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Experiments conducted in mice demonstrated that through its effects on mTORC1, the SPAR polypeptide helps regulate the muscle’s ability to regenerate and repair after injury. look at these guysSpecifically, expression of LINC00961 is blocked following muscle injury in mice, leading to reduced levels of SPAR and maximal mTORC1 activity to promote tissue regeneration. “The experimental approach we used allowed us to eliminate expression of the SPAR polypeptide, while maintaining expression of the host lncRNA,” said lead author Akinobu Matsumoto, PhD, research fellow at the Cancer Center at BIDMC and lead author of the study. “We are able to ascribe this function to the coding function of the lncRNA rather than any non-coding function it may also have.” The findings suggest that therapeutic strategies that restrict expression of SPAR in injured muscle may promote a more rapid regeneration of tissue. The results suggest that lncRNAs may have diverse roles and functions. Although they may not code for large proteins, lncRNAs may produce small polypeptides that can fine tune the activity of critical cellular components. The findings also expand the repertoire of peptide-coding genes in the human genome that should be studied and annotated. The study also provides insights on how mTORC1 activity may be attuned to meet the distinct needs of a specific tissue. check my site“An ability to target such modulators could be of great advantage from a therapeutic perspective, allowing for control of mTORC1 activity in cells or tissues that express such modulators while not affecting its activity and function in other tissue and cell types,” explained co-author John Clohessy, PhD, Instructor in Medicine at BIDMC and a senior member of Pandolfi’s research team. Indeed, a key feature of many lncRNAs is that their expression is often highly tissue-specific.
For the original version including any supplementary images or video, visit https://www.eurekalert.org/pub_releases/2016-12/bidm-rrt122316.php