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  • 1
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    Proapoptotic BAX and BAK: a requisite gateway to mitochondrial dysfunction and death (2001)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2001-04-28
    Description: Multiple death signals influence mitochondria during apoptosis, yet the critical initiating event for mitochondrial dysfunction in vivo has been unclear. tBID, the caspase-activated form of a "BH3-domain-only" BCL-2 family member, triggers the homooligomerization of "multidomain" conserved proapoptotic family members BAK or BAX, resulting in the release of cytochrome c from mitochondria. We find that cells lacking both Bax and Bak, but not cells lacking only one of these components, are completely resistant to tBID-induced cytochrome c release and apoptosis. Moreover, doubly deficient cells are resistant to multiple apoptotic stimuli that act through disruption of mitochondrial function: staurosporine, ultraviolet radiation, growth factor deprivation, etoposide, and the endoplasmic reticulum stress stimuli thapsigargin and tunicamycin. Thus, activation of a "multidomain" proapoptotic member, BAX or BAK, appears to be an essential gateway to mitochondrial dysfunction required for cell death in response to diverse stimuli.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3049805/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3049805/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wei, M C -- Zong, W X -- Cheng, E H -- Lindsten, T -- Panoutsakopoulou, V -- Ross, A J -- Roth, K A -- MacGregor, G R -- Thompson, C B -- Korsmeyer, S J -- 5T32AT09361/AT/NCCIH NIH HHS/ -- R01 HD036437-02/HD/NICHD NIH HHS/ -- R01 HD036437-03/HD/NICHD NIH HHS/ -- R01 HD036437-04/HD/NICHD NIH HHS/ -- R01 HD036437-05/HD/NICHD NIH HHS/ -- R01CA50239/CA/NCI NIH HHS/ -- R37CA4802/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 2001 Apr 27;292(5517):727-30.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, Departments of Pathology and Medicine, Harvard Medical School, Dana-Farber Cancer Institute, Boston, MA 02115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/11326099" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antibodies ; Antigens, CD95/immunology/physiology ; Apoptosis/*physiology ; BH3 Interacting Domain Death Agonist Protein ; Biopolymers ; Carrier Proteins/genetics/metabolism ; Cells, Cultured ; Cytochrome c Group/metabolism ; Endoplasmic Reticulum/metabolism ; Etoposide/pharmacology ; Hepatocytes/cytology/metabolism ; Intracellular Membranes/metabolism ; Membrane Proteins/genetics/*metabolism ; Mice ; Mitochondria/*metabolism ; Protein Structure, Tertiary ; Proto-Oncogene Proteins/genetics/*metabolism ; *Proto-Oncogene Proteins c-bcl-2 ; Signal Transduction ; Staurosporine/pharmacology ; Transfection ; Ultraviolet Rays ; bcl-2 Homologous Antagonist-Killer Protein ; bcl-2-Associated X Protein
    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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    Control of effector CD8+ T cell function by the transcription factor Eomesodermin (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-11-08
    Description: Activated CD8+ T cells play a critical role in host defense against viruses, intracellular microbes, and tumors. It is not clear if a key regulatory transcription factor unites the effector functions of CD8+ T cells. We now show that Eomesodermin (Eomes), a paralogue of T-bet, is induced in effector CD8+ T cells in vitro and in vivo. Ectopic expression of Eomes was sufficient to invoke attributes of effector CD8+ T cells, including interferon-gamma (IFN-gamma), perforin, and granzyme B. Loss-of-function analysis suggests Eomes may also be necessary for full effector differentiation of CD8+ T cells. We suggest that Eomesodermin is likely to complement the actions of T-bet and act as a key regulatory gene in the development of cell-mediated immunity.