Catálogo de publicaciones - revistas

<jats:title>SAMTOR joins the family</jats:title> <jats:p> The amino acid methionine is widely appreciated to have interesting effects on animal physiology. Diets low in methionine increase longevity and overall health, particularly glucose homeostasis. Gu <jats:italic>et al.</jats:italic> describe a potential molecular link between the effects of methionine restriction and the growth controller mTOR complex 1 (mTORC1), a well-validated regulator of life span and health span in many organisms. They identify a protein that they named SAMTOR as a component of the nutrient-sensing pathway upstream of mTORC1. SAMTOR directly binds S-adenosylmethionine (SAM), a metabolite made from methionine, and is necessary for regulating mTORC1 in response to methionine. </jats:p> <jats:p> <jats:italic>Science</jats:italic> , this issue p. <jats:related-article xmlns:xlink="http://www.w3.org/1999/xlink" ext-link-type="doi" issue="6364" page="813" related-article-type="in-this-issue" vol="358" xlink:href="10.1126/science.aao3265">813</jats:related-article> </jats:p>

<jats:p>A weekly roundup of information on newly offered instrumentation, apparatus, and laboratory materials of potential interest to researchers.</jats:p>

<jats:p> Cell death, including autophagy, necroptosis, and apoptosis, is a physiological process critical for normal development and function of multicellular organisms. Many of the signals that elicit cell death converge on mitochondria, which regulate cell death by a pivotal process called mitochondrial outer membrane permeabilization (MOMP). In apoptosis, MOMP is tightly regulated by the Bcl-2 family of proteins, composed of both proapoptotic (Bax, Bak, Bid, Bim) and antiapoptotic (Bcl-2, Bcl-xL, Bcl-W) members, which act in part by governing mitochondrial death signaling through cytochrome C release and subsequent activation of caspases. Irrespective of caspase activity, MOMP can lead to cell death by causing a progressive decline in mitochondrial function. Under certain circumstances, however, a cell can survive cell death; its survival may have pathophysiological consequences leading to cancer, autoimmunity, neurodegeneration, and resistance to cancer therapies. This webinar will examine how identification of dysregulated cell-death mechanisms underpinning various pathologies can be exploited to develop novel treatments for cancer and neurodegenerative diseases that directly activate the cell-death machinery. <jats:list list-type="bullet"> <jats:list-item> <jats:p> <jats:ext-link xmlns:xlink="http://www.w3.org/1999/xlink" ext-link-type="uri" xlink:href="http://www.sciencemag.org/custom-publishing/webinars/deciphering-cancer-investigating-cell-death-mechanisms">View the Webinar</jats:ext-link> </jats:p> </jats:list-item> </jats:list> </jats:p>