Publication for NFKBIA and TNFAIP3

Species	Symbol	Function*	Entrez Gene ID*	Other ID	Gene coexpression	CoexViewer
hsa	NFKBIA	NFKB inhibitor alpha	4792			[link]
hsa	TNFAIP3	TNF alpha induced protein 3	7128

Pubmed ID	Priority	Text
29402958	0.98	IkappaBalpha and A20 synthesis after poly(I:C) stimulation.
	0.98	A20- and IkappaBalpha-mediated negative feedbacks terminate LPS- or cytokine-induced signalling.
	0.97	A20 and IkappaBalpha, as well as against a phosphorylated (active) form of PKR (p-Thr451).
	0.94	IkappaBalpha and A20.
	0.94	IkappaBalpha and A20: NF-kappaB and IRF3 activity is controlled by negative feedbacks mediated by NF-kappaB-inducible inhibitors: IkappaBalpha and A20.
	0.92	IkappaBalpha and A20 synthesis, and thus allowing for stabilisation of NF-kappaB and IRF3 activity.
	0.86	IkappaBalpha) and Tnfaip3 (A20) mRNA expression peaks at 4-6 h post-stimulation, much later than for LPS stimulation (Fig. 1d).
	0.85	IkappaBalpha and A20 (Fig. 1b, d), which constitute the negative feedback loops terminating NF-kappaB signalling 1.5 h post LPS stimulation (Fig. 1c).
	0.79	IkappaBalpha and A20, leading to stabilisation of NF-kappaB and IRF3 signalling.
	0.74	IkappaBalpha and A20.
	0.64	IkappaBalpha and A20 feedbacks: The IkappaBalpha- and A20-mediated negative feedbacks are compromised when protein synthesis is suppressed and/or mRNA degradation is enhanced.
	0.64	IkappaBalpha and A20 with respect to naive cells, allowing for stabilisation of NF-kappaB and IRF3 activity (Supplementary Fig. 7).
	0.58	A20 and IkappaBalpha can be antagonised by positive-feedback mediators, OAS1A and PKR, which, when activated by poly(I:C), enhance mRNA degradation and inhibit translation.
	0.57	IkappaBalpha and A20, transform tonic TNFalpha, IL1 or LPS signals into oscillatory or pulse-like responses.
	0.54	IkappaBalpha and A20.
	0.51	IkappaBalpha and A20 lead to pulse-like cytoplasmic-to-nuclear NF-kappaB shuttling (Fig. 2e and Supplementary Fig. 5a).
27180651	0.98	A20 and IkappaBalpha genes is consistent with the notion that these genes are ready for rapid transcriptional induction.
	0.98	A20 and cIAP2 induced transcripts were reduced but those of IkappaBalpha, CXCL1 and IEX-1 were unchanged (Fig. 4d).
	0.97	IkappaBalpha and A20, are themselves negative regulators of NF-kappaB signalling.
	0.97	A20 and IkappaBalpha, while Spt5 is clearly essential (Fig. 3b) as previously reported.
	0.97	IkappaBalpha, CXCL1 and IEX-1 but not A20 and cIAP2 (Fig. 5b, bottom).
	0.92	A20 and IkappaBalpha genes is comparable to the level seen in the constitutively active gene GAPDH, and is restricted to the 5'end of the genes.
	0.86	A20, IkappaBalpha and cIAP2, whereas in CXCL1 and JunB they were relatively unchanged (Fig. 4c).
	0.84	A20, IkappaBalpha, cIAP2, IEX-1, CXCL1 but not JunB genes (Fig. 7a).
	0.84	A20 and IkappaBalpha.
	0.60	IkappaBalpha, A20 and beta-Tubulin proteins were analysed by western blot.
	0.59	A20 and cIAP2 are both TATA-less while IkappaBalpha, CXCL1 and IEX-1 are driven by TATA or TATA-like promoters.
	0.51	A20, IkappaBalpha, cIAP2, JunB and CXCL1.
	0.51	A20, IkappaBalpha, cIAP2, JunB and CXCL1.
25165885	0.98	IkappaBalpha and A20 stabilities.