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Pearce, Erika L -- Mullen, Alan C -- Martins, Gislaine A -- Krawczyk, Connie M -- Hutchins, Anne S -- Zediak, Valerie P -- Banica, Monica -- DiCioccio, Catherine B -- Gross, Darrick A -- Mao, Chai-An -- Shen, Hao -- Cereb, Nezih -- Yang, Soo Y -- Lindsten, Tullia -- Rossant, Janet -- Hunter, Christopher A -- Reiner, Steven L -- AI-042370/AI/NIAID NIH HHS/ -- GM-07229/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2003 Nov 7;302(5647):1041-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Abramson Family Cancer Research Institute, and Department of Medicine, University of Pennsylvania, Philadelphia, PA 19104, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/14605368" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Arenaviridae Infections/immunology ; Base Sequence ; CD8-Positive T-Lymphocytes/*immunology/physiology ; Cell Differentiation ; Cytotoxicity, Immunologic ; Gene Expression Regulation ; Granzymes ; Interferon-gamma/biosynthesis ; Lymphocyte Activation ; Lymphocytic choriomeningitis virus/immunology ; Membrane Glycoproteins/biosynthesis/genetics ; Mice ; Mice, Inbred BALB C ; Mice, Inbred C57BL ; Molecular Sequence Data ; Perforin ; Pore Forming Cytotoxic Proteins ; RNA, Messenger/genetics/metabolism ; Serine Endopeptidases/biosynthesis/genetics ; T-Box Domain Proteins/chemistry/genetics/*physiology ; Th2 Cells/immunology/physiology ; Transcription Factors/chemistry/genetics/physiology
    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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  • 3
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    The PP2A-associated protein alpha4 is an essential inhibitor of apoptosis (2004)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2004-10-23
    Description: Despite evidence that protein kinases are regulators of apoptosis, a specific role for phosphatases in regulating cell survival has not been established. Here we show that alpha4, a noncatalytic subunit of protein phosphatase 2A (PP2A), is required to repress apoptosis in murine cells. alpha4 is a nonredundant regulator of the dephosphorylation of the transcription factors c-Jun and p53. As a result of alpha4 deletion, multiple proapoptotic genes were transcribed. Either inhibition of new protein synthesis or Bcl-xL overexpression suppressed apoptosis initiated by alpha4 deletion. Thus, mammalian cell viability depends on repression of transcription-initiated apoptosis mediated by a component of PP2A.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kong, Mei -- Fox, Casey J -- Mu, James -- Solt, Laura -- Xu, Anne -- Cinalli, Ryan M -- Birnbaum, Morris J -- Lindsten, Tullia -- Thompson, Craig B -- New York, N.Y. -- Science. 2004 Oct 22;306(5696):695-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Abramson Family Cancer Research Institute, University of Pennsylvania, Philadelphia, PA 19104, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15499020" target="_blank"〉PubMed〈/a〉
    Keywords: Adipocytes/cytology ; Animals ; *Apoptosis ; Cell Differentiation ; Cell Line ; Cell Survival ; Cells, Cultured ; Cycloheximide/pharmacology ; Gene Deletion ; Gene Expression Profiling ; Liver/cytology/metabolism ; Mice ; Mice, Transgenic ; Oligonucleotide Array Sequence Analysis ; PPAR gamma/metabolism ; Phosphoprotein Phosphatases/*metabolism ; Phosphoproteins/*metabolism ; Phosphorylation ; Protein Phosphatase 2 ; Protein Synthesis Inhibitors/pharmacology ; Proto-Oncogene Proteins c-bcl-2/metabolism ; Proto-Oncogene Proteins c-jun/metabolism ; Transcription, Genetic ; Tumor Suppressor Protein p53/metabolism ; bcl-X Protein
    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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  • 4
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    Deficiency of Bax and Bak protects photoreceptors from light damage in vivo (2004)
    Springer Nature
    Details
    Publication Date: 2004-07-23
    Print ISSN: 1350-9047
    Electronic ISSN: 1476-5403
    Topics: Biology , Medicine
    Published by Springer Nature
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