JEFFREY WINKLES

Summary

Affiliation: University of Maryland
Country: USA

Publications

  1. ncbi request reprint Role of TWEAK and Fn14 in tumor biology
    Jeffrey A Winkles
    Department of Surgery, Center for Vascular and Inflammatory Diseases, University of Maryland School of Medicine, Baltimore, Maryland 21201, USA
    Front Biosci 12:2761-71. 2007
  2. pmc The HER2- and Heregulin β1 (HRG)-Inducible TNFR Superfamily Member Fn14 Promotes HRG-Driven Breast Cancer Cell Migration, Invasion, and MMP9 Expression
    Kaushal Asrani
    Department of Surgery, University of Maryland School of Medicine, 800 West Baltimore St, Room 320, Baltimore, MD 21201
    Mol Cancer Res 11:393-404. 2013
  3. ncbi request reprint TWEAK and Fn14: new molecular targets for cancer therapy?
    Jeffrey A Winkles
    Department of Surgery, University of Maryland Greenebaum Cancer Center, University of Maryland School of Medicine, Baltimore, 21201, USA
    Cancer Lett 235:11-7. 2006
  4. ncbi request reprint Differential regulation of polo-like kinase 1, 2, 3, and 4 gene expression in mammalian cells and tissues
    Jeffrey A Winkles
    Department of Surgery, University of Maryland Greenebaum Cancer Center, University of Maryland School of Medicine, Baltimore, MD 21201, USA
    Oncogene 24:260-6. 2005
  5. pmc The TWEAK-Fn14 cytokine-receptor axis: discovery, biology and therapeutic targeting
    Jeffrey A Winkles
    Department of Surgery, Center for Vascular and Inflammatory Diseases, and the Marlene and Stewart Greenebaum Cancer Center, 800 West Baltimore Street, University of Maryland School of Medicine, Baltimore, Maryland 21201, USA
    Nat Rev Drug Discov 7:411-25. 2008
  6. pmc A soluble Fn14-Fc decoy receptor reduces infarct volume in a murine model of cerebral ischemia
    Manuel Yepes
    Department of Surgery, University of Maryland School of Medicine, 15601 Crabbs Branch Way, Rockville, MD 20855, USA
    Am J Pathol 166:511-20. 2005
  7. pmc Full-length, membrane-anchored TWEAK can function as a juxtacrine signaling molecule and activate the NF-kappaB pathway
    Sharron A N Brown
    Department of Surgery and Physiology, Center for Vascular and Inflammatory Diseases, University of Maryland School of Medicine, Baltimore, Maryland 21201, USA
    J Biol Chem 285:17432-41. 2010
  8. pmc TWEAK binding to the Fn14 cysteine-rich domain depends on charged residues located in both the A1 and D2 modules
    Sharron A N Brown
    Department of Surgery, Center for Vascular and Inflammatory Diseases, University of Maryland School of Medicine, 800 W Baltimore St, Baltimore, MD 21201, USA
    Biochem J 397:297-304. 2006
  9. ncbi request reprint Soluble tumor necrosis factor-like weak inducer of apoptosis overexpression in HEK293 cells promotes tumor growth and angiogenesis in athymic nude mice
    David H Ho
    Department of Surgery and Physiology and the University of Maryland Greenebaum Cancer Center, University of Maryland School of Medicine, Baltimore, Maryland, USA
    Cancer Res 64:8968-72. 2004
  10. pmc TWEAK, via its receptor Fn14, is a novel regulator of mesenchymal progenitor cells and skeletal muscle regeneration
    Mahasweta Girgenrath
    Boston Biomedical Research Institute, Watertown, MA, USA
    EMBO J 25:5826-39. 2006

Research Grants

  1. The Fnk Kinase and Vascular Cell Growth Control
    JEFFREY WINKLES; Fiscal Year: 2004
  2. Role of TWEAK and Fn14 in Vascular Biology
    JEFFREY WINKLES; Fiscal Year: 2005
  3. The Fn14 Receptor and Brain Tumor Invasion
    JEFFREY WINKLES; Fiscal Year: 2007
  4. TWEAK-Fn14 Signaling in the Tumor Microenvironment
    Jeffrey A Winkles; Fiscal Year: 2010
  5. VASCULAR SMOOTH MUSCLE CELL PROLIFERATION
    JEFFREY WINKLES; Fiscal Year: 1993
  6. FGF SIGNAL TRANSDUCTION IN VASCULAR CELLS
    JEFFREY WINKLES; Fiscal Year: 2000
  7. The Fn14 Receptor and Brain Tumor Invasion
    Jeffrey A Winkles; Fiscal Year: 2011

