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A protein known as SIRT1 has an important role in the cell, but it is something of a double-edged sword - implicated in both combating ageing and promoting tumour growth, its activity needs to be tightly controlled. Two papers in Nature offer valuable insight into how this key protein is regulated.
The two groups, respectively comprising Junjie Chen and Wei Gu and their colleagues, have discovered that another protein, named DBC1, acts as a regulator of SIRT1 activity. DBC1 prevents SIRT1 from carrying out its normal function of removing special chemical tags, called acetyl groups, from other proteins inside the cell. The acetylation status of a molecule influences its particular function - for better or for worse - hence the seemingly duplicitous role of SIRT1. By inhibiting SIRT1, DBC1 allows damaged cells to self-destruct, which would be beneficial in combating cancer cells. It also makes normal cells more susceptible to oxidative stress, so agents designed to inhibit or activate SIRT1 could each be beneficial, depending on circumstances. CONTACT Junjie Chen (Yale University, New Haven, CT, USA) Author paper [9]
E-mail: junjie.chen@yale.edu Wei Gu (Columbia University, New York, NY, USA) Author paper [10]
E-mail: wg8@columbia.edu (C) Nature press release.
Message posted by: Trevor M. D'Souza
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