Gene interactions and pathways from curated databases and text-mining
FEBS Lett 2010, PMID: 19883644

Depletion of mammalian target of rapamycin (mTOR) via siRNA mediated knockdown leads to stabilization of beta-catenin and elicits distinct features of cardiomyocyte hypertrophy.

Hagenmueller, Marco; Malekar, Pratima; Fieger, Christiane; Weiss, Celine S; Buss, Sebastian J; Wolf, David; Katus, Hugo A; Hardt, Stefan E

Cardiac myocyte growth is under differential control of mammalian target of rapamycin (mTOR) and glycogen-synthase-kinase-3beta (GSK3beta). Whereas active GSK3beta negatively regulates growth and down-regulates cellular protein synthesis, activation of the mTOR pathway promotes protein expression and cell growth. Here we report that depletion of mTOR via siRNA mediated knockdown causes marked down-regulation of GSK3beta protein in cardiac myocytes. As a result, GSK3beta target protein beta-catenin becomes stabilized and translocates into the nucleus. Moreover, mTOR knockdown leads to increase in cardiac myocyte surface area and produces an up-regulation of the fetal gene program. Our findings suggest a new type of convergence of mTOR and GSK3beta activities, indicating that GSK3beta-dependent stabilization of beta-catenin in cardiac myocytes is influenced by mTOR.

Diseases/Pathways annotated by Medline MESH: Cardiomegaly
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Text Mining Data

beta-catenin ⊣ mammalian target of rapamycin (mTOR): " Depletion of mammalian target of rapamycin (mTOR) via siRNA mediated knockdown leads to stabilization of beta-catenin and elicits distinct features of cardiomyocyte hypertrophy "

beta-catenin → GSK3beta: " Our findings suggest a new type of convergence of mTOR and GSK3beta activities, indicating that GSK3beta dependent stabilization of beta-catenin in cardiac myocytes is influenced by mTOR "

Manually curated Databases

No curated data.