	0.94	A20 or IkappaBalpha effects.
	0.91	IkappaBalpha and A20 expression, important negative regulatory molecules that control the NF-kappaB response.
	0.88	A20 and IkappaBalpha.
	0.87	A20 and IkappaBalpha protein expressions in Jurkat T cells transduced with shControl or shRNF1 and 2.
	0.78	A20 and IkappaBalpha antibodies are presented as well as a corresponding quantification.
	0.75	A20 or IkappaBalpha inhibitors.
	0.68	A20 and IkappaBalpha inhibitors.
	0.59	A20 and IkappaBalpha expression.
	0.51	A20 and IkappaBalpha and could be the mechanism by which RNF114 regulates NF-kappaB pathway.
27381163	0.98	A20, IkappaBalpha, IkappaBe, Rel, RelB, NF-kappaB1 and NF-kappaB2) and cytokine response genes (CXCL2, CXCL1, IL8, TNFAIP6, CSF2, TNFalpha, LIF, IL-1beta and CCL2).
	0.96	A20 signalling (for example, A20 mRNA transcription, protein translation rates and half-lives, c1, c2, c3, c4; IKKK level, IKKKtott; A20-induced IKKK inhibition, kA20; half-maximal IKK activation, sIKKK, Fig. 4g shown in blue), but not the core NF-kappaB-IkappaBalpha or receptor signalling (see also Supplementary Fig. 28).
	0.96	A20/IKKK signalling (such as IKKKn recovery rate, m3, or total IKKK, IKKKt), but not IkappaBalpha (for example, protein half-life, c4a) were able to fit the measured refractory period distribution (Fig. 4i).
	0.96	IkappaBalpha, IkappaBe and A20) and a number of pro-inflammatory signalling molecules including cytokines and chemokines (IL8, CSF2, CCL2, CCL5, CXCL1, CXCL2, LIF, TNFalpha, TNFAIP6 and IL-1beta).
	0.96	IkappaBalpha, A20, CSF2, CXCL2 and IL8 transcript levels from data in d. Shown are mean expression levels (+-s.d.) per condition, respectively.
	0.94	A20 and IkappaBalpha highest with two-fold and 1.4-fold change, respectively).
	0.92	A20 (but not IkappaBalpha, Supplementary Fig. 21) levels effectively divided the solution space into 'responding' and 'non-responding' regimes (Fig. 4b).
24710104	0.98	TNFAIP3/a20 (p = 0.002) and NFKBIA/IkappaBalpha (p = 0.001): all cases are qualitatively matched under the RelA siRNA knockdown.
	0.97	IkappaBalpha and TNFAIP3 genes has shown that these genes are maintained in an open chromatin configuration and are regulated by a process involving transcriptional elongation.
	0.93	IkappaBalpha and TNFAIP3, the induction of IFNbeta and RIG-I mRNA are clearly delayed (Fig. 1A).
	0.91	TNFAIP3, RIG-I, and IkappaBalpha.
	0.89	TNFAIP3/A20, NFKBIA/IkappaBalpha, IL8, IL6, Grobeta and RANTES at 18 hr after electroporation.
	0.55	TNFAIP3/A20 and NFKBIA/IkappaBalpha genes; we noted that these selectively NF-kappaB dependent genes were the most rapidly induced, whose expression could be detected within 30 min of stimulation.
28166199	0.98	NFKBIA: 14q13.2, TNFAIP3: 6q23.3, TNIP1: 5q33.1 and TNIP2: 4p16.3) of these genes and concurrent gene copy number variation as a cause of their co-expression (Supplementary Figure 1A).
	0.96	NFKBIA and TNFAIP3, and to a less extent, of TNIP1 and TNIP2, in all the cell lines tested (Figures 3d-f).
	0.96	NFKBIA and TNFAIP3 in LN229 (d), BTSC23 (e), BTSC233 (f) cells expressing EV, KLF6-wt or KLF6-sv1.
	0.91	NFKBIA, TNFAIP3, TNIP1 and TNIP2 representing pairwise associations between each of these variables in 188 glioblastomas.
	0.86	NFKBIA, TNFAIP3, TNIP1 and TNIP2 in glioblastoma patients from The Cancer Genome Atlas (TCGA).
	0.82	NFKBIA, TNFAIP3, TNIP1 and TNIP2 to identify KLF6 as a common transactivator of NF-kappaB-negative regulatory genes.
