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Manel Joaquin

Researcher at Pompeu Fabra University

Publications -  18
Citations -  4986

Manel Joaquin is an academic researcher from Pompeu Fabra University. The author has contributed to research in topics: Cyclin-dependent kinase & Cyclin A. The author has an hindex of 15, co-authored 18 publications receiving 4678 citations. Previous affiliations of Manel Joaquin include Friedrich Miescher Institute for Biomedical Research & Ludwig Institute for Cancer Research.

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Absence of S6K1 protects against age- and diet-induced obesity while enhancing insulin sensitivity

TL;DR: It is reported that S6K1-deficient mice are protected against obesity owing to enhanced β-oxidation, however on a high fat diet, levels of glucose and free fatty acids still rise in S6k1- deficient mice, resulting in insulin receptor desensitization.
Journal Article

Absence of S6K1 protects against age- and diet-induced obesity while enhancing insulin sensitivity. [Erratum: 2004 Sept. 23, v. 431, no. 7007, p. 485.]

TL;DR: In this article, S6K1-deficient mice are protected against obesity owing to enhanced β-oxidation, but on a high fat diet, levels of glucose and free fatty acids still rise in S6k1-dependent mice, resulting in insulin receptor desensitization.
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Insulin Activation of Rheb, a Mediator of mTOR/S6K/4E-BP Signaling, Is Inhibited by TSC1 and 2

TL;DR: Evidence is provided that TSC1/2 is a GAP for the small GTPase Rheb and that insulin-mediated RheB activation is PI3K dependent and that Rhe b overexpression induces S6K1 phosphorylation and inhibits PKBosphorylation, as do loss-of-function mutations in TSC 1/2.
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Amino Acids Activate mTOR Complex 1 via Ca2+/CaM Signaling to hVps34

TL;DR: It is shown that AAs induce a rise in intracellular Ca(2+) ([Ca(2+)](i), which triggers mTOR Complex 1 and hVps34 activation, which increases the direct binding of Ca( 2+)/calmodulin (CaM) to an evolutionarily conserved motif in hVPS34 that is required for lipid kinase activity and increased mTOR complex 1 signaling.
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The p38 Pathway: From Biology to Cancer Therapy.

TL;DR: An extensive description of the main biological functions of p38 is provided and an updated overview of therapeutic strategies targeting p38 in cancer and promising alternatives currently being explored is provided.