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Validated All-in-One™ qPCR Primer for TNFAIP3(NM_001270507.2) Search again
Product ID:
HQP162166
(click here to view gene annotation page)
Powered by BiozSpecies:
Human
Symbol:
Alias:
A20, AIFBL1, AISBL, OTUD7C, TNFA1P2
Gene Description:
TNF alpha induced protein 3
Target Gene Accession:
NM_001270507.2(click here to view gene page)
Estimated Delivery:
Approximately 1-3 weeks, but may vary. Please email sales@genecopoeia.com or call 301-762-0888 to confirm ETA.
Important Note:
By default, qPCR primer pairs are designed to measure the expression level of the splice variant (accession number) you selected for this gene WITHOUT consideration of other possible variants of this gene. If this gene has multiple variants, and you would like to measure the expression levels of one particular variant, multiple variants, or all variants, please contact us for a custom service project at inquiry@genecopoeia.com.
Summary
This gene was identified as a gene whose expression is rapidly induced by the tumor necrosis factor (TNF). The protein encoded by this gene is a zinc finger protein, and has been shown to inhibit NF-kappa B activation as well as TNF-mediated apoptosis.
Gene References into function
- The zinc finger protein A20 is an NF-kappaB-inducible gene that can protect the IKKgamma-deficient cells from TNF-induced apoptosis by disrupting the recruitment of the death domain signaling molecules TRADD and RIP to the receptor signaling complex.
- In vitro, recombinant A20 inhibits NF-kappaB activation in mouse islets and protects from cytokine- and death receptor-mediated apoptosis; in vivo, A20 preserves mouse islet cell mass and function in diabetic mice in early post-transplantation period.
- redundant and distinct roles in regulating NFkappaB activation and apoptosis
- Our results suggest that A20 may function as a negative regulator of TLR-mediated inflammatory responses in the airway, thereby protecting the host against harmful overresponses to pathogens.
- A20 also protects from Fas/CD95 and significantly blunts natural killer cell-mediated endothelial cell apoptosis by inhibiting caspase 8 activation
- definition of a novel ubiquitin ligase domain and identification of two sequential mechanisms by which A20 downregulates NF-kappaB signalling
- A20 is a candidate negative regulator of the signaling cascade to interferon regulatory factor-3 activation in the innate antiviral response.
- A20 may be involved in the regulation of cell proliferation by tumor necrosis factor, Vitamin D, and androgen in prostate cancer.
- A1 and A20 are both required for optimal protection from apoptosis (A1) and inflammation (A20) in conditions leading to renal damage
- the virus-inducible, NF-kappaB-dependent activation of A20 functions as a negative regulator of RIG-I-mediated induction of the antiviral state
- Results suggest that A20 can effectively protect neurons from postischemic apoptosis and may function partly on death receptor caspase pathway.
- ABIN-1 physically links A20 to NEMO/IKKgamma and facilitates A20-mediated de-ubiquitination of NEMO/IKKgamma, thus resulting in inhibition of NF-kappaB
- A20 prevents neointimal hyperplasia through combined anti-inflammatory and antiproliferative functions in medial smooth muscle cells.
- A new role for A20 in regulating neovascularisation. We used RNA interference to inhibit A20 expression in primary human umbilical vein endothelial cells (HUVECs)and investigated the effect on tubule formation in two in vitro angiogenesis assays
- Using oligonucleotide microarrays and real-time PCR, we identified TNFAIP3/A20 as the most highly regulated antiapoptotic gene expressed in cytokine-stimulated human and mouse islets.
- These findings point to variability in the A20/TNFAIP3 gene as a modulator of CAD risk in type 2 diabetes. This effect is mediated by allelic differences in A20 expression.
- A20 is a new 17beta-estradiol-regulated gene.
- May act as a tumor suppressor gene in ocular adnexal marginal zone B cell lymphoma; loss of this gene may play an important role in lymphomagenesis.
- analysis of the crystal structure of the N-terminal OTU (ovarian tumour) deubiquitinase domain of A20
- These findings reveal a dynamic regulation of DSIF involving either E-box or NF-kappaB depending on the physiological circumstances.
- Molecular basis for the unique deubiquitinating activity of the NF-kapppaB inhibitor A20 is reported.
- results further define the molecular mechanisms that control activation of NF-kappaB and reveal a function for A20 in the regulation of CARMA and BCL10 activity in lymphoid and non-lymphoid cells
- Pre-treatment of human umbilical vein endothelial cells with an adenovirus containing A20 suppressed activation of NF-kappaB and induction of pro-inflammatory molecules by hypoxia/re-oxygenation.
- five genes (TNFSF10/TRAIL, IL1RN, IFI27, GZMB, and CCR5) were upregulated and three genes (CLK1, TNFAIP3 and BTG1) were downregulated in at least three out of four subpopulations during acute GVHD.
- Dendritic cells downregulated by A20 show higher activation of transcription factors NF-kappaB and activator protein-1, which results in increased and sustained production of interleukin (IL)-6, IL-10, and IL-12p70.
- RNF11, together with TAX1BP1 and Itch, is an essential component of an A20 ubiquitin-editing protein complex that ensures transient activation of inflammatory signalling pathways.
- These results establish that variants near TNFAIP3 contribute to differential risk of SLE and RA.
- We show that three independent SNPs in the TNFAIP3 region (rs13192841, rs2230926 and rs6922466) are associated with systemic lupus erythematosus (SLE) among individuals of European ancestry
- Expanded catalog of genetic loci implicated in psoriasis susceptibility.