Abstract:
:Human diploid fibroblasts (HDFs) possess Ca(2+)-dependent membrane currents. These currents were suppressed in late-passage normal (senescent) HDFs and prematurely senescent HDFs derived from a subject with Werner syndrome (WS), compared with early-passage normal (young) HDFs. When young HDFs were microinjected with mRNA transcribed in vitro from a cDNA (WS3-10) which encodes a protein bearing a putative Ca(2+)-binding site and whose endogenous gene is overexpressed in senescent and WS HDFs, membrane currents fell to levels present in senescent and WS HDFs. Thus, both replicative senescence and forced expression of the WS3-10 gene sequence lead to suppression of Ca(2+)-dependent membrane currents, which suggests that a causal connection exists between these two processes.
journal_name
Proc Natl Acad Sci U S Aauthors
Liu S,Thweatt R,Lumpkin CK Jr,Goldstein Sdoi
10.1073/pnas.91.6.2186subject
Has Abstractpub_date
1994-03-15 00:00:00pages
2186-90issue
6eissn
0027-8424issn
1091-6490journal_volume
91pub_type
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