17620405	0.98	A20, and IkappaBalpha) was influenced by knocking down endogenous UXT expression.
	0.93	A20 and IkappaBalpha as described in Materials and methods.
	0.86	IkappaBalpha super repressor (SR) and analyzed the amount of A20 or IL-8 mRNA induced by TNF-alpha, respectively, via quantitative real-time RT-PCR.
	0.86	A20, and IkappaBalpha were measured by real-time RT-PCR.
28473659	0.98	A20 significantly reduced pro-inflammatory cytokines expression and down-regulated phospho-IkappaBalpha and phospho-p65 in both cells.
	0.98	A20-overexpression cells demonstrated lower phospho-p65 and phospho-I-kappaBalpha levels compared with control (Figure 7A-7B).
	0.96	A20-knockdown cells enhanced NF-kappaB activation indicated by higher phospho-p65 and phospho-I-kappaBalpha levels (Figure 7C-7D).
30526650	0.98	IkappaB-alpha resulted in IkappaB-alpha degradation and subsequent nuclear translocation of NF-kappaB. These findings suggest that haploinsufficiency of TNFAIP3, which leads to impaired A20 expression, could be responsible for the TNF-alpha-induced increased degradation of IkappaB-alpha in the present case.
	0.85	IkappaB-alpha failed to maintain baseline levels compared with cells expressing wild-type A20 in response to extended TNF-alpha stimulation.
28791018	0.98	TNFAIP3 expression correlated positively with phosphorylated IkappaBalpha, phosphorylated MAP kinases, and unstimulated phosphorylated STAT3, but negatively with LPS or TNF-alpha-stimulated fold induction of phosphorylated STAT3.
21602809	0.97	A20, robust I-kappaBalpha resynthesis that rapidly terminated TLR4-induced NF-kappaB signaling, and by suppressing chromatin remodeling.
	0.97	A20 concentrations present at the time of cell stimulation, and the kinetics of I-kappaBalpha protein re-expression after stimulation.
	0.96	A20 and I-kappaBalpha (Fig. 8).
	0.92	A20- and I-kappaBalpha-mediated negative feedback that depends on prior stimulation of cells can explain the context-dependent function of GSK3 in regulating NF-kappaB and inflammation.
	0.90	A20 expression, rapid resynthesis of I-kappaBalpha, and suppression of chromatin remodeling at the IL6 locus.
	0.89	A20, which inhibits signaling upstream of IKKs, and I-kappaBalpha, whose resynthesis terminates NF-kappaB signaling.
	0.70	A20 and I-kappaBalpha expression.
24530305	0.97	TNFAIP3 and NFKBIA (Figures 4B and S4).
	0.96	NFKBIA and TNFAIP3, but not for IL8 (Figures 3G and S3; p = 10-18, 10-6 and 0.5 respectively, t-tests for 10 ng/ml TNF datasets).
	0.82	TNFAIP3 (but similar to the pattern for NFKBIA).
	0.81	TNFAIP3 and NFKBIA were recapitulated by altering the affinity of competitor for gene promoters.
	0.76	TNFAIP3, and NFKBIA (which respectively encode IL-8, A20 and IkappaBalpha), three NF-kappaB-dependent genes strongly expressed 1 hr after exposure to TNF.
	0.74	TNFAIP3 was minimal while transcription of NFKBIA varied (3 to 61 mRNAs/cell in parental HeLa; Figure 3F, G; Table S1).
	0.55	TNFAIP3 and NFKBIA (Figure 5D, E).
22099304	0.97	A20 and the parental (WT) HEK293 cells were stimulated with TNFalpha for the indicated time, then IKK complex was immunoprecipitated with a NEMO antibody for kinase assay using GST-IkappaBalpha N-terminus and gamma-32P-ATP as substrates.
	0.96	A20 does not require deubiquitination, IkappaBalpha degradation did not occur when either A20 WT or C103A was overexpressed (Figure 1D).
	0.96	A20, then washed and incubated with gamma-32P-ATP and GST-IkappaBalpha N-terminus or immunoblotted with the indicated antibodies.
24357803	0.97	A20 was due to the activity of NF-kappaB. We used the 'knock down' of IKKbeta and IkappaBalpha in MSCs to find out if modulation of the NF-kappaB pathway activity influenced the expression of A20.
