Derek Abbott

Summary

Affiliation: Case Western Reserve University
Country: USA

Publications

  1. ncbi The Crohn's disease protein, NOD2, requires RIP2 in order to induce ubiquitinylation of a novel site on NEMO
    Derek W Abbott
    Division of Gastrointestinal Pathology, Department of Pathology, Brigham and Women s Hospital, Harvard Medical School, Boston, MA, USA
    Curr Biol 14:2217-27. 2004
  2. ncbi A rapid method for determining protein kinase phosphorylation specificity
    Jessica E Hutti
    Division of Signal Transduction, Harvard Medical School, 330 Brookline Avenue, Boston, Massachusetts 02215, USA
    Nat Methods 1:27-9. 2004
  3. pmc Coordinated regulation of Toll-like receptor and NOD2 signaling by K63-linked polyubiquitin chains
    Derek W Abbott
    Department of Pathology, Case Western Reserve University School of Medicine, Room 5123 Wolstein Research Building, Cleveland, OH 44106, and Department of Pathology, Brigham and Women s Hospital, Boston, MA, USA
    Mol Cell Biol 27:6012-25. 2007
  4. pmc Phosphorylation of the tumor suppressor CYLD by the breast cancer oncogene IKKepsilon promotes cell transformation
    Jessica E Hutti
    Department of Systems Biology, Harvard Medical School, Boston, MA 02115, USA
    Mol Cell 34:461-72. 2009
  5. pmc RIP2 activity in inflammatory disease and implications for novel therapeutics
    Janice C Jun
    1 Case Western Reserve University School of Medicine, Wolstein Research Bldg, 2103 Cornell Rd, Room 6532, Cleveland, OH 44122, USA
    J Leukoc Biol 94:927-32. 2013
  6. ncbi NOD2 pathway activation by MDP or Mycobacterium tuberculosis infection involves the stable polyubiquitination of Rip2
    Yibin Yang
    Department of Pathology, Case Western University School of Medicine, Cleveland, Ohio 44106, USA
    J Biol Chem 282:36223-9. 2007
  7. pmc ITCH K63-ubiquitinates the NOD2 binding protein, RIP2, to influence inflammatory signaling pathways
    Mingfang Tao
    Department of Pathology, Case Western Reserve University School of Medicine, Cleveland, OH 44106, USA
    Curr Biol 19:1255-63. 2009
  8. pmc Feedback inhibition of Akt signaling limits the growth of tumors lacking Tsc2
    Brendan D Manning
    Department of Genetics and Complex Diseases, Harvard School of Public Health, Boston, Massachusetts 02115, USA
    Genes Dev 19:1773-8. 2005
  9. pmc IkappaB kinase beta phosphorylates the K63 deubiquitinase A20 to cause feedback inhibition of the NF-kappaB pathway
    Jessica E Hutti
    Department of Systems Biology, Harvard Medical School, Boston, Massachusetts, USA
    Mol Cell Biol 27:7451-61. 2007
  10. pmc Binding of pro-prion to filamin A disrupts cytoskeleton and correlates with poor prognosis in pancreatic cancer
    Chaoyang Li
    Department of Pathology, Case Western Reserve University, Cleveland, Ohio 44106, USA
    J Clin Invest 119:2725-36. 2009

Collaborators

  • Christopher Sassetti
  • Peter Storz
  • AVERIL I contact MA
  • Edward W Harhaj
  • Jessica E Hutti
  • Lewis C Cantley
  • John M Asara
  • Janice C Jun
  • Justine T Tigno-Aranjuez
  • Chaoyang Li
  • Mingfang Tao
  • Yibin Yang
  • Benjamin E Turk
  • Brendan D Manning
  • Fabio Cominelli
  • Rhine R Shen
  • Man Sun Sy
  • Shaoman Yin
  • Shuiliang Yu
  • Jinghua Xu
  • William C Hahn
  • Jill M Marinis
  • Wei Xin
  • ALAN TARTAKOFF
  • Amber A Petrolla
  • Kam M Sprott
  • Alicia Y Zhou
  • Lydia E Matesic
  • Fumihiko Nakamura
  • Peter C Scacheri
  • Neena Singh
  • Catherine Yin
  • Amit Pandey
  • Michelle A Kelliher
  • Alex I Lipovsky
  • M Nicole Logsdon
  • David J Kwiatkowski
  • James D Chang
  • Emily T Jarrell
  • Alex Toker

