General Information:

Id: 3,795 (click here to show other Interactions for entry)
Diseases: Diabetes mellitus, type II - [OMIM]
Insulin resistance
Mammalia
review
Reference: Avruch J et al.(2009) Amino acid regulation of TOR complex 1 Am. J. Physiol. Endocrinol. Metab. 4: E592-E602 [PMID: 18765678]

Interaction Information:

Comment Cellular stresses inhibit TORC1 through a variety of mechanisms, which also converge on the TSC complex; thus energy depletion or hypoxia, for example, activate the AMPK, which (in collaboration with GSK3) phosphorylates TSC2 and activates the TSC GAP function. Glucocorticoids, hypoxia, and other stresses induce expression of the REDD1 polypeptide, which binds 14-3-3 and thereby relieves 14-3-3 inhibition of the TSC GAP function. Thus, these negative regulatory inputs to TORC1 appear to operate largely through upregulation of the GTPase-activating function of the TSC complex.
Formal Description
Interaction-ID: 37685

increases_activity of

complex/PPI

AMPK

Comment Cellular stresses inhibit TORC1 through a variety of mechanisms, which also converge on the TSC complex; thus energy depletion or hypoxia, for example, activate the AMPK, which (in collaboration with GSK3) phosphorylates TSC2 and activates the TSC GAP function. Glucocorticoids, hypoxia, and other stresses induce expression of the REDD1 polypeptide, which binds 14-3-3 and thereby relieves 14-3-3 inhibition of the TSC GAP function. Thus, these negative regulatory inputs to TORC1 appear to operate largely through upregulation of the GTPase-activating function of the TSC complex.
Formal Description
Interaction-ID: 37688

increases_expression of

gene/protein

DDIT4