	0.60	IkappaBalpha, displayed an increased A20 expression (Figure 3d).
24324544	0.96	IkappaBalpha, IkappaBepsilon and A20.
	0.91	A20 expression, IKK retains its activity, which leads to the rapid degradation of the newly synthesized IkappaBalpha and destroys the NF-kappaB-IkappaBalpha feedback loop.
	0.90	A20-deficient cells the IKK activity remains at a high level preventing the accumulation of inhibitors IkappaBalpha and IkappaBepsilon.
	0.87	IkappaBalpha, A20, intracellular TNFalpha.
	0.80	A20-deficient cells do not exhibit limit cycle oscillation, but reach the active steady state, characterized by a high IKK activity, a high level of nuclear NF-kappaB and correspondingly high level of IkappaBalpha transcript, but low level of IkappaBalpha protein, which is constantly degraded due to the high IKK activity.
	0.64	A20 and IkappaBalpha, known for very rapid mRNA synthesis (see).
	0.61	IkappaBalpha and A20, which assure oscillatory responses, and by positive feedback loops arising due to the paracrine and autocrine regulation via TNFalpha, IL-1 and other cytokines.
29162874	0.96	IkappaBalpha and A20 mRNA at 3 hr/4 hr after TNF/LPS stimulation.
	0.93	IkappaBalpha and A20 were obtained using digital PCR measurements.
	0.90	IkappaBalpha (IkappaBalphadeg), NF-kappaBnuc, and A20 - all within first 30 min after TNF stimulation.
	0.89	IkappaBalpha and A20.
	0.87	IkappaBalpha and A20.
	0.87	IkappaBalpha (Nfkbia) and A20 (Tnfaip3) mRNA accumulate over 3-4 hours after TNF or LPS stimulation (Fig. 1d), indicating transcriptional activity, however, no IkappaBalpha proteins are visible in immunostaining images at the end of that period, and most of NF-kappaB reside in the nucleus (Fig. 1b), as also observed by Sung et al.. Notwithstanding, in cells stimulated with TNF or LPS without CHX pretreatment, IkappaBalpha mRNA profile peaks at about 1 hour, and IkappaBalpha protein accumulates over 3 hours and directs NF-kappaB out of the nucleus.
25005727	0.96	IkappaBalpha after virus infection was comparable between control and A20-knockdown cells, suggesting that under this high MOI condition, the NF-kB activity may be less effectively affected by A20 (Figure 4C, right panels).
	0.88	IkappaBalpha, A20, and beta-actin proteins were shown by immunoblotting (C).
16191192	0.96	IkappaBalpha Mut cells cultured in the absence of Dox, mRNA expression for all of these genes were significantly inhibited, with IL-6 being induced no more than 5- fold, and no detectable induction was seen for IL-8 and TNFAIP3/A20 (Figure 3a).
19077262	0.96	NFKBIA, TNFAIP3; TRD: HSPA1A/B, NFKBIA, GADD45A, SGK, JUN, MAP3K14) was changed.
21765415	0.96	A20 target important signaling intermediates upstream of IkappaBalpha to terminate NF-kappaB activation.
24083678	0.96	IkBalpha was accompanied by an increase in mRNA expression of NF-kappaB target genes A20, ICAM1 and IL-8, which was more pronounced with 50 or 120 muM sulindac sulfide (Figure 1D).
26725010	0.95	NFKBIA, and TNFAIP3) in response to TNF in the shNT and shKAP1 cell lines (Figure 4).
	0.93	NFKBIA and TNFAIP3 (Figures 4B and 4C; Figures S3B and S3C).
	0.88	NFKBIA or a slight reduction in HIV and TNFAIP3 RNA steady-state levels in response to KAP1 KD (Figures 3G-3I) without alterations in ACTB levels (Figure 3J).
31406604	0.95	IkappaB-alpha, IkappaB-epsilon or TNFAIP3, the gene encoding A20 (;9).
	0.94	IkappaB-alpha, IKK-alpha, IKK-beta, IKK-gamma/NEMO, NIK, A20), as well as their associations with EBV status and clinical outcome.
29900006	0.95	IkBalpha by pIKK, the production and degradation of IkBalpha mRNA, and, finally, the translation of A20 mRNA were introduced into the model yielding the TNFalpha signaling DCF model.
