E2L 6 (UBE2L6).