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Literature summary for 2.7.11.15 extracted from

  • Ciccarelli, M.; Chuprun, J.K.; Rengo, G.; Gao, E.; Wei, Z.; Peroutka, R.J.; Gold, J.I.; Gumpert, A.; Chen, M.; Otis, N.J.; Dorn, G.W.; Trimarco, B.; Iaccarino, G.; Koch, W.J.
    G protein-coupled receptor kinase 2 activity impairs cardiac glucose uptake and promotes insulin resistance after myocardial ischemia (2011), Circulation, 123, 1953-1962.
    View publication on PubMedView publication on EuropePMC
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Protein Variants

Protein Variants Comment Organism
K220R kinase-dead mutant fails to alter Akt activation and GLUT4 membrane translocation in response to insulin Mus musculus

Natural Substrates/ Products (Substrates)

Natural Substrates Organism Comment (Nat. Sub.) Natural Products Comment (Nat. Pro.) Rev. Reac.
ATP + insulin receptor substrate-1 Mus musculus
-
 ADP + phosphorylated-insulin receptor substrate-1
-
 ?

Organism

Organism UniProt Comment Textmining
Mus musculus
-
-
-

Substrates and Products (Substrate)

Substrates Comment Substrates Organism Products Comment (Products) Rev. Reac.
ATP + insulin receptor substrate-1
-
 Mus musculus ADP + phosphorylated-insulin receptor substrate-1
-
 ?

Synonyms

Synonyms Comment Organism
GRK2
-
 Mus musculus

General Information

General Information Comment Organism
malfunction transgenic mice with cardiac-specific overexpression of GRK2 negatively impact cardiac metabolism by inhibiting glucose uptake and desensitization of insulin signaling, which increases after ischemic injury and precedes heart failure development. Mechanistically, GRK2 interacts with and directly phosphorylates insulin receptor substrate-1 (IRS1) in cardiomyocytes causing insulin-dependent negative signaling feedback including inhibition of membrane translocation of the glucose transporter, GLUT4 Mus musculus