J Moscat

Summary

Affiliation: University of Cincinnati
Country: USA

Publications

  1. doi request reprint Of the atypical PKCs, Par-4 and p62: recent understandings of the biology and pathology of a PB1-dominated complex
    J Moscat
    Department of Cancer and Cell Biology, University of Cincinnati College of Medicine, Cincinnati, Ohio 45267, USA
    Cell Death Differ 16:1426-37. 2009
  2. doi request reprint p62 at the crossroads of autophagy, apoptosis, and cancer
    Jorge Moscat
    Department of Cancer and Cell Biology, University of Cincinnati College of Medicine, Cincinnati, OH 45267, USA
    Cell 137:1001-4. 2009
  3. ncbi request reprint Cell signaling and function organized by PB1 domain interactions
    Jorge Moscat
    Centro de Biologia Molecular Severo Ochoa, Consejo Superior de Investigaciones Cientificas, Universidad Autonoma, Cantoblanco, 28049 Madrid, Spain
    Mol Cell 23:631-40. 2006
  4. ncbi request reprint Signal integration and diversification through the p62 scaffold protein
    Jorge Moscat
    Department of Genome Science, Genome Research Institute, University of Cincinnati, 2180 E Galbraith Road, Cincinnati, OH 45237, USA
    Trends Biochem Sci 32:95-100. 2007
  5. doi request reprint The signaling adaptor p62 is an important NF-kappaB mediator in tumorigenesis
    Angeles Duran
    Department of Molecular Oncogenesis, Genome Research Institute, University of Cincinnati College of Medicine, Cincinnati, OH 45229, USA
    Cancer Cell 13:343-54. 2008
  6. ncbi request reprint Akt regulation and lung cancer: a novel role and mechanism of action for the tumor suppressor Par-4
    Maria T Diaz-Meco
    Department of Cancer and Cell Biology, University of Cincinnati College of Medicine, Cincinnati, Ohio 45267, USA
    Cell Cycle 7:2817-20. 2008
  7. pmc Loss of PKC lambda/iota impairs Th2 establishment and allergic airway inflammation in vivo
    Jun Qi Yang
    Department of Cancer and Cell Biology, University of Cincinnati College of Medicine, Cincinnati, OH 45267, USA
    Proc Natl Acad Sci U S A 106:1099-104. 2009
  8. pmc Protein kinase Czeta represses the interleukin-6 promoter and impairs tumorigenesis in vivo
    Anita S Galvez
    Department of Cancer and Cell Biology, University of Cincinnati College of Medicine, 3125 Eden Ave, Cincinnati, OH 45267, USA
    Mol Cell Biol 29:104-15. 2009
  9. pmc Par-4 inhibits Akt and suppresses Ras-induced lung tumorigenesis
    Jayashree Joshi
    Department of Cancer and Cell Biology, University of Cincinnati College of Medicine, Cincinnati, OH 45267, USA
    EMBO J 27:2181-93. 2008
  10. pmc PKCzeta-regulated inflammation in the nonhematopoietic compartment is critical for obesity-induced glucose intolerance
    Sang Jun Lee
    Department of Cancer and Cell Biology, University of Cincinnati College of Medicine, 3125 Eden Avenue, Cincinnati, OH 45267, USA
    Cell Metab 12:65-77. 2010

Collaborators

  • M W Wooten
  • Maria T Diaz-Meco
  • G Pages
  • Armando Albert
  • Manuel Collado
  • Juan F Linares
  • Angeles Duran
  • Sang Jun Lee
  • Jun Qi Yang
  • Michael Leitges
  • Anita S Galvez
  • Ruben Nogueiras
  • Ji Young Kim
  • Matthias H Tschop
  • Ramars Amanchy
  • Peterson Pathrose
  • Jayashree Joshi
  • Kenneth Greis
  • Jacques Pouyssegur
  • Jason K Kim
  • Susanna M Hofmann
  • Diego Perez-Tilve
  • Dae Young Jung
  • Hongzhu Liu
  • Angela Drew
  • Paul T Pfluger
  • Hwi Jin Ko
  • Shadi Abu-Baker
  • Elias A Castilla
  • Pablo J Fernandez-Marcos
  • Clara Salas
  • Kathryn Wikenheiser
  • Juana M Flores
  • Anita Galvez
  • Manuel Serrano
  • Marta Canamero

