Antisense Depletion of Death-associated Protein Kinase Promotes Apoptosis *
Journal of Biological Chemistry, ISSN: 0021-9258, Vol: 278, Issue: 51, Page: 51587-51593
2003
- 40Citations
- 26Captures
- 1Mentions
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Example: if you select the 1-year option for an article published in 2019 and a metric category shows 90%, that means that the article or review is performing better than 90% of the other articles/reviews published in that journal in 2019. If you select the 3-year option for the same article published in 2019 and the metric category shows 90%, that means that the article or review is performing better than 90% of the other articles/reviews published in that journal in 2019, 2018 and 2017.
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Metrics Details
- Citations40
- Citation Indexes40
- 40
- CrossRef37
- Captures26
- Readers26
- 26
- Mentions1
- References1
- 1
Article Description
Death-associated protein kinases (DAPK) are serine/threonine protein kinases that have an important role in regulating cell death. In this study two antisense approaches were employed to down-regulate expression of the endogenous DAPK-α and DAPK-β proteins. Transient expression of an antisense DAPK cDNA or antisense morpholino oligonucleotides in HeLa, 3T3, or primary human vascular smooth muscle cells demonstrate that decreased DAPK expression promotes a spontaneous, caspase-mediated apoptosis as evidenced by increased activities of caspases-3 and -9. Clonal HeLa cell lines with attenuated levels of DAPK expression, obtained following selection in the presence of antisense DAPK cDNA, are more sensitive to tumor necrosis factor-induced caspase-mediated apoptosis, and their sensitivity is inversely related to DAPK expression. In contrast, HeLa cells with reduced DAPK expression are moderately resistant to cell death induced by interferon-γ. This finding is consistent with previous studies showing that DAPK has a role in promoting caspase-independent cell death. Together, these studies demonstrate that the cellular activities of DAPK are critical for antagonizing caspase-dependent apoptosis to promote cell survival under normal cell growth conditions.
Bibliographic Details
http://www.sciencedirect.com/science/article/pii/S0021925820754232; http://dx.doi.org/10.1074/jbc.m309165200; http://www.scopus.com/inward/record.url?partnerID=HzOxMe3b&scp=0347064290&origin=inward; http://www.ncbi.nlm.nih.gov/pubmed/14530257; https://linkinghub.elsevier.com/retrieve/pii/S0021925820754232; http://www.jbc.org/lookup/doi/10.1074/jbc.M309165200; https://syndication.highwire.org/content/doi/10.1074/jbc.M309165200; https://dx.doi.org/10.1074/jbc.m309165200
Elsevier BV
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