Collaborators

  • Steven R Wiley
  • MANUEL SALVADOR YEPES
  • Jennifer S Michaelson
  • Timothy S Zheng
  • Ann Zeuner
  • Max Costa
  • Marta Ruiz-Ortega
  • Wei Dai
  • Alberto Ortiz
  • Linda C Burkly
  • Aniela Jakubowski
  • Sharron A N Brown
  • Nhan L Tran
  • Wendy S McDonough
  • Heather N Hanscom
  • Patrick J Donohue
  • Hong Vu
  • Rohini Polavarapu
  • Kaushal Asrani
  • Gregory F Alberts
  • Michael E Berens
  • Arundhati Ghosh
  • Amanda L Willis
  • Ana Belen Sanz
  • Yali Yang
  • Xiaohui Zhang
  • Shannon P Fortin
  • Heather E Cunliffe
  • Mahasweta Girgenrath
  • Benjamin A Savitch
  • Nadia Felli
  • Dominique B Hoelzinger
  • David H Ho
  • Katsuhisa Tanabe
  • Christine M Richards
  • Rebeca Galisteo
  • Sarah J Morgan
  • Ruth A Keri
  • Luo Lu
  • Ying Huang
  • Nichole Charlton
  • Joshua R Niska
  • Ning Jiang
  • Elena Komissarova
  • Julia Blanco
  • Pilar Justo
  • Matthias Kreztler
  • Jingxiang Bai
  • Luis Miguel Blanco-Colio
  • Julie M Chatigny
  • Maria Dolores Sanchez-Nino
  • Jesus Egido
  • Rulong Shen
  • Michael A Black
  • Kyungmin Hahm
  • Xiao Jiang Li
  • Meyer Friedman
  • Maria C Gongora
  • Martin L Scott
  • Christopher A Lipinski
  • Marc Symons
  • Luigi Mariani
  • Jessica L Rennert
  • Shelesa A Brew
  • Mitsutoshi Nakada
  • Joseph C Loftus
  • Shawn Weng
  • Monica Wang
  • Yen Ming Hsu
  • Norm Allaire
  • Beth Browning
  • Jeffrey Boone Miller
  • Pascal Schneider
  • Richard A Flavell
  • Christine A Kostek
  • Hideo Yagita
  • Galen Hostetter
  • Ugo Testa
  • Eleonora Petrucci
  • Maria Carolina Gongora
  • Thomas F Sawyer
  • Mauro Biffoni
  • Cesare Peschle
  • Andrea Di Cataldo
  • Ruggero De Maria
  • Francesca Pedini
  • Concetta Conticello
  • Theresa J Berens
  • Timothy Hla
  • Stephen M Strittmatter