Detail Information

Publications13

  1. doi request reprint Of the atypical PKCs, Par-4 and p62: recent understandings of the biology and pathology of a PB1-dominated complex
    J Moscat
    Department of Cancer and Cell Biology, University of Cincinnati College of Medicine, Cincinnati, Ohio 45267, USA
    Cell Death Differ 16:1426-37. 2009
    ..All this published information is shedding new light on the proposed pathological implications of these PB1-regulators in disease and shows their important role in cell physiology...
  2. doi request reprint p62 at the crossroads of autophagy, apoptosis, and cancer
    Jorge Moscat
    Department of Cancer and Cell Biology, University of Cincinnati College of Medicine, Cincinnati, OH 45267, USA
    Cell 137:1001-4. 2009
    ..2009) now show that the modulation of p62 by autophagy is a key factor in tumorigenesis. These findings place p62 at critical decision points that control cell death and survival...
  3. ncbi request reprint Cell signaling and function organized by PB1 domain interactions
    Jorge Moscat
    Centro de Biologia Molecular Severo Ochoa, Consejo Superior de Investigaciones Cientificas, Universidad Autonoma, Cantoblanco, 28049 Madrid, Spain
    Mol Cell 23:631-40. 2006
    ..Also, recent data suggest that PB1 domains may serve to orchestrate signaling cascades not involving other PB1 domains, such as the MEK5-ERK5 and p62-ERK1 interactions...
  4. ncbi request reprint Signal integration and diversification through the p62 scaffold protein
    Jorge Moscat
    Department of Genome Science, Genome Research Institute, University of Cincinnati, 2180 E Galbraith Road, Cincinnati, OH 45237, USA
    Trends Biochem Sci 32:95-100. 2007
    ..The availability of mice in which p62 has been genetically inactivated is providing new insight into the mechanism and function of p62 at a whole-organism level...
  5. doi request reprint The signaling adaptor p62 is an important NF-kappaB mediator in tumorigenesis
    Angeles Duran
    Department of Molecular Oncogenesis, Genome Research Institute, University of Cincinnati College of Medicine, Cincinnati, OH 45229, USA
    Cancer Cell 13:343-54. 2008
    ....
  6. ncbi request reprint Akt regulation and lung cancer: a novel role and mechanism of action for the tumor suppressor Par-4
    Maria T Diaz-Meco
    Department of Cancer and Cell Biology, University of Cincinnati College of Medicine, Cincinnati, Ohio 45267, USA
    Cell Cycle 7:2817-20. 2008
    ....
  7. pmc Loss of PKC lambda/iota impairs Th2 establishment and allergic airway inflammation in vivo
    Jun Qi Yang
    Department of Cancer and Cell Biology, University of Cincinnati College of Medicine, Cincinnati, OH 45267, USA
    Proc Natl Acad Sci U S A 106:1099-104. 2009
    ..Therefore PKC lambda/iota emerges as a critical regulator of Th 2 activation...
  8. pmc Protein kinase Czeta represses the interleukin-6 promoter and impairs tumorigenesis in vivo
    Anita S Galvez
    Department of Cancer and Cell Biology, University of Cincinnati College of Medicine, 3125 Eden Ave, Cincinnati, OH 45267, USA
    Mol Cell Biol 29:104-15. 2009
    ..We also show that PKCzeta represses histone acetylation at the C/EBPbeta element in the IL-6 promoter. Therefore, PKCzeta, by controlling the production of IL-6, is a critical signaling molecule in tumorigenesis...
  9. pmc Par-4 inhibits Akt and suppresses Ras-induced lung tumorigenesis
    Jayashree Joshi
    Department of Cancer and Cell Biology, University of Cincinnati College of Medicine, Cincinnati, OH 45267, USA
    EMBO J 27:2181-93. 2008
    ....
  10. pmc PKCzeta-regulated inflammation in the nonhematopoietic compartment is critical for obesity-induced glucose intolerance
    Sang Jun Lee
    Department of Cancer and Cell Biology, University of Cincinnati College of Medicine, 3125 Eden Avenue, Cincinnati, OH 45267, USA
    Cell Metab 12:65-77. 2010
    ..These results establish PKCzeta as a critical negative regulator of IL-6 in the control of obesity-induced inflammation in adipocytes...
  11. pmc NBR1 is a new PB1 signalling adapter in Th2 differentiation and allergic airway inflammation in vivo
    Jun Qi Yang
    Department of Cancer and Cell Biology, University of Cincinnati College of Medicine, Cincinnati, OH, USA
    EMBO J 29:3421-33. 2010
    ..These results establish NBR1 as a novel PB1 adapter in Th2 differentiation and asthma...
  12. doi request reprint A functional role for the p62-ERK1 axis in the control of energy homeostasis and adipogenesis
    Sang Jun Lee
    Department of Cancer and Cell Biology, The Vontz Center for Molecular Studies, University of Cincinnati College of Medicine, Cincinnati, Ohio 45267, USA
    EMBO Rep 11:226-32. 2010
    ..These results establish genetically that p62 is a crucial regulator of ERK1 in metabolism...
  13. pmc Phosphorylation of p62 by cdk1 controls the timely transit of cells through mitosis and tumor cell proliferation
    Juan F Linares
    Department of Cancer and Cell Biology, University of Cincinnati College of Medicine, Vontz Center for Molecular Studies, 3125 Eden Avenue, Cincinnati, OH 45267, USA
    Mol Cell Biol 31:105-17. 2011
    ..Therefore, p62 emerges as a node for the control of not only cell survival but also cell transit through mitosis...