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Ankyrin repeat domain 2
ANKRD2 belongs to the conserved muscle ankyrin repeat protein (MARP) family. Expression of MARPs is induced in response to physiologic stress, injury, and hypertrophy (Miller et al., 2003 [PubMed 14583192]).[supplied by OMIM, Mar 2008] (from
Kojic et al., Belgrade, Serbia. In Histochem Cell Biol, Jun 2015
Muscle-specific mechanosensors Ankrd2/Arpp (ankyrin repeat protein 2) and Ankrd1/CARP (cardiac ankyrin repeat protein) have an important role in transcriptional regulation, myofibrillar assembly, cardiogenesis and myogenesis.
Moorhead et al., Calgary, Canada. In Biochem Biophys Res Commun, Apr 2015
PP2A containing the B55 subunit is a key regulator of mitosis and must be inhibited by phosphorylated α-endosulfine (ENSA) or cyclic AMP-regulated 19 kDa phosphoprotein (ARPP-19) to allow passage through mitosis.
Re-expression of miR-320a was sufficient to sensitize TamR cells to tamoxifen by targeting cAMP-regulated phosphoprotein (ARPP-19) and estrogen-related receptor gamma (ERRγ) as well as their downstream effectors, c-Myc and Cyclin D1.
Labeit et al., Mannheim, Germany. In Biomed Res Int, 2014
Expression patterns of 8 mechanoptotic machinery-associated titin ligands (ANKRD1, ANKRD2, TRIM63, TRIM55, NBR1, MLP, FHL2, and TCAP) were quantitated in endomyocardial biopsies from 25 patients with advanced IDCM.
Hunt, Schwäbisch Hall, Germany. In Adv Biol Regul, 2013
Control of this phosphatase is achieved by an inhibitor protein (α-endosulfine or ARPP-19) that becomes inhibitory when phosphorylated by a protein kinase called Greatwall, which is itself a substrate of CDK1.
Jessus et al., Paris, France. In Results Probl Cell Differ, 2010
PP2A-B55δ is the major phosphatase controlling exit from mitosis; it is negatively regulated by the kinase Greatwall that phosphorylates the small protein ARPP-19 and converts it into a potent PP2A inhibitor.
Moriyama et al., Ōita, Japan. In Histochem Cell Biol, 2008
The Ankrd2 accumulated in the nuclei of myofibers located adjacent to severely damaged myofibers after muscle injury. Ankrd2 may translocate from the I-band to the nucleus in response to muscle damage and in the regulation of gene expression.