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evidence for HBV-induced HCC susceptibility gene TNIP1 in the Chinese Han population
Our data suggest that ABIN1 protects human leukaemia T-cells by allowing them to resist the apoptosis induced by T. gondii ME-49 and that the T. gondii ME-49 strain induces the apoptosis of human leukaemia T-cells via A20-mediated downregulation of ABIN1 expression.
ABIN-1 negatively regulates MOR function in vitro and in vivo
this review discusses the role of TNIP1 in autoimmune diseases as a regulator of Toll-like receptor signaling
Results showed that ABIN1 acted as a modulator to down-regulate HDAC1 ubiquitination via three different sites, thereby stabilizing HDAC1 by inhibiting its lysosomal and proteasomal degradation.
Results provide evidence that TNIP1 SNP (rs7708392) might be associated with the development of lupus nephritis in Egyptian SLE patients.
cell viability and apoptosis in the hepatic cell line L02 were detected after hypoxia/reoxygenation (H/R) treatment, and MTT assay showed that cell viability was inhibited after H/R treatment, but reversed after TNIP1 transfection
association of TNIP1 was stronger in AIH without HLA-DRB1*04:05 allele (P = 0.0063, Q = 0.0127, OR 1.48, 95% CI: 1.12-1.96), though the association was not detected in AIH with DRB1*04:05
Naf1 contributes to the maintenance of HIV-1 latency by inhibiting long terminal repeat driven HIV-1 gene transcription in a nuclear factor kappa B-dependent manner.
the risk allele for the TNIP1 rs7708392 polymorphism was associated with systemic lupus erythematosus susceptibility.
C/EBP beta LAP isoform expression was increased and LIP/TNFAIP3/TNIP1 expression was decreased in systemic lupus erythematosus (SLE) patients. LAP expression was positively correlated with SLE disease activity; TNFAIP3 and TNIP1 expression was negatively correlated with SLE disease activity.
genetic variation in TNIP1 gene is associated with gastric carcinoma
An association of the GPX3-TNIP1 locus with ALS is identified using cross-ethnic meta-analyses. [Meta-Analysis]
These studies define a novel role for ABIN1 dysfunction and NF-kappaB in mediating glomerulonephritis through proinflammatory activation of podocytes.
IM could upregulate A20 protein to inhibit the activation of NF-kappaB pathway in Jurkat T cells, which was independent of the ABIN1 protein.
LILRB1 ligation during monocyte differentiation to dendritic cells in vitro increases ABIN1 expression. Increased ABIN1 expression occurs in "immunosuppressive" monocytes of patients with non-Hodgkin lymphoma ex vivo. ABIN1 siRNA allows dendritic cells and immunosuppressive monocytes to respond to stimulation by allowing NF-kappaB translocation to the nucleus, more phagocytosis, cytokine secretion, and T-cell stimulation.
These findings show ABIN1 as an intrinsic suppressor of HIV-1 mRNA transcription by regulating the ubiquitination of Tat.
Polymorphisms in TNIP1 are associated with GPP in Chinese Han population. However, no association with PPP was found. These findings suggest that TNIP1 might be a susceptibility gene for GPP.
The findings of this study suggested that TNIP1 is a new potential predisposing gene to spina bifida (SB) and its pathway needs to be investigated in human NTD in order to confirm its role and to plan appropriate counseling to families
Data suggest that reduced TNFalpha-induced protein 3-interacting protein 1 (TNIP1) expression may have a role in the pathogenesis of myasthenia gravis (MG)for patients with thymoma.
It has been proposed that ABIN-1 provides a critical link between methionine1 ubiquitylation mediated by the LUBAC complex and lysine63 deubiquitylation by phospho-A20 to modulate the activation of RIPK1.
Reduced expression of TNIP1 was determined in hepatic ischemia/reperfusion (I/R) injury compared to normal mice. Then, TNIP1 transgene mice were used to determine the effects of TNIP1 on mice after treatment for I/R.
the data establish Tnip1 as a critical regulator of IL-17 biology and reveal a causal role of keratinocytes in the pathogenesis of psoriasis.
Suppression of IRAK1 or IRAK4 Catalytic Activity, but Not Type 1 IFN Signaling, Prevents Lupus Nephritis in Mice Expressing a Ubiquitin Binding-Defective Mutant of ABIN1
These results suggest that the ABIN1-mediated hyperactivation of IKKs and MAPKs might mediate chronic inflammation and CVD development.
studies link ABIN-1 with IL-23 and IL-17, and they provide cellular and molecular mechanisms by which ABIN-1 regulates susceptibility to psoriasis.
data reveal ABIN1 as an essential anti-inflammatory component of TLR-signaling pathways that controls C/EBPbeta activity
ABIN1 requires its ubiquitin binding domain and cooperates with TAX1BP1 and A20 to restrict antiviral signaling.
the interaction of ABIN1 with polyubiquitin is required to limit the activation of TLR-MyD88 pathways and prevent autoimmunity
Using a murine model of allergen-induced asthma, we have demonstrated that adenovirus-mediated delivery of ABIN-1 to the lung epithelium results in a reduction of allergen-induced eosinophil infiltration into the lungs.
ABIN-1 inhibits caspase 8 recruitment to FADD (Fas-associated death domain-containing protein) in TNF-induced signalling complexes, preventing caspase 8 cleavage and programmed cell death.
we cloned the pig ABIN-1 gene to investigate its potential effects on pig reproduction traits.
This gene encodes an A20-binding protein which plays a role in autoimmunity and tissue homeostasis through the regulation of nuclear factor kappa-B activation. Mutations in this gene have been associated with psoriatic arthritis, rheumatoid arthritis, and systemic lupus erythematosus. Multiple transcript variants encoding different isoforms have been found for this gene.
A20-binding inhibitor of NF-kappa-B activation 1
, HIV-1 Nef-interacting protein
, Nef-associated factor 1 SNP
, TNFAIP3-interacting protein 1
, virion-associated nuclear shuttling protein
, A20-binding inhibitor of NF-kappa B activation
, Nef-associated factor 1
, TNFAIP3 interacting protein 1
, A20 binding and inhibitor of NF-kB protein 1
, TNFAIP3-interacting protein 1-like