21618526	0.94	IkappaBalpha and silencing of p65 inhibited HGF-dependent A20 upregulation.
	0.85	A20 by HGF was NF-kappaB/RelA dependent as it was abolished by overexpressing IkappaBalpha or silencing p65/RelA. Unlike TNFalpha, HGF caused minimal IkappaBalpha and p65/RelA phosphorylation, with moderate IkappaBalpha degradation.
	0.82	A20, IkappaBalpha (to confirm transgene expression) and betaactin (as loading control).
	0.79	IkappaBalpha using recombinant adenovirus (rAd.) mediated gene transfer, or silencing the p65/RelA subunit of NF-kappaB, on HGF-mediated upregulation of A20.
	0.65	IkappaBalpha and p65 phosphorylation that support HGF-induced upregulation of A20, we investigated which signaling pathway triggered by HGF is responsible for mediating NF-kappaB activation and increased A20 expression.
32218782	0.94	IkappaBalpha degradation in A20 depleted cells within 15-min post-infection which was followed by its recovery to near resting levels by 6 h (Figures 4A-D).
	0.91	A20 overexpressing TIGKs displayed increased levels of IkappaBalpha after P. gingivalis infection compared to control cells (Figure 4F).
	0.91	IkappaBalpha levels (E) in A20 overexpressing TIGKs infected with P. gingivalis and relative density of IkappaBalpha levels from five independent experiments as indicated were plotted with mean and standard errors (F).
	0.66	IkappaBalpha levels were significantly decreased for approximately 1.5-2 fold in A20 depleted cells compared to control cells after 1 h post infection (Figures 4B,D).
21342546	0.94	A20, IkBa, IL1 and TNF are longer than other reactions in Table 1.
	0.87	A20 and IkBa could suppress NFkB's activity.
	0.87	A20 and IkBa to suppress the IKK activities.
23737552	0.94	IkappaBalpha and nuclear import of NF-kappaB. In IL-1 and TLR signaling, A20 limits MAPK activation by targeting TRAF6 for degradation.
	0.93	A20 inhibited IL-17-mediated activation of NF-kappaB, we monitored IL-17-dependent IkappaBalpha degradation in A20-/- MEFs that were reconstituted with EV or with A20.
25774694	0.94	A20, and phosphorylation and degradation of IkappaBalpha, were normal and transient in empty vector or Tax expressing Cadm1-deficient MEFs stimulated with TNF-alpha (Fig. 7) or IL-1beta (S4 Fig.).
	0.92	A20, TAK-1, phospho-TAK1, IkappaBalpha, phospho-IkappaBalpha, and beta-actin expression.
22187158	0.94	IkappaB-alpha and ubiquitin-editing protein A20.
26918963	0.94	A20 overexpression substantially inhibited NF-kappaB activation and decreased expression of several NF-kappaB target genes, such as E-selectin, ICAM-1, IL-8 and IkappaBalpha.
20185725	0.92	A20, IkappaBalpha,or beta-actin.
	0.79	IkappaBalpha, A20, TAX1BP1, Ubc13, UbcH5c, RNF11, Itch, and beta-actin.
26189496	0.91	A20 expression and suppresses degradation of I-kappaBalpha and NF-kappaB signaling in response to RANKL stimulation.
	0.65	A20 and I-kappaBalpha, and IgG crosslinking regulates both A20 and I-kappaBalpha.
27529070	0.91	A20 overexpression attenuates HMBA-enhanced IkappaBalpha degradation which was induced by prostratin.
28355270	0.91	NFKBIA, NFKBIAZ, TNFAIP3, MAP3K8 (TPL-2/COT), ZC3H12A (MCPIP1)).
29853534	0.90	IkBalpha, while co-transfected with si-TNFAIP3 reversed the effects of MiR-128-3p inhibitor (Figure 4B).
	0.70	TNFAIP3, while cells co-transfected with MiR-128-3p inhibitor and si-TNFAIP3 altered the level of p-IkBalpha, indicating that MiR-128-3p regulated the NF-kappaB pathway is through regulating the expression of TNFAIP.
26170170	0.89	IkappaBalpha and A20.
