Publication for BIRC3 and NFKBIA

Species	Symbol	Function*	Entrez Gene ID*	Other ID	Gene coexpression	CoexViewer
hsa	BIRC3	baculoviral IAP repeat containing 3	330			[link]
hsa	NFKBIA	NFKB inhibitor alpha	4792

Pubmed ID	Priority	Text
27180651	0.98	IkappaBalpha, cIAP2, CXCL1 and IEX-1 while the mutants in NGN, KOW1+2 and KOW2+4 domains failed to do so (Fig. 2b).
	0.98	IkappaBalpha, cIAP2, JunB and CXCL1.
	0.97	cIAP2, IkappaBalpha, CXCL1, JunB, GAPDH and RANTES genes.
	0.97	IkappaBalpha, cIAP2, JunB and CXCL1.
	0.96	cIAP2 induced transcripts were reduced but those of IkappaBalpha, CXCL1 and IEX-1 were unchanged (Fig. 4d).
	0.96	IkappaBalpha, CXCL1 and IEX-1 but not A20 and cIAP2 (Fig. 5b, bottom).
	0.96	IkappaBalpha, cIAP2, IEX-1, CXCL1 but not JunB genes (Fig. 7a).
	0.94	IkappaBalpha, cIAP2, JunB and CXCL1.
	0.92	IkappaBalpha, cIAP2, JunB and CXCL1.
	0.62	cIAP2 was dependent on H3K4me3 but not H4K5Ac, while the exact opposite was found for IkappaBalpha, CXCL1 and IEX-1.
	0.60	cIAP2 are both TATA-less while IkappaBalpha, CXCL1 and IEX-1 are driven by TATA or TATA-like promoters.
21224428	0.98	IkappaBalpha siRNA (Figure 4), and indicate that the nuclear IkappaBalpha regulates transcription of cIAP1 and cIAP2, but not Bcl-2, in Hut-78 cells.
	0.96	cIAP2 and IkappaBalpha protein expression in whole cell extracts of Hut-78 cells treated 24 h with increasing concentrations of bortezomib.
	0.90	cIAP2 promoters was significantly reduced by the bortezomib-induced nuclear IkappaBalpha, whereas its recruitment to Bcl-2 promoter was not affected.
	0.88	cIAP2 mRNA expression analyzed by real time RT-PCR (A) and total cellular protein levels analyzed by western blotting and densitometry normalized to actin (B) in Hut-78 cells transfected with NS (empty column) or IkappaBalpha siRNA (full columns) and treated 24 h with increasing concentrations of bortezomib.
	0.79	cIAP2 expression in IkappaBalpha siRNA transfected Hut-78 cells treated with increasing concentrations of bortezomib
	0.75	cIAP2 mRNA and protein levels decreased with increasing bortezomib concentrations; however, transfection with IkappaBalpha siRNA reduced this bortezomib-induced decrease.
	0.71	cIAP2 promoters, while the Bcl-2 promoter is occupied only by p50 NFkappaB. Thus, these results indicate that the cIAP1 and cIAP2 promoters associate with NFkappaB p65/50 heterodimers, and this binding and transcription are inhibited by the bortezomib-induced nuclear IkappaBalpha.
	0.67	cIAP2, as well as IkappaBalpha and control actin, in whole cell extracts prepared from Hut-78 cells treated 24 h with increasing concentrations of bortezomib (Figure 5B).
	0.62	cIAP2 regulation by nuclear IkappaBalpha, we analyzed Bcl-2, cIAP1 and cIAP2 mRNA and protein levels in cells that were transfected with non-silencing or IkappaBalpha siRNA and treated with increasing concentrations of bortezomib (Figure 6) or MG132 (data not shown).
27770821	0.98	cIAP-2 complex and leading to IKKalpha/beta-mediated IkBalpha phosphorylation and degradation (Fig. 7b).
	0.98	c-IAP2 at the protein level by inhibiting its auto-ubiquitination and the increased expression of c-IAP2 enhances the phosphorylation of IkappaBalpha that favours its subsequent proteasomal degradation leading to activation of the canonical NFkappaB pathway.
	0.98	cIAP2-XIAP complex formation increases IkBalpha expression leading to NFkappaB inactivation and apoptosis induction
	0.98	cIAP2-XIAP complex formation increased IkBalpha expression leading to NFkappaB inhibition and apoptosis induction by reducing survivin and FLIP, a caspase 8 inhibitor as confirmed by microarray analysis (Fig. 8).
	0.97	cIAP2-XIAP complex formation and IkBalpha degradation and leading to NFkappaB pathway inactivation.
	0.96	c-IAP2 at the protein level by inhibiting its auto-ubiquitination and the increased expression of c-IAP2 enhances the phosphorylation of IkappaBalpha that favours its subsequent proteasomal degradation leading to activation of the canonical NFkappaB pathway.
	0.91	cIAP2 complex leading to IKKalpha/beta-mediated IKBalpha phosphorylation and NFkappaB activation as it blocked RF-Id-mediated XIAP degradation.
