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TNIP3 expression is significantly upregulated in human masticatory mucosa during wound healing
recombinant transgene facilitates the transcription of pro-inflammatory cytokines in fibroblast-like synoviocytes in rheumatoid arthritis
ABIN-3 is a novel negative feedback regulator of LPS-induced NF-kappaB activation
ABIN-3 is, thus, an IL-10-induced gene product capable of attenuating NF-kappaB in human macrophages yet is inoperative in mice and represents a basis for species-specific differences in IL-10 actions.
Enhanced expression of ABIN-3 in monocytes is associated with sepsis
This review defines ABIN-3 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.
adiponectin augmented the expression of A20, suppressor of cytokine signaling (SOCS) 3, B-cell CLL/lymphoma (BCL) 3, TNF receptor-associated factor (TRAF) 1, and TNFAIP3-interacting protein (TNIP) 3.
Binds to zinc finger protein TNFAIP3 and inhibits NF- kappa-B activation induced by tumor necrosis factor, Toll-like receptor 4 (TLR4), interleukin-1 and 12-O-tetradecanoylphorbol-13- acetate. Overexpression inhibits NF-kappa-B-dependent gene expression in response to lipopolysaccharide at a level downstream of TRAF6 and upstream of IKBKB. NF-kappa-B inhibition is independent of TNFAIP3 binding.
TNFAIP3 interacting protein 3
, A20-binding inhibitor of NF-kappa-B activation 3
, ABIN-3 beta
, Listeria induced
, TNFAIP3-interacting protein 3
, TNFAIP3-interacting protein 3 beta
, TNIP3 beta
, listeria-induced gene protein
, RIKEN cDNA 9030611K07