	0.88	A20 (left) and IkappaBalpha (right) were measured by qPCR at indicated time points after TNFalpha treatment.
	0.80	A20, we identified IkappaBalpha in our PAR-CLIP as an additional RC3H1 target transcript (Fig. 6a,b).
	0.51	A20, IkappaBalpha and NFKBIZ, are targets of RC3H1.
28569771	0.89	A20 KD CNE2 cells transfected with plasmid expressing IkappaBalpha and control cells.
	0.83	A20 KD significantly enhanced the phosphorylated levels of IKKalpha/beta, IkappaBalpha, and p65, the nuclear translocation of p-p65 and NF-kappaB luciferase reporter activity in the CNE2 cells, whereas either miR-125b inhibitor or A20 OE significantly reduced the phosphorylated levels of IKKalpha/beta, IkappaBalpha, and p65, the nuclear translocation of p-p65 and NF-kappaB luciferase reporter activity in the CNE2-IR cells (Figures 6a-d).
	0.69	IkappaBa overexpression or BAY11-7082 abolished the effects of A20 KD on NPC proliferation and apoptosis, whereas p65 (RelA) overexpression abolished the effects of A20 overexpression on NPC cell proliferation and apoptosis.
19857199	0.89	A20 controls IKK and thus the degradation of IkappaBalpha.
	0.53	A20 is one of the feedback regulators of NF-kappaB. A20 shares some similarities with IkappaBalpha, another feedback regulator.
17925009	0.88	A20 and IkappaBalpha, shown in Fig. 1.
	0.82	A20 expression, the IKK retains activity which leads to rapid degradation of the newly resynthesized IkappaBalpha, which destroys the NF-kappaB-IkappaBalpha feedback loop.
	0.79	IkappaBalpha and A20 genes.
	0.73	IkappaBalpha, Panel E: Nuclear NF-kappaB, Panel F: IkappaBalpha gene activity, Panel G: A20 gene activity, Panel H: IkappaBalpha mRNA, Panel I: A20 mRNA, Panel J: A20 protein.
	0.65	IkappaBalpha and NF-kappaB-A20-IKK feedback loops, arise because both IkappaBalpha and A20 genes are directly regulated by NF-kappaB binding.
	0.62	A20 (or IkappaBalpha) gene expression.
	0.51	IkappaBalpha and A20 promoters are "pre-loaded"- already bound by general transcription factors, coactivators and RNA Pol II, waiting for the presence of NF-kappaB binding to activate expression.
19152111	0.88	A20 protects against TNFalpha-mediated cell death, macrophages were co-infected with a control adenoviral vector or one expressing A20 (Ad A20) plus Ad-IkappaBalpha or Ad-control.
	0.80	zinc-finger protein A20 was the most highly expressed at 2 hours and its induction was prevented by the super repressor IkappaBalpha (Figure 6B).
26648169	0.88	A20 over-expression significantly reversed IL-1alpha-induced phosphorylation of ERK, JNK, and p38, but did not affect IL-1alpha-induced degradation of IkappaB-alpha (Fig. 9g).
	0.52	A20 over-expression did not reverse IL-1beta-induced degradation of IkappaB-alpha (Fig. 9f).
30761389	0.88	IkappaBalpha, A20 and Regnase-1/MCPIP1, all of which are regulated by NF-kappaB. ABIN-1 is also a known NF-kappaB target gene, raising the possibility that IL-17 might also induce its expression.
	0.51	A20), NFKBIA (encoding IkappaBalpha) and TNIP1 (encoding ABIN-1).
27759429	0.88	TNFAIP3, PTGS2, and NFKBIA were related to cellular apoptosis and regulation of apoptosis.
24039598	0.87	TNFAIP3 promoter and was accompanied by a concomitant increase in A20 protein and phospho-IkappaBalpha expression (Figure 3C).
	0.68	A20 (Figure 5B) and increased basal NF-kappaB pathway activity as measured by IkappaBalpha phosphorylation in homozygous risk cell lines (Figure 5C).
29505600	0.85	A20 transcript levels and NFKBIA expression, as measured by RNAseq, in ART-treated participants (n = 19).
	0.81	A20 and related genes (e.g., IkappaBalpha) demonstrated a positive association with epithelial function.
28178345	0.82	A20, p-IkappaBalpha, total IkappaBalpha, p-BTK and total BTK was analyzed using Simple Western.
