MEKK1 Is Essential for DT40 Cell Apoptosis in Response to Microtubule Disruption
AUTOR(ES)
Kwan, Raymond
FONTE
American Society for Microbiology
RESUMO
Vinblastine and other microtubule-damaging agents, such as nocodazole and paclitaxel, cause cell cycle arrest at the G2/M transition and promote apoptosis in eukaryotic cells. The roles of these drugs in disrupting microtubule dynamics and causing cell cycle arrest are well characterized. However, the mechanisms by which these agents promote apoptosis are poorly understood. We disrupted the MEKK1 kinase domain in chicken bursal B-cell line DT40 by homologous recombination and have shown that it is essential for both vinblastine-mediated apoptosis and vinblastine-mediated c-Jun N-terminal protein kinase activation. In addition, our data indicate that vinblastine-mediated apoptosis in DT40 cells requires new protein synthesis but does not require G2/M arrest, suggesting that vinblastine-mediated cell cycle arrest and apoptosis are two independent processes.
ACESSO AO ARTIGO
http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=99893Documentos Relacionados
- MEKK1 is essential for cardiac hypertrophy and dysfunction induced by Gq
- MEKK1 suppresses oxidative stress-induced apoptosis of embryonic stem cell-derived cardiac myocytes
- The Organelle Proteome of the DT40 Lymphocyte Cell Line*S⃞
- The chicken HPRT gene: a counter selectable marker for the DT40 cell line.
- DT40 cells lacking the Ca2+-binding protein annexin 5 are resistant to Ca2+-dependent apoptosis