	0.86	cIAP2 complex by inhibiting NFkappaB pathway, we evaluated the effects of RF-Id on either XIAP, cIAP2 and XIAP -cIAP2 complex expression and on IKKalpha/beta, IKBalpha and NFkappaB activation and expression.
	0.69	cIAP2-XIAP complex formation and IkBalpha degradation by leading to NFkappaB inhibition and caspase activation.
19584916	0.98	BIRC3 and NFKBIA were directly involved in the apoptosis pathway.
	0.98	BIRC3, and NFKBIA, were upregulated by rCFES treatment.
	0.97	BIRC3, and NFKBIA in terms of up- or downregulation (Pearson correlations: 0.66 ~ 0.82).
	0.93	BIRC3, and NFKBIA.
	0.92	BIRC3 and NFKBIA were the downstream genes of PIK3R3.
	0.81	BIRC3, and NFKBIA, suggesting that these proteins may play an essential role in the cytotoxic process in the rCFES-treated WI-38 cells.
19746155	0.98	IkappaBalpha and cIAP2 is identified early following 3 hours of doxorubicin treatment, and subsequently declines.
	0.97	IkappaBalpha and cIAP2.
	0.96	cIAP2 and IkappaBalpha.
	0.79	cIAP2, which mirror the results seen with IkappaBalpha.
	0.57	IkappaBalpha and cIAP2, decreased transcription of XIAP, Survivin, Bcl-xL, and Bcl2, and did not alter cIAP1 transcription (black bars).
	0.52	IkappaBalpha and cIAP2, but had no effect on the doxorubicin-mediated repression of the other anti-apoptotic genes (gray bars).
22768179	0.98	IkappaB-alpha, cIAP1, cIAP-2 and survivin.
30018081	0.98	cIAP2 could initiate phosphorylation of IkappaBalpha but were unable to maintain sustained IkappaBalpha phosphorylation at all time points (Fig. 2D).
14641910	0.97	NFKBIA, GSTA4, BIRC3, MMP3, TNFRSF10B, DAD1.
	0.95	NFKBIA, GSTA4, BIRC3, MMP3, TNFRSF10B, DAD1 and glutathione S-transferase.
23538445	0.97	IkappaBalpha-SR resulted in increased NIK levels accompanied by profound downregulation of cIAP2 expression (Figure 4c).
24565101	0.97	IkappaBalpha and p65 (Figure 4B), and induced the expression of c-IAP1 and c-IAP2 (Figure 4C).
27070702	0.97	cIAP2 decreased phosphorylation of IKKbeta and stabilized the IKK substrate IkappaBalpha, indicating lower activity of the classical NF-kappaB pathway (Figure 2F).
28295868	0.97	cIAP2 showed significantly increased IkappaBalpha and p65 levels following TNF-alpha stimulation with GAPDH as a protein marker.
19077262	0.96	NFKBIA, PPP1R15A, GADD45A, AXL, SGK, DUSP1, JUN, IRF1, MYC, BAG5, BIRC3).
23349769	0.96	NFKBIA, PRIC285 and BIRC3, showed modest mRNA inducibility by dexamethasone alone, the majority revealed either no effect or repression of basal expression (Table S2, Figure S1).
23573150	0.96	IkappaBalpha degradation, NF-kappaB p65 phosphorylation and nuclear translocation, but also downregulated TNF-alpha-induced NF-kappaB-dependent genes expression involving cancer cell proliferation (c-myc and cyclin D1), cell invasion (MMP-9 and ICAM-1), angiogenesis (COX-2 and VEGF), and anti-apoptosis (survivin, c-IAP2, Bcl-2, Bcl-xL and XIAP), leading to induction of apoptosis, and blockage of cell invasion and angiogenesis.
25446254	0.96	cIAP2 (KMS-28PE) were treated with TRAIL (100 ng/ml) as indicated, and the phosphorylation of IkappaBalpha and JNK was examined by Western blotting.
23770847	0.95	API2-MALT1-induced RIP1 and NEMO ubiquitination, as well as IkappaBalpha phosphorylation, in a dose-dependent manner (Figure 5D).
	0.91	API2-MALT1 expression, which also correlated with loss of IKK complex activation and IkappaBalpha phosphorylation (Figure 2A).
	0.88	IkappaBalpha phosphorylation in response to API2-MALT1 expression (Figure 5B).
	0.71	API2-MALT1-induced NF-kappaB activation, completely blocked API2-MALT1-induced RIP1 and NEMO ubiquitination (Figure 5C) as well as phosphorylation of IkappaBalpha (Supplementary Figure S5).
	0.54	API2-MALT1-induced RIP1 and NEMO ubiquitination and phosphorylation of IkappaBalpha.
26015393	0.95	BIRC3 is associated with a decline in the levels of phosphorylated IkappaBalpha and active NFkappaB family members detectable in the nuclear compartment.
	0.91	BIRC3/cIAP2 - an effect not seen with either compound alone - which was associated with subsequent decreases in IkappaBalpha phosphorylation, p65 and p52 nuclear translocation (Figure 5B).
	0.86	BIRC3, IkappaBalpha, A20, and CYLD (Table 1), suggesting that the combination may effectively target the NFkappaB pathway.
