Requirement of JNK for stress-induced activation of the cytochrome c-mediated death pathway.

By C. Tournier, P. Hess, Derek D. Yang, Jie Xu, Tod K. Turner, A. Nimnual, D. Bar-Sagi, Stephen N. Jones, R. Flavell, R. Davis. Science, 2000

1,834 citations recorded by the source corpus.

Subfields: Molecular Biology, Oncology

View Paper: https://www.semanticscholar.org/paper/b209285698bafc562ae043e5779bf3d8b7144850

How researchers see this paper

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In Molecular Biology

1. E. Wagner
2. J. Avruch
3. J. Kyriakis
4. A. Nebreda
5. H. Beere
6. Josef M. Penninger
7. T. Wada
8. Beth Levine

In Oncology

1. E. Wagner
2. J. Avruch
3. J. Kyriakis
4. B. Kaina
5. W. Roos
6. A. Nebreda
7. C. Weston
8. Beth Levine

Citations in the corpus

• AP-1 in cell proliferation and survival (2001, background): “Correspondingly, c-jun7/7 and Jnk17/7 Jnk27/7 cells (which are defective in c-Jun induction) are resistant to UV induced apoptosis but retain full sensitivity to other pro-apoptotic stimuli (Shaulian et al., 2000; Tournier et al., 2000).”
• Anthracyclines: Molecular Advances and Pharmacologic Developments in Antitumor Activity and Cardiotoxicity (2004, background): “Although controversy exists on the pro- or antiapoptotic consequences of Bcl-2 phosphorylation (Kharbanda et al., 2000; Tournier et al., 2000; Deng et al., 2001), the activity of MEN 10755 in MX-1 xenografts clearly reflected phosphorylation events.”
• Cellular response to oxidative stress: Signaling for suicide and survival * (2002, background): “While some of the MAPKK and MAPKKK are selective for one pathway or the other, others are common to both JNK and p38 (Tournier et al., 2000).”
• Signal integration by JNK and p38 MAPK pathways in cancer development (2009, background): “As cytoplasmic injection of cytochrome c rescued the apoptotic defects of JNK-deficient fibroblasts, JNK pro-apoptotic functions were proposed to be mediated by the mitochondrial pathwa”
• MAPK signal pathways in the regulation of cell proliferation in mammalian cells (2002, background): “It has been reported that UV-induced apoptosis in fibroblasts requires JNK for cytochrome C release from the motochondria[27].”
• Mammalian MAP kinase signalling cascades (2001, background): “JNK1 and JNK2 are required for apoptosis of ultraviolet-irradiated fibroblasts, in which they have been suggested to activate directly the apoptotic machiner”
• CK2 Is a C-Terminal IκB Kinase Responsible for NF-κB Activation during the UV Response (2003, neutral): “Both function. of these processes require activation of JNK, a member of the MAP kinase (MAPK) family (Dérijard et al., 1994; Results Hibi et al., 1993; Tournier et al., 2000).”
• Mammalian MAPK signal transduction pathways activated by stress and inflammation: a 10-year update. (2012, background): “Indeed, mouse embryo fibroblasts (MEFs in contrast to the situation described below for T lymphocytes), in which both mkk3 and mkk6 are disrupted, show a profound defect in all known mechanisms of p38␣ activation.”
• Cardiotoxicity of the cancer therapeutic agent imatinib mesylate (2006, background): “JNKs interact with the intrinsic cell death pathway at several points and have been shown to be both sufficient and necessary for release of cytochrome c from mitochondria in response to various stimul”