Literature summary for 3.9.1.3 extracted from

Srivastava, S.; Li, Z.; Soomro, I.; Sun, Y.; Wang, J.; Bao, L.; Coetzee, W.A.; Stanley, C.A.; Li, C.; Skolnik, E.Y.
Regulation of KATP channel trafficking in pancreatic bea-cells by protein histidine phosphorylation (2018), Diabetes, 67, 849-860 .

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Organism

Organism	UniProt	Comment	Textmining
Mus musculus	Q9DAK9	-	-

Synonyms

Synonyms	Comment	Organism
PHPT-1	-	Mus musculus

General Information

General Information	Comment	Organism
malfunction	PHPT-1(-/-) mice exhibit neonatal hyperinsulinemic hypoglycemia due to impaired trafficking of K(ATP) channels to the plasma membrane in pancreatic beta-cells in response to low glucose and leptin. The defect in K(ATP) channel trafficking in PHPT-1(-/-) beta-cells is due to the failure of PHPT-1 to directly activate transient receptor potential channel 4 (TRPC4), resulting in decreased Ca2+ influx and impaired downstream activation of AMPK	Mus musculus
physiological function	critical role for PHPT-1 in normal pancreatic b-cell function	Mus musculus

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Release 2023.1 (January 2023)