Signaling pathways: the benefits of good communication.
Recent studies show that hyperactivated mTOR, the 'target of rapamycin' that senses nutrient availability in eukaryotic cells, inhibits signaling by insulin receptor substrates. This crosstalk reveals how hyperactivated mTOR may suppress metastasis locally, while causing systemic insulin resistance that can progress to diabetes.
Fisher
Tracey L
TL
Howard Hughes Medical Institute, Division of Endocrinology, Children's Hospital Boston, Harvard Medical School, 300 Longwood Avenue, Boston, Massachusetts 02115, USA.
White
Morris F
MF
D000818:Animals; D004789:Enzyme Activation / Q000502:physiology*; D020690:GTPase-Activating Proteins / Q000378:metabolism; D006801:Humans; D007333:Insulin Resistance / Q000502:physiology; D008954:Models, Biological; D009154:Mutation / Q000235:genetics; D009362:Neoplasm Metastasis / Q000503:physiopathology*; D011494:Protein Kinases / Q000378:metabolism*; D011506:Proteins / Q000235:genetics; D011972:Receptor, Insulin / Q000037:antagonists & inhibitors*; D015398:Signal Transduction / Q000502:physiology*; D058570:TOR Serine-Threonine Kinases; D014402:Tuberous Sclerosis / Q000378:metabolism* / Q000503:physiopathology; D000077004:Tuberous Sclerosis Complex 1 Protein; D025521:Tumor Suppressor Proteins
D020690:GTPase-Activating Proteins; D011506:Proteins; D000077004:Tuberous Sclerosis Complex 1 Protein; D025521:Tumor Suppressor Proteins; D011494:Protein Kinases; C546842:MTOR protein, human; D011972:Receptor, Insulin; D058570:TOR Serine-Threonine Kinases