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findings underscore the specific and prominent role of SKIP and GRP78 (Montrer HSPA5 Kits ELISA) in the regulation of insulin (Montrer INS Kits ELISA)-dependent PI 3 (Montrer PI3 Kits ELISA)-kinase signaling in skeletal muscle
prominent role of SKIP in the development of insulin (Montrer INS Kits ELISA) resistance in skeletal muscle
the physiological role of Pak1 (Montrer PAK1 Kits ELISA)-SKIP binding is in the regulation of insulin (Montrer INS Kits ELISA) signaling in skeletal muscle
SKIP controls the IGF-II-PI 3 (Montrer PI3 Kits ELISA)-kinase-Akt (Montrer AKT1 Kits ELISA)-mTOR (Montrer FRAP1 Kits ELISA) auto-regulation loop during myogenesis.
Specific suppression of insulin (Montrer INS Kits ELISA) signaling is achieved via the spatiotemporal regulation of SKIP through the scaffolding function of Pak1 (Montrer PAK1 Kits ELISA).
Regulation of insulin signaling and glucose transporter 4 (GLUT4) exocytosis by phosphatidylinositol 3,4,5-trisphosphate (PIP3) phosphatase, skeletal muscle, and kidney enriched inositol polyphosphate phosphatase (SKIP).
Results indicate that Inpp5k 5-phosphatase is important for the control of the arginine vasopressin (Montrer AVP Kits ELISA)/aquaporin-2 (Montrer AQP2 Kits ELISA) signalling pathway and water transport in kidney collecting ducts.
Silencer of death domains (SODD (Montrer BAG4 Kits ELISA)) inhibits skeletal muscle and kidney enriched inositol 5-phosphatase (SKIP) and regulates phosphoinositide 3-kinase (PI3K)/Akt (Montrer AKT1 Kits ELISA) signaling to the actin cytoskeleton.
These results imply that SKIP regulates insulin (Montrer INS Kits ELISA) signaling in skeletal muscle.
results suggest that SKIP (skeletal muscle and kidney-enriched inositol phosphatase) plays a negative regulatory role in Akt (Montrer AKT1 Kits ELISA)/ GSK-3beta (Montrer GSK3b Kits ELISA)/GS (glycogen synthase) pathway leading to glycogen (Montrer GYS1 Kits ELISA) synthesis in myocytes
In individuals exhibiting congenital muscular dystrophy, early-onset cataracts, and mild intellectual disability but normal cranial magnetic resonance imaging, we identified bi-allelic mutations in INPP5K, encoding inositol polyphosphate-5-phosphatase K.
Mutations in INPP5K cause a congenital muscular dystrophy syndrome with short stature, cataracts, and intellectual disability.
These findings suggest a model by which GRP78 (Montrer HSPA5 Kits ELISA) regulates intracellular localization of SKIP and how SKIP binds to Pak1 (Montrer PAK1 Kits ELISA) on insulin (Montrer INS Kits ELISA) stimulation.
The authors report that HBV core protein interacts with a cellular SKIP (skeletal muscle and kidney enriched inositol phosphatase) protein, an endoplasmic reticulum-located phosphoinositide 5-phosphatase, both in vivo and in vitro.
This gene encodes a protein with 5-phosphatase activity toward polyphosphate inositol. The protein localizes to the cytosol in regions lacking actin stress fibers. It is thought that this protein may negatively regulate the actin cytoskeleton. Alternatively spliced transcript variants encoding different isoforms have been identified.
, inositol polyphosphate 5-phosphatase K
, putative phosphoinositide 5-phosphatase type II
, putative phosphoinositide 5-phosphatase type II; C62
, skeletal muscle and kidney enriched inositol phosphatase
, PI-5-phosphatase related
, putative PI-5-phosphatase
, skeletal muscle and kidney enriched inositol polyphosphate phosphatase
, skeletal muscle and kidney-enriched inositol phosphatase