TSC1/TSC2

Gene/Protein · 8 studies in the Atlas · also known as TSC1, TSC2, TSC1-TSC2, TSC complex, hamartin, tuberin

Tuberin-hamartin tumor suppressor complex; acts as a GTPase-activating protein for Rheb; integrates growth-factor and energy signals to control mTORC1.

Evidence at a glance

Tier	What it means	Studies
B	Direct human evidence	1
C	Animal in vivo	2
D	Mechanistic / in vitro / review	5

Studies

Study	Year	Tier	Finding
KRU2010	2010	B	In patients whose TSC1/TSC2 mutations cause brain tumors, everolimus shrank tumor volume by 30%+ in three-quarters of patients.
CHE2008	2008	C	Showed why blood stem cells must keep mTOR LOW. Deleting TSC1 (which unleashes mTOR) drove resting stem cells into rapid division, flooded them with reactive oxygen species, and burned out their abili
KAP2004	2004	C	Genetically reducing TOR pathway activity extends fruit fly lifespan, overlapping with dietary restriction effects.
HOW2017	2017	D	Pinned down HOW the diabetes drug metformin - a major longevity candidate - actually reaches mTOR. In the liver, metformin lowers cellular energy, and at low doses this shuts down mTORC1 specifically
GWI2008	2008	D	Found a SECOND way the energy sensor AMPK shuts mTORC1 down. Besides acting through TSC2, AMPK directly phosphorylates Raptor - the core mTORC1 subunit - to halt growth when energy runs low. This 'met
INO2003	2003	D	Established the energy-sensing arm of the pathway. When energy runs low, AMPK phosphorylates TSC2, boosting its ability to shut mTOR down - protecting the cell from burning through resources and from
TEE2003	2003	D	TSC1-TSC2 acts as a GTPase-activating protein (GAP) for Rheb; when TSC is inactive, Rheb accumulates in its active GTP-bound form and directly activates mTORC1.
INO2002	2002	D	Akt directly phosphorylates and inactivates TSC2, disrupting the TSC1-TSC2 complex and releasing its inhibition of mTOR - the link between growth-factor/insulin signaling and mTORC1 activation.

Related entities

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