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Literature summary for 2.7.11.17 extracted from

  • Aiba, T.; Hesketh, G.G.; Liu, T.; Carlisle, R.; Villa-Abrille, M.C.; ORourke, B.; Akar, F.G.; Tomaselli, G.F.
    Na+ channel regulation by Ca2+/calmodulin and Ca2+/calmodulin-dependent protein kinase II in guinea-pig ventricular myocytes (2010), Cardiovasc. Res., 85, 454-463.
    View publication on PubMedView publication on EuropePMC
Search for more literature for 2.7.11.17

Inhibitors

Inhibitors Comment Organism Structure
autocamtide-2-related inhibitory peptide specific CaMKII inhibitor Cavia porcellus

Organism

Organism UniProt Comment Textmining
Cavia porcellus
-
-
-

Source Tissue

Source Tissue Comment Organism Textmining
myocyte ventricular myocyte Cavia porcellus
-

Substrates and Products (Substrate)

Substrates Comment Substrates Organism Products Comment (Products) Rev. Reac.
ATP + alpha-subunit of the cardiac Na+ channel NaV1.5-GST fusion peptide phosphorylated in vitro by CaMKII predominantly on the I-II linker Cavia porcellus ADP + phosphorylated alpha-subunit of the cardiac Na+ channel NaV1.5-GST fusion peptide
-
 ?
additional information CaMKII induces changes of Na+ channel gating Cavia porcellus ?
-
 ?

Synonyms

Synonyms Comment Organism
Ca2+/CaM-dependent protein kinase II
-
 Cavia porcellus
CaMKII
-
 Cavia porcellus

Cofactor

Cofactor Comment Organism Structure
ATP
-
 Cavia porcellus

General Information

General Information Comment Organism
malfunction chronic overactivity of CaMKII is associated with left ventricular hypertrophy and dysfunction and lethal arrhythmias Cavia porcellus