TNFAIP3-interacting protein 2

Definition:

Inhibits NF-kappa-B activation by blocking the interaction of RIPK1 with its downstream effector NEMO/IKBKG. Forms a ternary complex with NFKB1 and MAP3K8 but appears to function upstream of MAP3K8 in the TLR4 signaling pathway that regulates MAP3K8 activation. Involved in activation of the MEK/ERK signaling pathway during innate immune response; this function seems to be stimulus- and cell type specific. Required for stability of MAP3K8. Involved in regulation of apoptosis in endothelial cells; promotes TEK agonist-stimulated endothelial survival. May act as transcriptional coactivator when translocated to the nucleus. Enhances CHUK-mediated NF-kappa-B activation involving NF-kappa-B p50-p65 and p50-c-Rel complexes.

References:

[1]. Wei-Kuang Liu, et al. The inhibitor ABIN-2 disrupts the interaction of receptor-interacting protein with the kinase subunit IKKgamma to block activation of the transcription factor NF-kappaB and potentiate apoptosis. Biochem J. 2004 Mar 15;378(Pt 3):867-76. [Content Brief]

[2]. Laurent Leotoing, et al. A20-binding inhibitor of nuclear factor-kappaB (NF-kappaB)-2 (ABIN-2) is an activator of inhibitor of NF-kappaB (IkappaB) kinase alpha (IKKalpha)-mediated NF-kappaB transcriptional activity. J Biol Chem. 2011 Sep 16;286(37):32277-88. [Content Brief]

[3]. Wei-Kuang Liu, et al. An LKB1-interacting protein negatively regulates TNFalpha-induced NF-kappaB activation. J Biomed Sci. 2003 Mar-Apr;10(2):242-52. [Content Brief]

[4]. Amir Tadros, et al. ABIN-2 protects endothelial cells from death and has a role in the antiapoptotic effect of angiopoietin-1. Blood. 2003 Dec 15;102(13):4407-9. [Content Brief]

[5]. Chia-Yi Chien, et al. The A20-binding protein ABIN-2 exerts unexpected function in mediating transcriptional coactivation. FEBS Lett. 2003 May 22;543(1-3):55-60. [Content Brief]

[6]. V Lang, et al. ABIN-2 forms a ternary complex with TPL-2 and NF-kappa B1 p105 and is essential for TPL-2 protein stability. Mol Cell Biol. 2004 Jun;24(12):5235-48. [Content Brief]

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