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GYS1 — PRKAB1

Pathways - manually collected, often from reviews:

• WikiPathways AMP-activated Protein Kinase (AMPK) Signaling: Complex of PRKAG3-PRKAA1-PRKAG2-PRKAG1-PRKAB2-PRKAB1-PRKAA2 → GYS1/GYS2 (mim-inhibition) Halse et al., Diabetes 2003, Carling et al., Biochim Biophys Acta 1989

Protein-Protein interactions - manually collected from original source literature:

Studies that report less than 10 interactions are marked with *

• IRef Biogrid Interaction: PRKAB1 — GYS1 (physical association, affinity chromatography technology) Ewing et al., Molecular systems biology 2007
• IRef Intact Interaction: PRKAB1 — GYS1 (physical association, anti bait coimmunoprecipitation) Ewing et al., Molecular systems biology 2007

Text-mined interactions from Literome

Wojtaszewski et al., Diabetes 2002 : Although the data do not exclude a role of other kinases/phosphatases, they suggest that glycogen synthase may be a target for AMPK in vivo
Wojtaszewski et al., Biochem Soc Trans 2003 : Transgenic models -- a scientific tool to understand exercise induced metabolism : the regulatory role of AMPK ( 5'-AMP activated protein kinase ) in glucose transport and glycogen synthase activity in skeletal muscle
Cammisotto et al., American journal of physiology. Renal physiology 2008 (Diabetes Mellitus, Experimental) : The present study aims to determine whether adiponectin and AMPK are involved in the regulation of glycogen synthase ( GS ) in these structures
Zhang et al., J Biol Chem 2011 : AMP activated protein kinase (AMPK) activation and glycogen synthase kinase-3ß ( GSK-3ß ) inhibition induce Ca2+ independent deposition of tight junction components at the plasma membrane ... We find that in the absence of extracellular Ca ( 2+ ), AMP activated protein kinase (AMPK) activation and glycogen synthase kinase ( GSK ) -3ß inhibition independently induce the localization of epithelial tight junction components to the plasma membrane