D K Morrison

Summary

Affiliation: National Cancer Institute
Country: USA

Publications

  1. ncbi request reprint Raf-1 without MEK?
    M S Murakami
    Regulation of Cell Growth Laboratory, National Cancer Institute, Frederick Cancer Research and Development Center, Frederick, MD 21702, USA
    Sci STKE 2001:pe30. 2001
  2. ncbi request reprint KSR: a MAPK scaffold of the Ras pathway?
    D K Morrison
    Regulation of Cell Growth Laboratory, National Cancer Institute, Frederick Cancer Reseach and Development Center, Frederick, MD 21702, USA
    J Cell Sci 114:1609-12. 2001
  3. ncbi request reprint C-TAK1 regulates Ras signaling by phosphorylating the MAPK scaffold, KSR1
    J Muller
    Regulation of Cell Growth Laboratory, Center for Cancer Research, NCI Frederick, Frederick, MD 21702, USA
    Mol Cell 8:983-93. 2001
  4. pmc Identification of constitutive and ras-inducible phosphorylation sites of KSR: implications for 14-3-3 binding, mitogen-activated protein kinase binding, and KSR overexpression
    A M Cacace
    Molecular Basis of Carcinogenesis Laboratory, ABL Basic Research Program, National Cancer Institute, Frederick Cancer Research and Development Center, Frederick, Maryland 21702, USA
    Mol Cell Biol 19:229-40. 1999
  5. pmc Identification of B-KSR1, a novel brain-specific isoform of KSR1 that functions in neuronal signaling
    J Muller
    Regulation of Cell Growth Laboratory, National Cancer Institute, Frederick Cancer Research and Development Center, Frederick, Maryland 21702, USA
    Mol Cell Biol 20:5529-39. 2000
  6. ncbi request reprint The complexity of Raf-1 regulation
    D K Morrison
    Molecular Basis of Carcinogenesis Laboratory, ABL Basic Research Program, National Cancer Institute, Frederick Cancer Research and Development Center, Frederick, MD 21702, USA
    Curr Opin Cell Biol 9:174-9. 1997
  7. pmc Mammalian Raf-1 is activated by mutations that restore Raf signaling in Drosophila
    R E Cutler
    Molecular Basis of Carcinogenesis Laboratory, ABL Basic Research Program, National Cancer Institute, Frederick Cancer Research and Development Center, MD 21702, USA
    EMBO J 16:1953-60. 1997
  8. ncbi request reprint Opposing actions of CSW and RasGAP modulate the strength of Torso RTK signaling in the Drosophila terminal pathway
    V Cleghon
    Molecular Basis of Carcinogenesis Laboratory, National Cancer Institute, Frederick Cancer Research and Development Center, Maryland 21702, USA
    Mol Cell 2:719-27. 1998
  9. pmc Autoregulation of the Raf-1 serine/threonine kinase
    R E Cutler
    Molecular Basis of Carcinogenesis Laboratory, Advanced BioSciences Laboratories Basic Research Program, National Cancer Institute Frederick Cancer Research and Development Center, Frederick, MD 21702, USA
    Proc Natl Acad Sci U S A 95:9214-9. 1998
  10. ncbi request reprint Integrating signals from RTKs to ERK/MAPK
    M M McKay
    Laboratory of Cell and Developmental Signaling, NCI Frederick, Frederick, MD 21702, USA
    Oncogene 26:3113-21. 2007

Collaborators

  • J Muller
  • M Lee
  • N Perrimon
  • ILARIA L REBAY
  • M Therrien
  • G M Rubin
  • M M McKay
  • R E Cutler
  • N R Michaud
  • M S Murakami
  • A M Cacace
  • V Cleghon
  • A F Ferrier
  • R M Stephens
  • T F Franke
  • T D Copeland
  • A M Wong
  • K Mathes
  • T Copeland
  • M R Saracino
  • C Ghiglione
  • P Feldmann
  • D A Hughes
  • D R Lowy
  • T Laverty
  • A Tang
  • D A Wassarman
  • H C Chang
  • D R Kaplan
  • J E DeClue
  • G Benvenuto
  • W B Anderson
  • F Karim
  • T O Chan
  • P N Tsichlis
  • A Kazlauskas
  • S I Yang
  • K Datta
  • G Sithanandam
  • U R Rapp

