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Human Polyclonal TNIP2 Primary Antibody für ICC, IF - ABIN442650
Banks, Boanca, Lee, Florens, Washburn: Proteins interacting with cloning scars: a source of false positive protein-protein interactions. in Scientific reports 2015
Show all 2 Pubmed References
the data indicated that TNIP2 is significantly decreased in MODS following severe trauma, and it plays a protective role in MODS development by inhibiting the inflammation response and oxidative stress by preventing NFkappaB activation.
RelAp43 interacts with the p105-ABIN2-TPL2 complex and we observe a strong perturbation of this complex in presence of M protein.
Study reports the crystal structure of hABIN2 in complex with linear triubiquitin, which shows the ubiquitins with M1-linkage could form a right-handed helical trimer when bridging two hABIN2 dimers, and thus allow the assembly of a higher-order signaling complex with A20.
Findings suggest an expanded role for the NF-kappaB network hub protein TNIP2 and reveals an association between TNIP2 and YLPM1, TNIP2 and ESCRT-I, together with many RNA processing proteins and a distinct set of mRNAs.
miR-1180 might act as a tumor promoter by targeting TNIP2 during development of hepatocellular carcinoma.
miR let-7a-regulated USP35 can inhibit NF-kappaB activation by deubiquitination and stabilization of ABIN-2 protein
ABIN-2 acts as a positive regulator of NF-kappaB-dependent transcription by activating IKKalpha.
A20, ABIN-1/2, and CARD11 mutations have prognostic value in gastrointestinal diffuse large B-cell lymphoma
transcription repressed by promyelocytic leukemia protein expression
FLIP1 has a role in the regulation of NF-kappaB activity related to the role of LKB1 in tumor suppression
Endothelial tyrosine kinase Tie2 interacts with ABIN-2.
ABIN-2 exerts unexpected function in mediating transcriptional coactivation.
ABIN-2 was found to inhibit endothelial apoptosis and rescue cells from death following growth factor deprivation. Deletion of the carboxy-terminus of ABIN-2 removed its ability to inhibit apoptosis.
optimal TPL-2 stability in vivo requires interaction with ABIN-2 as well as p105
ABIN-2 may function as a negative regulator that downregulates NF-kappaB activation during liver regeneration
Thus, CIH-mediated NF-kappaB activation may be a molecular mechanism linking OSA and cardiovascular pathologies seen in OSA patients.
Thus the present results showed a correlation between NF-kappaB activation and the repair of sublethal damage in split-dose irradiation.
role for an ABIN-sensitive non-classical NF-kappaB signalling pathway in the proliferation of EGFR-overexpressing tumour cells.
This review defines ABIN-2 based on three different parameters: ability to bind A20; ability to inhibit NF-kappaB activation upon overexpression; the presence of specific short amino acid regions of strong homology, designated ABIN homology domains.
Authors found that TNIP2 was correlated with the activation of NF-kappaB in cerulein-stimulated AR42J cells, and TNIP2 over-expression inhibited the inflammatory response caused by cerulein. Moreover, results suggest that TNIP2 over-expression relieved the cerulein-triggered inflammatory response and AP-induced myocardial injury in mice.
ABIN-2 acts to positively regulate the Erk signaling potential by stabilizing TPL-2.
TNIP2 binds to the C-terminal zinc finger domain of A20 (TNFAIP3\; MIM 191163) and is involved in activation of the ERK (see MAPK3\; MIM 601795) MAP kinase pathway in various cell types (Van Huffel et al., 2001
TNFAIP3-interacting protein 2
, TNFAIP3 interacting protein 2
, A20-binding inhibitor of NF-kappaB activation 2
, A20-binding inhibitor of NF-kappa-B activation 2
, A20-binding inhibitor of NF-kappaB activation-2
, fetal liver LKB1-interacting protein
, A20 binding inhibitor of NF-kappaB activation-2