P Vito

Summary

Country: Switzerland

Publications

  1. ncbi request reprint Cloning of AIP1, a novel protein that associates with the apoptosis-linked gene ALG-2 in a Ca2+-dependent reaction
    P Vito
    T Cell Molecular Biology Unit, Laboratory of Cellular and Molecular Immunology, NIAID, National Institutes of Health, Bethesda, Maryland 20892, USA
    J Biol Chem 274:1533-40. 1999
  2. ncbi request reprint Requirement of the familial Alzheimer's disease gene PS2 for apoptosis. Opposing effect of ALG-3
    P Vito
    T Cell Molecular Biology Unit, Laboratory of Cellular and Molecular Immunology, NIAID, National Institutes of Health, Maryland 20892, USA
    J Biol Chem 271:31025-8. 1996
  3. ncbi request reprint Interaction of Alzheimer's presenilin-1 and presenilin-2 with Bcl-X(L). A potential role in modulating the threshold of cell death
    B J Passer
    T Cell Apoptosis Unit, Laboratory of Cellular and Molecular Immunology, NIAID, National Institutes of Health, Bethesda, Maryland 20892, USA
    J Biol Chem 274:24007-13. 1999
  4. ncbi request reprint Generation of anti-apoptotic presenilin-2 polypeptides by alternative transcription, proteolysis, and caspase-3 cleavage
    P Vito
    T Cell Molecular Biology Unit, Laboratory of Cellular and Molecular Immunology, NIAID, National Institutes of Health, Bethesda, Maryland 20892, USA
    J Biol Chem 272:28315-20. 1997
  5. ncbi request reprint Participation of presenilin 2 in apoptosis: enhanced basal activity conferred by an Alzheimer mutation
    B Wolozin
    Unit on Alzheimer Biology, Laboratory of Clinical Science, National Institute of Mental Health, Building 10, Room 3D41, 9000 Rockville Pike, Bethesda, MD 20892, USA
    Science 274:1710-3. 1996
  6. ncbi request reprint Interfering with apoptosis: Ca(2+)-binding protein ALG-2 and Alzheimer's disease gene ALG-3
    P Vito
    T Cell Molecular Biology Unit, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892, USA
    Science 271:521-5. 1996
  7. ncbi request reprint c-E10 is a caspase-recruiting domain-containing protein that interacts with components of death receptors signaling pathway and activates nuclear factor-kappaB
    A Costanzo
    Fondazione A Cesalpino, I Clinica Medica, V le Policlinico 155, 00161 Roma, Italy
    J Biol Chem 274:20127-32. 1999
  8. pmc Caspase recruitment domain (CARD)-dependent cytoplasmic filaments mediate bcl10-induced NF-kappaB activation
    C Guiet
    Basel Institute for Immunology, Postfach CH 4005, Basel, Switzerland
    J Cell Biol 148:1131-40. 2000
  9. ncbi request reprint c-FLIP efficiently rescues TRAF-2-/- cells from TNF-induced apoptosis
    C Guiet
    Basel Institute for Immunology, Grenzacherstrasse 487, Postfach CH 4005, Basel, Switzerland
    Cell Death Differ 9:138-44. 2002
  10. ncbi request reprint The expression of the sarco/endoplasmic reticulum Ca2+-ATPases in thyroid and its down-regulation following neoplastic transformation
    F Pacifico
    Dipartimento di Scienze e Tecnologie Biologiche ed Ambientali, Facoltà di Scienze Matematiche Fisiche e Naturali, Universita degli Studi di Lecce, Strada Provonciale Lecce Monteroni, 73100 Lecce, Italy
    J Mol Endocrinol 30:399-409. 2003

