Title : Insulin-sensitive phospholipid signaling systems and glucose transport. Update II.

Pub. Date : 2001 Apr

PMID : 11368419






1 Functional Relationships(s)
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1 Atypical PKCs and PKB are rapidly activated by insulin in adipocytes, liver, skeletal muscles, and other cell types by a mechanism requiring PI3K and its downstream effector, 3-phosphoinositide-dependent protein kinase-1 (PDK-1), which, in conjunction with PIP3, phosphorylates critical threonine residues in the activation loops of atypical PKCs and PKB. Threonine insulin Homo sapiens