Disease relevance of TNIP2

• Identification of a novel mechanism of NF-kappaB inactivation by progesterone through progesterone receptors in Hec50co poorly differentiated endometrial cancer cells: induction of A20 and ABIN-2 [1].

High impact information on TNIP2

• ABIN-2 inhibits nuclear factor-kappaB (NF-kappaB) activity and is a possible effector of A20 regulation of NF-kappaB [2].
• ABIN-2 also interacts with the endothelial receptor Tie2 [2].
• ABIN-2 protects endothelial cells from death and has a role in the antiapoptotic effect of angiopoietin-1 [2].
• Although A20 is a potent inhibitor of endothelial apoptosis, the effect of ABIN-2 on apoptosis is not known [2].
• We identified ABIN2 and Ier2/pip92 mRNAs as candidate targets of AUF1 in the rat uterus [3].

Biological context of TNIP2

• Deletion of the carboxy-terminus of ABIN-2 removed its ability to inhibit apoptosis [2].
• We have also found that BAF60a, a component of chromatin-remodeling complex, interacts with ABIN-2 by the yeast two-hybrid analysis [4].
• Here we report that ABIN-2 has the potential to enter the nucleus and plays a role in mediating transcriptional activation in both yeast and mammalian cells [4].
• In the first part of this work [Heinrich, R., Montero, F., Klipp, E., Waddell, T. G. & Melendez-Hevia, E. (1997) Eur. J. Biochem. 243, 191-201] the kinetic and thermodynamic constraints under which an optimal glycolysis must be designed have been analysed [5].

Anatomical context of TNIP2

• The inhibitors of phosphatidylinositol-3 kinase, wortmannin and LY294002, suppressed ABIN-2 inhibition of endothelial cell death [2].
• Coexpression of Tie2 and ABIN-2 in CHO cells confirmed the interaction occurs in mammalian cells [6].
• The L6 skeletal muscle cell line has been identified as a suitable model to study the action of insulin on glucose uptake in muscle [Klip, Li & Logan (1984) Am. J. Physiol. 247, E291-E296] [7].

Associations of TNIP2 with chemical compounds

• The antiinflammatory endothelial tyrosine kinase Tie2 interacts with a novel nuclear factor-kappaB inhibitor ABIN-2 [6].
• The tumorigenic inflammatory and anti-apoptotic effects of NFkappaB are inhibited by progesterone/PRB through the transcriptional control of binding proteins A20 and ABIN-2 [1].
• Immunostaining for putative targets of NF-kappaB was as follows: Bcl-xL, 76.2% (p = 0.001); Flip 43.0%; Cyclin D1, 64.79%. p65 immunostaining correlated with increased immunoreaction for steroid hormone receptors [8].
• The PED PAH concentrations were also used to calculate porewater PAH concentrations that allowed for the estimation of a linear free-energy relationship between the lipid-water distribution coefficient (Klip) and the octanol-water distribution coefficient (KOW) for PAH uptake in marine polychaetes (R2 = 0.94, p < 0.0001) [9].

Physical interactions of TNIP2

• The A20-binding protein ABIN-2 exerts unexpected function in mediating transcriptional coactivation [4].

Other interactions of TNIP2

• Here we examine the effects of ABIN-2 on endothelial cell apoptosis and its potential involvement in Tie2-mediated endothelial survival [2].
• In contrast, Tie1 did not interact with ABIN-2 in the yeast two-hybrid system or mammalian cells [6].
• In this report, we describe the identification of a putative human LKB1-interacting protein, FLIP1, using the yeast two-hybrid system [10].

References