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Dr. Finkel In The News

November 25, 2013 : AAAS News
AAAS council elects 388 new AAAS Fellows
NHLBI intramural investigators Toren Finkel and Herbert Geller were among the 388 newly-elected AAAS Fellows who were recognized by their peers for their efforts to advance science or its applications. The new AAAS Fellows will be honored at the AAAS Fellows Forum on Saturday, 15 February during the AAAS Annual Meeting in Chicago, where they will receive a certificate and a blue and gold rosette as a symbol of their distinguished accomplishments

two mice side by side

August 29, 2013
Single gene change increases mouse lifespan by 20 percent
By lowering the expression of a single gene, researchers at the National Institutes of Health have extended the average lifespan of a group of mice by about 20 percent. The research team targeted a gene called mTOR, which is involved in metabolism and energy balance, and may be connected with the increased lifespan associated with caloric restriction.

August 29, 2013 : Cell Reporter
Longer life with less mTor - and a twist
Stephen Matheson
In a paper just published in Cell Reports, J. Julie Wu and colleagues from Toren Finkel’s group at the NHLBI use a hypomorphic allele of mTor to probe the effects of reduced mTor expression in mice. They found that reduced mTOR did lead to a significant increase in lifespan, but age-related improvements varied from tissue to tissue.

February 22, 2013 : Cell Press
Cell Press webinar: signaling and mitochondria
co-presented by Toren Finkel, M.D., Ph.D., Center for Molecular Medicine
Recent years have witnessed a growing excitement in the field of mitochondrial biology with a dramatic increase in our appreciation of the diversity and complexity of mitochondrial function. Rather than simply acting as isolated energy-generating organelles, as once thought, we now know that these organelles form a dynamic network that is subject to continuous remodeling and is integrated into cellular signaling pathways. This webinar will focus on recent developments in signaling at mitochondria, specifically the role of oxidative stress signalling in metabolism, the regulation of mitochondrial calcium dynamics, and the contribution of the ubiquitin-proteasome system in modulating mitochondrial dynamics.

December 14, 2012 : Nature
The NAD-dependent deacetylase SIRT2 is required for programmed necrosis
co-authored by Toren Finkel, Elizabeth Murphy, and Michael Sack
Although initially viewed as unregulated, increasing evidence suggests that cellular necrosis often proceeds through a specific molecular program. In particular, death ligands such as tumour necrosis factor (TNF)-α activate necrosis by stimulating the formation of a complex containing receptor-interacting protein 1 (RIP1) and receptor-interacting protein 3 (RIP3). Relatively little is known regarding how this complex formation is regulated. Here, we show that the NAD-dependent deacetylase SIRT2 binds constitutively to RIP3 and that deletion or knockdown of SIRT2 prevents formation of the RIP1–RIP3 complex in mice.

February 12, 2003
NHLBI Study Finds Possible New Indicator of Heart Disease Risk
Levels of a type of adult stem cell in the bloodstream may indicate a person's risk of developing cardiovascular disease, according to a study supported by the National Heart, Lung, and Blood Institute (NHLBI), part of the National Institutes of Health in Bethesda, MD.

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Last Updated: April 24, 2012