Detail Information

Publications11

  1. ncbi The Crohn's disease protein, NOD2, requires RIP2 in order to induce ubiquitinylation of a novel site on NEMO
    Derek W Abbott
    Division of Gastrointestinal Pathology, Department of Pathology, Brigham and Women s Hospital, Harvard Medical School, Boston, MA, USA
    Curr Biol 14:2217-27. 2004
    ..NOD2 can both strongly activate and negatively attenuate NF-kB signaling. The biochemical mechanism for this dual function of NOD2 is unknown...
  2. ncbi A rapid method for determining protein kinase phosphorylation specificity
    Jessica E Hutti
    Division of Signal Transduction, Harvard Medical School, 330 Brookline Avenue, Boston, Massachusetts 02215, USA
    Nat Methods 1:27-9. 2004
    ..Here we describe a combinatorial peptide library method that allows rapid generation of phosphorylation motifs for serine/threonine kinases...
  3. pmc Coordinated regulation of Toll-like receptor and NOD2 signaling by K63-linked polyubiquitin chains
    Derek W Abbott
    Department of Pathology, Case Western Reserve University School of Medicine, Room 5123 Wolstein Research Building, Cleveland, OH 44106, and Department of Pathology, Brigham and Women s Hospital, Boston, MA, USA
    Mol Cell Biol 27:6012-25. 2007
    ..These findings suggest a biochemical mechanism for the faulty cytokine balance seen in Crohn's disease...
  4. pmc Phosphorylation of the tumor suppressor CYLD by the breast cancer oncogene IKKepsilon promotes cell transformation
    Jessica E Hutti
    Department of Systems Biology, Harvard Medical School, Boston, MA 02115, USA
    Mol Cell 34:461-72. 2009
    ..Together, these observations define IKKepsilon and CYLD as an oncogene-tumor suppressor network that participates in tumorigenesis...
  5. pmc RIP2 activity in inflammatory disease and implications for novel therapeutics
    Janice C Jun
    1 Case Western Reserve University School of Medicine, Wolstein Research Bldg, 2103 Cornell Rd, Room 6532, Cleveland, OH 44122, USA
    J Leukoc Biol 94:927-32. 2013
    ..This article reviews the role that the NOD2:RIP2 complex plays in inflammatory disease, with an emphasis on the inhibition of this signaling pathway as a novel pharmaceutical target in inflammatory disease. ..
  6. ncbi NOD2 pathway activation by MDP or Mycobacterium tuberculosis infection involves the stable polyubiquitination of Rip2
    Yibin Yang
    Department of Pathology, Case Western University School of Medicine, Cleveland, Ohio 44106, USA
    J Biol Chem 282:36223-9. 2007
    ..tuberculosis-induced Rip2 polyubiquitination appears MyD88-independent. Collectively, these data reveal that the NOD2 pathway is ubiquitin-regulated and that Rip2 employs a ubiquitin-dependent mechanism to achieve NF-kappaB activation...
  7. pmc ITCH K63-ubiquitinates the NOD2 binding protein, RIP2, to influence inflammatory signaling pathways
    Mingfang Tao
    Department of Pathology, Case Western Reserve University School of Medicine, Cleveland, OH 44106, USA
    Curr Biol 19:1255-63. 2009
    ....
  8. pmc Feedback inhibition of Akt signaling limits the growth of tumors lacking Tsc2
    Brendan D Manning
    Department of Genetics and Complex Diseases, Harvard School of Public Health, Boston, Massachusetts 02115, USA
    Genes Dev 19:1773-8. 2005
    ..However, Pten haploinsufficiency restores Akt signaling in these tumors and dramatically enhances their severity. This study demonstrates that attenuation of the PI3K-Akt pathway in tumors lacking TSC2 contributes to their benign nature...
  9. pmc IkappaB kinase beta phosphorylates the K63 deubiquitinase A20 to cause feedback inhibition of the NF-kappaB pathway
    Jessica E Hutti
    Department of Systems Biology, Harvard Medical School, Boston, Massachusetts, USA
    Mol Cell Biol 27:7451-61. 2007
    ..Phosphorylation of A20 by IKKbeta thus represents part of a novel feedback loop that regulates the duration of NF-kappaB signaling following activation of innate immune signaling pathways...
  10. pmc Binding of pro-prion to filamin A disrupts cytoskeleton and correlates with poor prognosis in pancreatic cancer
    Chaoyang Li
    Department of Pathology, Case Western Reserve University, Cleveland, Ohio 44106, USA
    J Clin Invest 119:2725-36. 2009
    ..We propose that binding of pro-PrP to FLNa perturbs FLNa function, thus contributing to the aggressiveness of PDAC. Prevention of this interaction could provide an attractive target for therapeutic intervention in human PDAC...
  11. pmc Inhibition of RIP2's tyrosine kinase activity limits NOD2-driven cytokine responses
    Justine T Tigno-Aranjuez
    Department of Pathology, Case Western Reserve University School of Medicine, Cleveland, Ohio 44106, USA
    Genes Dev 24:2666-77. 2010
    ....

Research Grants8

  1. RIP2 kinase's function in Innate Immunity
    Derek Abbott; Fiscal Year: 2007
    ..This grant application aims to define the preferred peptide phosphorylation sites of RIP2, to map the phosphorylation site of TRAF6 and to identify the physiologic significance of RIP2's phosphorylation of TRAF6. ..
  2. RIP2 kinase's function in Innate Immunity
    Derek Abbott; Fiscal Year: 2006
    ..This grant application aims to define the preferred peptide phosphorylation sites of RIP2, to map the phosphorylation site of TRAF6 and to identify the physiologic significance of RIP2's phosphorylation of TRAF6. ..
  3. Innate immune signal transduction specificity in inflammatory disease
    Derek Abbott; Fiscal Year: 2009
    ..This work aims to help determine the causes of inflammatory disease and aims to identify novel targets for pharmaceutical intervention in these debilitating disorders. ..
  4. Innate immune signal transduction specificity in inflammatory disease
    Derek W Abbott; Fiscal Year: 2010
    ..This work aims to help determine the causes of inflammatory disease and aims to identify novel targets for pharmaceutical intervention in these debilitating disorders. ..
  5. Innate immune signal transduction specificity in inflammatory disease
    Derek W Abbott; Fiscal Year: 2011
    ..This work aims to help determine the causes of inflammatory disease and aims to identify novel targets for pharmaceutical intervention in these debilitating disorders. ..
  6. Innate immune signal transduction specificity in inflammatory disease
    Derek W Abbott; Fiscal Year: 2010
    ..This work aims to help determine the causes of inflammatory disease and aims to identify novel targets for pharmaceutical intervention in these debilitating disorders. ..