![]() These results imply that genetic or environmental factors that alter hTR levels can directly affect immune cell function to influence health and disease. Hence, we propose that hTR can function as a noncoding RNA that protects from apoptosis independent of its function in telomerase enzymatic activity and long-term telomere maintenance in normal human immune cells. Strikingly, overexpression of hTERT protein caused apoptosis that was rescued by overexpression of enzymatically inactive hTR mutants. In contrast, hTERT knockdown did not induce apoptosis. Furthermore, hTR knockdown reproducibly induced apoptosis in the absence of any detectable telomere shortening or DNA damage response. We report that overexpression of enzymatically inactive hTR mutants protected against dexamethasone-induced apoptosis in stimulated CD4 T cells. It is unknown, however, whether telomerase, in addition to its long-term requirement for telomere maintenance, is also necessary for short-term immune cell proliferation and survival. Low telomerase activity in circulating peripheral blood mononuclear cells has been associated with a variety of diseases. It contains two core canonical components: the essential RNA component, hTR, which provides the template for DNA synthesis, and the reverse transcriptase protein component, hTERT. Telomerase is a ribonucleoprotein complex that adds telomeric DNA to the ends of linear chromosomes. ![]()
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