Regulation of experimental autoimmune encephalomyelitis by TPL-2 kinase.
London, United Kingdom. In J Immunol, 2014
Importantly, using a newly generated mouse strain expressing a kinase-inactive form of TPL-2, we demonstrated that stimulation of EAE was dependent on the catalytic activity of TPL-2 and not its adaptor function to stabilize the associated ubiquitin-binding protein ABIN-2.
The biology of A20-binding inhibitors of NF-kappaB activation (ABINs).
In Adv Exp Med Biol, 2013
The family of A20-Binding Inhibitors of NF-kappaB (ABINs) consists of three proteins, ABIN-1, ABIN-2 and ABIN-3, which were originally identified as A20-binding proteins and inhibitors of cytokines and Lipopolysaccharide (LPS) induced NF-kappaB activation.
A20 inactivation in ocular adnexal MALT lymphoma.
Cambridge, United Kingdom. In Haematologica, 2012
It is also unknown whether ABIN-1 and ABIN-2, the components of the A20 NF-κB inhibitor complex, are inactivated by genetic changes in ocular adnexal mucosa-associated lymphoid tissue lymphoma.
IκB kinase regulation of the TPL-2/ERK MAPK pathway.
London, United Kingdom. In Immunol Rev, 2012
TPL-2 is stoichiometrically complexed with the NF-κB inhibitory protein, NF-κB1 p105, and the ubiquitin-binding protein ABIN-2, both of which are required to maintain TPL-2 protein stability.
Regulation and function of TPL-2, an IκB kinase-regulated MAP kinase kinase kinase.
London, United Kingdom. In Cell Res, 2011
In unstimulated cells, TPL-2 is stoichiometrically complexed with the NF-κB inhibitory protein NF-κB1 p105, which blocks TPL-2 access to its substrate MEK, and the ubiquitin-binding protein ABIN-2 (A20-binding inhibitor of NF-κB 2), both of which are required to maintain TPL-2 protein stability.
ABINs: A20 binding inhibitors of NF-kappa B and apoptosis signaling.
Gent, Belgium. In Biochem Pharmacol, 2009
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.