Detail Information

Publications17

  1. ncbi request reprint Raf-1 without MEK?
    M S Murakami
    Regulation of Cell Growth Laboratory, National Cancer Institute, Frederick Cancer Research and Development Center, Frederick, MD 21702, USA
    Sci STKE 2001:pe30. 2001
    ..Murakami and Morrison examine these recent findings and discuss their implications, as well as other possible conclusions that may be drawn from the published data...
  2. ncbi request reprint KSR: a MAPK scaffold of the Ras pathway?
    D K Morrison
    Regulation of Cell Growth Laboratory, National Cancer Institute, Frederick Cancer Reseach and Development Center, Frederick, MD 21702, USA
    J Cell Sci 114:1609-12. 2001
    ..Thus, while Kinase Suppressor of Ras may be its name, phosphorylation may not be its game...
  3. ncbi request reprint C-TAK1 regulates Ras signaling by phosphorylating the MAPK scaffold, KSR1
    J Muller
    Regulation of Cell Growth Laboratory, Center for Cancer Research, NCI Frederick, Frederick, MD 21702, USA
    Mol Cell 8:983-93. 2001
    ....
  4. pmc Identification of constitutive and ras-inducible phosphorylation sites of KSR: implications for 14-3-3 binding, mitogen-activated protein kinase binding, and KSR overexpression
    A M Cacace
    Molecular Basis of Carcinogenesis Laboratory, ABL Basic Research Program, National Cancer Institute, Frederick Cancer Research and Development Center, Frederick, Maryland 21702, USA
    Mol Cell Biol 19:229-40. 1999
    ..Therefore, the biological function of KSR as a positive effector of Ras-dependent signaling appears to be dependent on maintaining KSR protein expression at low or near-physiological levels...
  5. pmc Identification of B-KSR1, a novel brain-specific isoform of KSR1 that functions in neuronal signaling
    J Muller
    Regulation of Cell Growth Laboratory, National Cancer Institute, Frederick Cancer Research and Development Center, Frederick, Maryland 21702, USA
    Mol Cell Biol 20:5529-39. 2000
    ....
  6. ncbi request reprint The complexity of Raf-1 regulation
    D K Morrison
    Molecular Basis of Carcinogenesis Laboratory, ABL Basic Research Program, National Cancer Institute, Frederick Cancer Research and Development Center, Frederick, MD 21702, USA
    Curr Opin Cell Biol 9:174-9. 1997
    ..The picture clearly emerging is that Raf-1 activity can be regulated by multiple mechanisms...
  7. pmc Mammalian Raf-1 is activated by mutations that restore Raf signaling in Drosophila
    R E Cutler
    Molecular Basis of Carcinogenesis Laboratory, ABL Basic Research Program, National Cancer Institute, Frederick Cancer Research and Development Center, MD 21702, USA
    EMBO J 16:1953-60. 1997
    ..Finally, we present evidence that the most activating suppressor mutation (G498S) increases Raf-1 activity by introducing a novel phosphorylation site into the L12 activation loop of the Raf-1 kinase domain...
  8. ncbi request reprint Opposing actions of CSW and RasGAP modulate the strength of Torso RTK signaling in the Drosophila terminal pathway
    V Cleghon
    Molecular Basis of Carcinogenesis Laboratory, National Cancer Institute, Frederick Cancer Research and Development Center, Maryland 21702, USA
    Mol Cell 2:719-27. 1998
    ..The opposing actions of CSW and RasGAP modulate the strength of the Torso signal, contributing to the establishment of precise boundaries for terminal structure development...
  9. pmc Autoregulation of the Raf-1 serine/threonine kinase
    R E Cutler
    Molecular Basis of Carcinogenesis Laboratory, Advanced BioSciences Laboratories Basic Research Program, National Cancer Institute Frederick Cancer Research and Development Center, Frederick, MD 21702, USA
    Proc Natl Acad Sci U S A 95:9214-9. 1998
    ....
  10. ncbi request reprint Integrating signals from RTKs to ERK/MAPK
    M M McKay
    Laboratory of Cell and Developmental Signaling, NCI Frederick, Frederick, MD 21702, USA
    Oncogene 26:3113-21. 2007
    ..Together, these factors contribute to the diversity of biological responses generated by RTK signaling...
  11. ncbi request reprint Sequential modification of serines 621 and 624 in the Raf-1 carboxyl terminus produces alterations in its electrophoretic mobility
    A F Ferrier
    Laboratory of Cellular Oncology, National Cancer Institute, Bethesda, Maryland 20892 4040, USA
    J Biol Chem 272:2136-42. 1997
    ..These results demonstrate that a mitogen-activated protein kinase kinase-induced event involving modification of serines 621 and 624 leads to the mobility shift of Raf-1...
  12. ncbi request reprint Signal transduction downstream from Ras in Drosophila
    G M Rubin
    Howard Hughes Medical Institute, University of California, Berkeley 94720 3200, USA
    Cold Spring Harb Symp Quant Biol 62:347-52. 1997
  13. pmc A genetic screen for modifiers of a kinase suppressor of Ras-dependent rough eye phenotype in Drosophila
    M Therrien
    Howard Hughes Medical Institute and Department of Molecular and Cell Biology, University of California, Berkeley, California 94720 3200, USA
    Genetics 156:1231-42. 2000
    ..One of them corresponds to the kismet locus, which encodes a putative chromatin remodeling factor. The relevance of these loci with respect to the function of KSR and the Ras1 pathway in general is discussed...
  14. ncbi request reprint KSR modulates signal propagation within the MAPK cascade
    M Therrien
    Howard Hughes Medical Institute, Department of Molecular and Cell Biology, University of California at Berkeley, 94720 3200, USA
    Genes Dev 10:2684-95. 1996
    ..Together, our findings indicate that mKSR1 is an integral component of the MAPK module functioning via a novel mechanism to modulate signal propagation between Raf-1, MEK1, and MAPK...
  15. ncbi request reprint The protein kinase encoded by the Akt proto-oncogene is a target of the PDGF-activated phosphatidylinositol 3-kinase
    T F Franke
    Fox Chase Cancer Center, Philadelphia, Pennsylvania 19111, USA
    Cell 81:727-36. 1995
    ..These results identify Akt as a novel target of PI 3-kinase and suggest that the Akt PH domain may be a mediator of PI 3-kinase signaling...
  16. ncbi request reprint Direct activation of the serine/threonine kinase activity of Raf-1 through tyrosine phosphorylation by the PDGF beta-receptor
    D K Morrison
    Department of Medicine, Howard Hughes Medical Institute, University of California, San Francisco 94143
    Cell 58:649-57. 1989
    ..This is the first demonstration of the direct modulation of a protein activity by a growth factor receptor tyrosine kinase...
  17. pmc 95-kilodalton B-Raf serine/threonine kinase: identification of the protein and its major autophosphorylation site
    R M Stephens
    Molecular Mechanisms of Carcinogenesis Laboratory, National Cancer Institute Frederick Cancer Research and Development Center, Maryland
    Mol Cell Biol 12:3733-42. 1992
    ..A threonine residue is present at similar positions in all three mammalian Raf family members and may represent a regulatory site for these proteins...