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  • 1
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    Apaf-1 and caspase-9 in p53-dependent apoptosis and tumor inhibition (1999)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1999-04-02
    Description: The ability of p53 to promote apoptosis in response to mitogenic oncogenes appears to be critical for its tumor suppressor function. Caspase-9 and its cofactor Apaf-1 were found to be essential downstream components of p53 in Myc-induced apoptosis. Like p53 null cells, mouse embryo fibroblast cells deficient in Apaf-1 and caspase-9, and expressing c-Myc, were resistant to apoptotic stimuli that mimic conditions in developing tumors. Inactivation of Apaf-1 or caspase-9 substituted for p53 loss in promoting the oncogenic transformation of Myc-expressing cells. These results imply a role for Apaf-1 and caspase-9 in controlling tumor development.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Soengas, M S -- Alarcon, R M -- Yoshida, H -- Giaccia, A J -- Hakem, R -- Mak, T W -- Lowe, S W -- CA13106/CA/NCI NIH HHS/ -- CA64489/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1999 Apr 2;284(5411):156-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Cold Spring Harbor Laboratory, Cold Spring Harbor, NY 11724, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10102818" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Apoptosis ; Apoptotic Protease-Activating Factor 1 ; Caspase 9 ; Caspases/genetics/*physiology ; Cell Division ; Cell Transformation, Neoplastic ; Cells, Cultured ; Cytochrome c Group/metabolism ; Genes, myc ; *Genes, p53 ; Genes, ras ; Mice ; Mice, Nude ; Mitochondria/metabolism ; Mutation ; Neoplasms, Experimental/genetics/metabolism/*pathology ; Proteins/genetics/*physiology ; Tumor Suppressor Protein p53/metabolism
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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  • 2
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    DNA damage-induced activation of p53 by the checkpoint kinase Chk2 (2000)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2000-03-10
    Description: Chk2 is a protein kinase that is activated in response to DNA damage and may regulate cell cycle arrest. We generated Chk2-deficient mouse cells by gene targeting. Chk2-/- embryonic stem cells failed to maintain gamma-irradiation-induced arrest in the G2 phase of the cell cycle. Chk2-/- thymocytes were resistant to DNA damage-induced apoptosis. Chk2-/- cells were defective for p53 stabilization and for induction of p53-dependent transcripts such as p21 in response to gamma irradiation. Reintroduction of the Chk2 gene restored p53-dependent transcription in response to gamma irradiation. Chk2 directly phosphorylated p53 on serine 20, which is known to interfere with Mdm2 binding. This provides a mechanism for increased stability of p53 by prevention of ubiquitination in response to DNA damage.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hirao, A -- Kong, Y Y -- Matsuoka, S -- Wakeham, A -- Ruland, J -- Yoshida, H -- Liu, D -- Elledge, S J -- Mak, T W -- GM44664/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2000 Mar 10;287(5459):1824-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉The Amgen Institute, Ontario Cancer Institute, and Departments of Medical Biophysics and Immunology, University of Toronto, 620 University Avenue, Suite 706, Toronto, Ontario, M5G 2C1, Canada.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10710310" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Apoptosis ; Ataxia Telangiectasia Mutated Proteins ; Cell Cycle Proteins ; Checkpoint Kinase 2 ; *DNA Damage ; DNA-Binding Proteins ; G1 Phase ; G2 Phase ; Gamma Rays ; Gene Expression Regulation ; Gene Targeting ; Genes, Tumor Suppressor ; Genes, p53 ; Humans ; *Interphase ; Mice ; *Nuclear Proteins ; Phosphorylation ; Phosphoserine/metabolism ; *Protein Kinases ; Protein-Serine-Threonine Kinases/*metabolism ; Proto-Oncogene Proteins/metabolism ; Proto-Oncogene Proteins c-mdm2 ; Stem Cells/cytology/metabolism ; T-Lymphocytes/cytology ; Transcription, Genetic ; Tumor Suppressor Protein p53/*metabolism ; Tumor Suppressor Proteins
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
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