Title : Activation of Akt rescues endoplasmic reticulum stress-impaired murine cardiac contractile function via glycogen synthase kinase-3β-mediated suppression of mitochondrial permeation pore opening.

Pub. Date : 2011 Nov 1

PMID : 21542787






3 Functional Relationships(s)
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1 RESULTS: Wild-type and transgenic mice with cardiac-specific overexpression of the active mutant of Akt (Myr-Akt) were subjected to the ER stress inducer tunicamycin (1 or 3 mg/kg). Tunicamycin thymoma viral proto-oncogene 1 Mus musculus
2 Treatment with tunicamycin also dephosphorylated Akt and its downstream signal glycogen synthase kinase 3beta (GSK3beta) (leading to activation of GSK3beta), the effect of which was abrogated by Akt activation and TUDCA. Tunicamycin thymoma viral proto-oncogene 1 Mus musculus
3 Treatment with tunicamycin also dephosphorylated Akt and its downstream signal glycogen synthase kinase 3beta (GSK3beta) (leading to activation of GSK3beta), the effect of which was abrogated by Akt activation and TUDCA. Tunicamycin thymoma viral proto-oncogene 1 Mus musculus