Detail Information

Publications25

  1. ncbi request reprint Role of TWEAK and Fn14 in tumor biology
    Jeffrey A Winkles
    Department of Surgery, Center for Vascular and Inflammatory Diseases, University of Maryland School of Medicine, Baltimore, Maryland 21201, USA
    Front Biosci 12:2761-71. 2007
    ..In this paper, we first summarize the general properties of these two proteins and then review the available data implicating TWEAK and Fn14 in multiple aspects of tumor biology...
  2. pmc The HER2- and Heregulin β1 (HRG)-Inducible TNFR Superfamily Member Fn14 Promotes HRG-Driven Breast Cancer Cell Migration, Invasion, and MMP9 Expression
    Kaushal Asrani
    Department of Surgery, University of Maryland School of Medicine, 800 West Baltimore St, Room 320, Baltimore, MD 21201
    Mol Cancer Res 11:393-404. 2013
    ..Together, these results indicate that Fn14 may be an important downstream regulator of HER2/HER3-driven breast cancer cell migration and invasion. Mol Cancer Res; 11(4); 393-404. ©2013 AACR...
  3. ncbi request reprint TWEAK and Fn14: new molecular targets for cancer therapy?
    Jeffrey A Winkles
    Department of Surgery, University of Maryland Greenebaum Cancer Center, University of Maryland School of Medicine, Baltimore, 21201, USA
    Cancer Lett 235:11-7. 2006
    ..In this article, we review recent studies indicating that TWEAK and Fn14 may be potential regulators of human tumorigenesis...
  4. ncbi request reprint Differential regulation of polo-like kinase 1, 2, 3, and 4 gene expression in mammalian cells and tissues
    Jeffrey A Winkles
    Department of Surgery, University of Maryland Greenebaum Cancer Center, University of Maryland School of Medicine, Baltimore, MD 21201, USA
    Oncogene 24:260-6. 2005
    ..These results indicate that the differential regulation of Plk family member gene expression is one cellular strategy for controlling Plk activity in mammalian cells...
  5. pmc The TWEAK-Fn14 cytokine-receptor axis: discovery, biology and therapeutic targeting
    Jeffrey A Winkles
    Department of Surgery, Center for Vascular and Inflammatory Diseases, and the Marlene and Stewart Greenebaum Cancer Center, 800 West Baltimore Street, University of Maryland School of Medicine, Baltimore, Maryland 21201, USA
    Nat Rev Drug Discov 7:411-25. 2008
    ..This Review provides an overview of TWEAK-Fn14 axis biology and summarizes the available data supporting the proposal that both TWEAK and Fn14 should be considered as potential targets for the development of novel therapeutics...
  6. pmc A soluble Fn14-Fc decoy receptor reduces infarct volume in a murine model of cerebral ischemia
    Manuel Yepes
    Department of Surgery, University of Maryland School of Medicine, 15601 Crabbs Branch Way, Rockville, MD 20855, USA
    Am J Pathol 166:511-20. 2005
    ..We conclude that the cytokine TWEAK may play an important role in ischemia-induced brain injury and that inhibition of TWEAK expression or function in the brain may represent a novel neuroprotective strategy to treat ischemic stroke...
  7. pmc Full-length, membrane-anchored TWEAK can function as a juxtacrine signaling molecule and activate the NF-kappaB pathway
    Sharron A N Brown
    Department of Surgery and Physiology, Center for Vascular and Inflammatory Diseases, University of Maryland School of Medicine, Baltimore, Maryland 21201, USA
    J Biol Chem 285:17432-41. 2010
    ..Thus, TWEAK can act in a juxtacrine manner to initiate cellular responses, and this property may be important for TWEAK function during physiological wound repair and disease pathogenesis...
  8. pmc TWEAK binding to the Fn14 cysteine-rich domain depends on charged residues located in both the A1 and D2 modules
    Sharron A N Brown
    Department of Surgery, Center for Vascular and Inflammatory Diseases, University of Maryland School of Medicine, 800 W Baltimore St, Baltimore, MD 21201, USA
    Biochem J 397:297-304. 2006
    ..These results indicate that the TWEAK-Fn14 interaction is highly dependent on multiple Fn14 residues located in both CRD modules...
  9. ncbi request reprint Soluble tumor necrosis factor-like weak inducer of apoptosis overexpression in HEK293 cells promotes tumor growth and angiogenesis in athymic nude mice
    David H Ho
    Department of Surgery and Physiology and the University of Maryland Greenebaum Cancer Center, University of Maryland School of Medicine, Baltimore, Maryland, USA
    Cancer Res 64:8968-72. 2004
    ..This result suggests that the TWEAK-Fn14 signaling system may be a potential regulator of human tumorigenesis...
  10. pmc TWEAK, via its receptor Fn14, is a novel regulator of mesenchymal progenitor cells and skeletal muscle regeneration
    Mahasweta Girgenrath
    Boston Biomedical Research Institute, Watertown, MA, USA
    EMBO J 25:5826-39. 2006
    ....