	0.85	IkappaBalpha and BIRC3 is an important mechanism of myeloma cell survival, and confirms the central role of NFkappaB signalling in myeloma pathogenesis.
	0.83	IkappaBalpha, A20, CYLD, and most markedly BIRC3.
21119000	0.95	IkappaBalpha and IP-10 but that efficient expression of some other NF-kappaB target genes such as ICAM-1 and cIAP2 requires TRAF2 phosphorylation-dependent prolonged IKK activation.
	0.90	IkappaBalpha, IP-10, cIAP2, cFLIP, RANTES, and ICAM-I were determined by real-time RT-PCR.
	0.86	IkappaBalpha and IP-10 expression occurred very quickly, peaking within 1 h after stimulation, whereas ICAM-1, cIAP2, and cFLIP expression continuously increased through 3 h, the final time point that was tested.
	0.75	IkappaBalpha and IP-10 but that it is required for efficient expression of RANTES, ICAM-1, cIAP2, and cFLIP at later time points (Figure 3, A-F).
20102612	0.95	cIAP2 mRNA and protein in the IkappaBalpha mutant cell line by real time PCR and western blot, and found that cIAP2 levels were specifically down-regulated when compared to control cells (Fig. 7B-C).
	0.51	cIAP2 reporter gene and either an expression vector coding for a dominant negative mutant of IkappaBalpha, IkappaBalpha-SR(S32A/S36A) or an expression vector coding for a dominant negative of c-JUN (TAM-67), to test whether 9-cis-RA inducibility was impaired.
25659587	0.95	BIRC3 gene (B), NFKBIA gene (C), and IL8 gene (D) with reference sequence annotation below.
	0.92	BIRC3, expression of NFKBIA was also markedly higher following CD30L than SM (12-fold increase and 7-fold increase, respectively) (Fig. 3C, Table S1, S2).
25951128	0.94	IkappaB-alpha gene expression in cancer cells, and reduce the expression of Bcl-2, Bcl-xL, XIAP, cIAP-1, cIAP-2, survivin and NF-kappaB.
	0.93	IkappaB-alpha expression levels were the highest, and Bcl-2, Bcl-xL, XIAP, cIAP-1, cIAP-2, survival, and NF-kappaB expression levels were the lowest.
29535419	0.93	BIRC3, CCL20, CXCL3, NFKBIA, TNF, and TNFAIP3) in SW480-EV and SW480-DDX27 (or HCT116-shCTL and HCT116-shDDX27) cells were measured by qPCR.
	0.93	BIRC3, CCL20, CXCL3, NFKBIA, TNF, and TNFAIP3 are NF-kB target genes which were further validated to be significantly up-regulated by ectopic expression of DDX27 in HCT116 by qPCR (Fig. S2).
	0.87	BIRC3 (c-IAP2) has been shown to exert positive feedback control on NF-kappaB via targeting IkappaBalpha for degradation and facilitate cell survival by suppressing caspase-8 activation.
	0.86	BIRC3, CCL20, CXCL3, NFKBIA, TNF, and TNFAIP3) induced by TNF-alpha.
25873381	0.93	BIRC3 (cIAP2) (+182-fold), ENPP2 (+47-fold), EGFR (+9-fold), RGS2 (+8.5-fold), NFKB2 p100 (+6.6-fold), the ephrin receptor B1 (EPHB1) (+4.7-fold), NFKBIA (IkappaBalpha) (+4.5-fold), RELB (+3-fold), and NFKBIZ (+2.9-fold) (Table S1).
27197231	0.93	cIAP2 (Fig.S7), downregulation of cIAP1 had similar effects as C9b on NF-kappaB signaling as well as the AIG capacity of NSCLC cells: increased the processing of the NF-kappaB2 p100 to p52, elevated the level of NIK and IkappaBalpha (Fig. 4A), decreased nuclear p65 level whereas elevated nuclear p52 level(Fig.
24675460	0.91	BIRC3 promoters, but not the IkappaBalpha promoter.
	0.80	BIRC3, but not IkappaBalpha and several other NF-kappaB target genes (Figures 4 and 5 and data not shown).
29497034	0.88	IkappaBalpha (pIkappaBalpha) and JNK1/JNK2 (pJNK1/2), along with rapid depletion of cIAP1 and cIAP2 (Fig. 4a).
19891769	0.85	API-2 or siRNA against Akt, overexpression of Aur-A however failed to reduce IkappaBalpha or raise Bcl-xL expression in comparison to the vector control (Fig. 6e and 6f).
30939781	0.83	IkappaBalpha phosphorylation and the NF-kappaB-DNA binding activity, and the expression of NF-kappaB target genes cIAP1, cIAP2 and survivin were also evaluated.
30210622	0.71	BIRC3, p-P65, p-IkappaBalpha and c-Myc, were detected by western blotting.
18694378	0.67	cIAP-2, XIAP, survivin, Bcl-2, Bcl-xL, Bfl-1/A1, and TRAF2 through suppression of constitutively active NF-kappaB through inhibition of IKK and the phosphorylation of IkappaBalpha and of p65 in human myeloma cell lines.