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The Journal of Immunology, 2001, 166: 4826-4830.
Copyright © 2001 by The American Association of Immunologists


CUTTING EDGE

Cutting Edge: Telomerase Activation in Human T Lymphocytes Does Not Require Increase in Telomerase Reverse Transcriptase (hTERT) Protein But Is Associated with hTERT Phosphorylation and Nuclear Translocation

Kebin Liu*, Richard J. Hodes{dagger} and Nan-ping Weng1,*

* Laboratory of Immunology, National Institute on Aging, National Institutes of Health, Baltimore, MD 21224; and {dagger} Experimental Immunology Branch, National Cancer Institute, and National Institute on Aging, National Institutes of Health, Bethesda, MD 20892

Capacity for cellular replication is critically important for lymphocyte function and can be regulated by telomerase-dependent maintenance of telomere length. In contrast to most normal human somatic cells that do not express telomerase due to the failure to transcribe telomerase reverse transcriptase (hTERT), lymphocytes express telomerase in a highly regulated fashion yet constitutively transcribe hTERT during development and activation. Here, we report that hTERT protein is present in both thymocytes and blood T cells at equivalent levels despite their substantial differences in telomerase activity, and that induction of telomerase activity in resting CD4+ T cells is not dependent on net hTERT protein increase. Moreover, hTERT is phosphorylated and translocated from cytoplasm to nucleus during CD4+ T cell activation. Thus, human T lymphocytes regulate telomerase function through novel events independent of hTERT protein levels, and hTERT phosphorylation and nuclear translocation may play a role in regulation of telomerase function in lymphocytes.




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