	0.58	A20 loss, this leads to p-IkappaBalpha upregulation demonstrated by some slight resistance to PI3K or BTK inhibition alone.
26991692	0.81	A20 siRNA lead to more prominent NF-kappaB/RelA in the nucleus and more weakened IkappaB-alpha expression (Fig. 6C and D).
	0.73	A20 on EC regulation and NF-kappaB signalling in vitro is correlated back to reduced IkappaB-alpha in vivo.
	0.71	A20 against NF-kappaB translocation and activation was suggested to be depending on a level upstream of IkappaB-alpha degradation 41, 44.
	0.66	A20 on NF-kappaB activation was determined by NF-kappaB/RelA translocation and IkappaB-alpha degradation.
24224954	0.80	IkappaB-alpha, A20 and IL-8 was inhibited in hepatocytes pre-treated with Ado+Hcy (Fig. 3C).
	0.72	A20 and IkappaB-alpha were not activated, NFkappaB remained in the nucleus for much longer.
	0.71	A20 is analogous to IkappaB-alpha: both genes are activated by NFkappaB, and both encode proteins that terminate NFkappaB signaling.
	0.61	IkappaB-alpha, A20 and IL-8 mRNA (Figs. 3B and 3C) and lack of expression of the NFkappaB-dependent luciferase reporter (Fig. 3A).
24529102	0.79	A20 and IkappaBalpha expression in RC-K8 cells.
	0.70	A20, CCR7, NFKBIA, TRAF1, and TNFalpha mRNAs was significantly increased (1.1- to 1.5-fold; p < 0.05) in p300 knockdown cells, relative to control RC-K8 cells.
	0.55	A20 and IkappaBalpha, two genes that have been shown to limit the growth of RC-K8 cells when overexpressed.
	0.51	A20 and anti-IkappaBalpha Western blotting to determine whether the increases in mRNA seen in these cells resulted in increases in protein levels.
	0.50	A20, BCL2A1, CCR7, NFKBIA [encoding IkappaBalpha], LTA, TNF, TRAF1) in RC-K8 cells expressing p300 shRNA to control cells (Figure 4d).
26681923	0.79	I-kappaBalpha expression in U937-A20 shRNA cells and control cells after 0.5 mmol/L FFAs treatment for the indicated times. (D2) and (D3) Corrected densitometry of p-p65/GAPDH, p-I-kappaBalpha/GAPDH in (D1), respectively.
	0.68	A20-overexpression cells showed impaired activation of NF-kappaB in response to FFAs as indicated by lower phospho-p65 levels and lower phospho-I-kappaBalpha levels (Fig. 3A and C).
	0.67	I-kappaBalpha expression in HepG2-A20 shRNA cells and control cells after 0.5 mmol/L FFAs treatment for the indicated times.
32028675	0.79	A20 expression had downregulated canonical NF-kappaB signaling, which was validated via the decreased IkappaBalpha phosphorylation and degradation at all analyzed time points (Figure 4A), independent of the presence of IAP antagonist.
29109532	0.71	A20, a zinc finger protein that exerts inhibitory effects on TNF signaling, significantly inhibited TNF-alpha-stimulated IkappaBalpha degradation (Fig. 3C and Supplementary Fig. 4).
23901138	0.69	IkappaBalpha and IkappaBbeta, causing their proteolysis and the subsequent nuclear translocation and activation of NF-kappaB. IkappaBalpha and A20 are immediate transcriptional targets of NF-kappaB that assist in the negative feedback control of the NF-kappaB signaling pathway.
19380639	0.68	TNFAIP3, KM-H2 cells also harbor inactivating mutations in NFKBIA (IkappaBalpha).
24586164	0.56	IkappaBalpha and A20 (13.5 ng).
22396652	0.54	A20 deficient cells showed enhanced NF-kappaB activation as indicated by increased phosphorylation and sustained degradation of IkappaBalpha (figure 1B).
30837480	0.51	A20, IkappaBalpha in the HTLV-1-infected T-cell line MT2 after transfection with various concentrations of shRNA-expression vector for Tax (shTax) or a shRNA expression vector for luciferase (shLuc) as a control.