Molecular and cellular biochemistry

https://eutils.ncbi.nlm.nih.gov/entrez/eutils/efetch.fcgi?db=pubmed&id=16283515&retmode=xml&tool=Litmetric&email=readroberts32@gmail.com&api_key=61f08fa0b96a73de8c900d749fcb997acc09 162835152007030120181113

0300-81772791-22005NovMolecular and cellular biochemistryMol Cell BiochemInvolvement of the p38 MAP kinase in Cr(VI)-induced growth arrest and apoptosis.697369-73Hexavalent chromium [Cr(VI)] is a carcinogenic genotoxin commonly found in industry and the environment. DNA damage resulting from Cr(VI) exposure triggers numerous stress responses, including activation of cell cycle checkpoints and initiation of apoptosis. Mechanisms controlling these responses, while extensively studied, have yet to be fully elucidated. Here, we demonstrate that the p38 mitogen-activated protein kinase (MAPK) is activated by Cr(VI) exposure and that inhibition of p38 function using the selective inhibitor SB203580 results in abrogation of S-phase and G2 cell cycle checkpoints in response to Cr(VI). Also, we observe that inhibition of p38 results in decreased cell survival and increased percentage of apoptotic cells following Cr(VI) treatment. Taken together, these results indicate that p38 function is critical for optimal stress response induced by Cr(VI) exposure.WakemanTimothy PTPDepartment of Genetics, and Department of Biochemistry and Molecular Biology, LSU Health Sciences Center, New Orleans, Louisiana, USA.WyczechowskaDorotaDXuBoBengR03 ES013301-02ESNIEHS NIH HHSUnited StatesP20 RR020152RRNCRR NIH HHSUnited StatesR03 ES013301ESNIEHS NIH HHSUnited StatesR03 ES013301-01ESNIEHS NIH HHSUnited StatesP20 RR020152-020003RRNCRR NIH HHSUnited StatesP20 RR020152-010003RRNCRR NIH HHSUnited StatesP20 RR020152-037528RRNCRR NIH HHSUnited StatesR03 ES013301-03ESNIEHS NIH HHSUnited StatesJournal ArticleResearch Support, N.I.H., ExtramuralResearch Support, Non-U.S. Gov'tResearch Support, U.S. Gov't, P.H.S.

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