Collaborators

Detail Information

Publications10

  1. ncbi request reprint Cloning of AIP1, a novel protein that associates with the apoptosis-linked gene ALG-2 in a Ca2+-dependent reaction
    P Vito
    T Cell Molecular Biology Unit, Laboratory of Cellular and Molecular Immunology, NIAID, National Institutes of Health, Bethesda, Maryland 20892, USA
    J Biol Chem 274:1533-40. 1999
    ....
  2. ncbi request reprint Requirement of the familial Alzheimer's disease gene PS2 for apoptosis. Opposing effect of ALG-3
    P Vito
    T Cell Molecular Biology Unit, Laboratory of Cellular and Molecular Immunology, NIAID, National Institutes of Health, Maryland 20892, USA
    J Biol Chem 271:31025-8. 1996
    ..Thus, the PS2 gene is required for some forms of cell death in diverse cell types, and its function is opposed by ALG-3...
  3. ncbi request reprint Interaction of Alzheimer's presenilin-1 and presenilin-2 with Bcl-X(L). A potential role in modulating the threshold of cell death
    B J Passer
    T Cell Apoptosis Unit, Laboratory of Cellular and Molecular Immunology, NIAID, National Institutes of Health, Bethesda, Maryland 20892, USA
    J Biol Chem 274:24007-13. 1999
    ..Together, these data support a possible role of the Alzheimer's presenilins in modulating the anti-apoptotic effects of Bcl-X(L)...
  4. ncbi request reprint Generation of anti-apoptotic presenilin-2 polypeptides by alternative transcription, proteolysis, and caspase-3 cleavage
    P Vito
    T Cell Molecular Biology Unit, Laboratory of Cellular and Molecular Immunology, NIAID, National Institutes of Health, Bethesda, Maryland 20892, USA
    J Biol Chem 272:28315-20. 1997
    ..Thus, whereas PS2 is required for apoptosis, PS2s and PS2Ccas oppose this process, and the balance between PS2 and these COOH-terminal fragments may dictate the cell fate...
  5. ncbi request reprint Participation of presenilin 2 in apoptosis: enhanced basal activity conferred by an Alzheimer mutation
    B Wolozin
    Unit on Alzheimer Biology, Laboratory of Clinical Science, National Institute of Mental Health, Building 10, Room 3D41, 9000 Rockville Pike, Bethesda, MD 20892, USA
    Science 274:1710-3. 1996
    ..This gain of function might accelerate the process of neurodegeneration that occurs in Alzheimer's disease, leading to the earlier age of onset characteristic of familial Alzheimer's disease...
  6. ncbi request reprint Interfering with apoptosis: Ca(2+)-binding protein ALG-2 and Alzheimer's disease gene ALG-3
    P Vito
    T Cell Molecular Biology Unit, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892, USA
    Science 271:521-5. 1996
    ..These findings suggest that ALG-2 may mediate Ca(2+)-regulated signals along the death pathway and that cell death may play a role in Alzheimer's disease...
  7. ncbi request reprint c-E10 is a caspase-recruiting domain-containing protein that interacts with components of death receptors signaling pathway and activates nuclear factor-kappaB
    A Costanzo
    Fondazione A Cesalpino, I Clinica Medica, V le Policlinico 155, 00161 Roma, Italy
    J Biol Chem 274:20127-32. 1999
    ..Thus, our results suggest that c-E10 is an adapter protein that activates NF-kappaB through a molecular pathway involved in death receptor signaling...
  8. pmc Caspase recruitment domain (CARD)-dependent cytoplasmic filaments mediate bcl10-induced NF-kappaB activation
    C Guiet
    Basel Institute for Immunology, Postfach CH 4005, Basel, Switzerland
    J Cell Biol 148:1131-40. 2000
    ..We also show that cytoskeleton elements regulate bcl10 signaling.Thus, organized assemblage of proteins in ordered structures linked to the cytoskeleton network may represent a general mechanism for intracellular signaling...
  9. ncbi request reprint c-FLIP efficiently rescues TRAF-2-/- cells from TNF-induced apoptosis
    C Guiet
    Basel Institute for Immunology, Grenzacherstrasse 487, Postfach CH 4005, Basel, Switzerland
    Cell Death Differ 9:138-44. 2002
    ..Our results strengthen the role of c-FLIP in protecting cells from the cytotoxic effect of TNF and have implication for the treatment of inflammatory and proliferative disorders...
  10. ncbi request reprint The expression of the sarco/endoplasmic reticulum Ca2+-ATPases in thyroid and its down-regulation following neoplastic transformation
    F Pacifico
    Dipartimento di Scienze e Tecnologie Biologiche ed Ambientali, Facoltà di Scienze Matematiche Fisiche e Naturali, Universita degli Studi di Lecce, Strada Provonciale Lecce Monteroni, 73100 Lecce, Italy
    J Mol Endocrinol 30:399-409. 2003
    ..This pattern of expression was basically reproduced in fully differentiated thyroid cells in culture and was sensitive to neoplastic transformation...