Gene interactions and pathways from curated databases and text-mining
Semin Cell Dev Biol 2005, PMID: 15659337

mTOR, translational control and human disease.

Tee, Andrew R; Blenis, John

Many human diseases occur when the precise regulation of cell growth (cell mass/size) and proliferation (rates of cell division) is compromised. This review highlights those human disorders that occur as a result of inappropriate cellular signal transduction through the mammalian target of rapamycin (mTOR), a major pathway that coordinates proper cell growth and proliferation by regulating ribosomal biogenesis and protein translation. Recent studies reveal that the tuberous sclerosis complex (TSC)-1/2, PTEN, and LKB1 tumor suppressor proteins tightly control mTOR. Loss of these tumor suppressors leads to an array of hamartoma syndromes as a result of heightened mTOR signaling. Since mTOR plays a pivotal role in maintaining proper cell size and growth, dysregulation of mTOR signaling results in these benign tumor syndromes and an array of other human disorders.

Diseases/Pathways annotated by Medline MESH: Disease, Hamartoma, Hypertrophy, Left Ventricular, Neovascularization, Pathologic
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Text Mining Data

(TSC)-1/2 — mTOR: " Recent studies reveal that the tuberous sclerosis complex (TSC)-1/2 , PTEN, and LKB1 tumor suppressor proteins tightly control mTOR "

(TSC)-1/2 — mTOR: " Recent studies reveal that the tuberous sclerosis complex (TSC)-1/2 , PTEN, and LKB1 tumor suppressor proteins tightly control mTOR "

tuberous sclerosis complex (TSC)-1/2 — mTOR: " Recent studies reveal that the tuberous sclerosis complex (TSC)-1/2 , PTEN, and LKB1 tumor suppressor proteins tightly control mTOR "

mTOR — PTEN: " Recent studies reveal that the tuberous sclerosis complex (TSC)-1/2, PTEN , and LKB1 tumor suppressor proteins tightly control mTOR "

Manually curated Databases

No curated data.