  11. ncbi request reprint The tumor necrosis factor-like weak inducer of apoptosis (TWEAK)-fibroblast growth factor-inducible 14 (Fn14) signaling system regulates glioma cell survival via NFkappaB pathway activation and BCL-XL/BCL-W expression
    Nhan L Tran
    Neurogenomics Division, The Translational Genomics Research Institute, Phoenix, Arizona 85004, USA
    J Biol Chem 280:3483-92. 2005
    ..Targeted therapy against Fn14 as an adjuvant to surgery may improve management of invasive glioma cells and advance the outcome of this devastating cancer...
  12. ncbi request reprint TWEAK, a member of the TNF superfamily, is a multifunctional cytokine that binds the TweakR/Fn14 receptor
    Steven R Wiley
    Amgen Corporation, Seattle, WA 98101, USA
    Cytokine Growth Factor Rev 14:241-9. 2003
    ..Although these studies have contributed a significant amount of new information, numerous questions still remain regarding the role of TWEAK in both normal physiology and the pathogenesis of human disease...
  13. ncbi request reprint Inhibition of TWEAK activity as a new treatment for inflammatory and degenerative diseases
    Manuel Yepes
    Department of Neurology and Center for Neurodegenerative Disease, Emory University School of Medicine, Atlanta, Georgia 30322, USA
    Drug News Perspect 19:589-95. 2006
    ..In this review we first introduce the TWEAK-Fn14 signaling system and then focus on the potential therapeutic utility of soluble Fn14-Fc fusion proteins and TWEAK neutralizing antibodies...
  14. pmc The cytokine TWEAK modulates renal tubulointerstitial inflammation
    Ana Belen Sanz
    Unidad de Dialisis, Fundacion Jimenez Diaz, Avda Reyes Catolicos 2, 28040 Madrid, Spain
    J Am Soc Nephrol 19:695-703. 2008
    ..Moreover, blockade of TWEAK reduces tubular chemokine expression and macrophage infiltration, suggesting that TWEAK modulates acute kidney injury by regulating the inflammatory response...
  15. pmc Polo-like kinase 3 functions as a tumor suppressor and is a negative regulator of hypoxia-inducible factor-1 alpha under hypoxic conditions
    Yali Yang
    Department of Environmental Medicine, New York University School of Medicine, Tuxedo, New York 10987, USA
    Cancer Res 68:4077-85. 2008
    ....
  16. pmc The fibroblast growth factor-inducible 14 receptor is highly expressed in HER2-positive breast tumors and regulates breast cancer cell invasive capacity
    Amanda L Willis
    Cancer and Cell Biology Division, The Translational Genomics Research Institute, 445 North Fifth Street, Phoenix, AZ 85004, USA
    Mol Cancer Res 6:725-34. 2008
    ..Expression profiling of the Fn14-depleted cells revealed deregulation of NF-kappaB activity. Our findings support a role for Fn14-mediated NF-kappaB pathway activation in breast tumor invasion and metastasis...
  17. ncbi request reprint Increased fibroblast growth factor-inducible 14 expression levels promote glioma cell invasion via Rac1 and nuclear factor-kappaB and correlate with poor patient outcome
    Nhan L Tran
    Cancer and Cell Biology Division, Translational Genomics Research Institute, Phoenix, AZ 85004, USA
    Cancer Res 66:9535-42. 2006
    ..Such a feedback loop argues for aggressive targeting of the Fn14 axis as a unique and specific driver of glioma malignant behavior...
  18. ncbi request reprint TWEAK-Fn14 pathway inhibition protects the integrity of the neurovascular unit during cerebral ischemia
    Xiaohui Zhang
    Department of Neurology and Center for Neurodegenerative Disease, Emory University School of Medicine, Atlanta, GA 30322, USA
    J Cereb Blood Flow Metab 27:534-44. 2007
    ..These findings show that the cytokine TWEAK plays a role in the disruption of the structure of the NVU during cerebral ischemia and that TWEAK antagonism is a potential therapeutic strategy for acute cerebral ischemia...
  19. ncbi request reprint Tumor necrosis factor-like weak inducer of apoptosis increases the permeability of the neurovascular unit through nuclear factor-kappa B pathway activation
    Rohini Polavarapu
    Department of Neurology, Center for Neurodegenerative Disease, Emory University School of Medicine, Atlanta, Georgia 30322, USA
    J Neurosci 25:10094-100. 2005
    ..We conclude that the cytokine TWEAK plays a role in the disruption of the structure and permeability of the NVU during physiological and pathological conditions...
  20. ncbi request reprint Multiple members of the TNF superfamily contribute to IFN-gamma-mediated inhibition of erythropoiesis
    Nadia Felli
    Department of Hematology, Oncology and Molecular Medicine, Istituto Superiore di Sanita, Rome, Italy
    J Immunol 175:1464-72. 2005
    ....
  21. ncbi request reprint Murine FGF-inducible kinase is rapidly degraded via the nuclear ubiquitin-proteosome system when overexpressed in NIH 3T3 cells
    Gregory F Alberts
    Department of Vascular Biology, Jerome H Holland Laboratory for the Biomedical Sciences, American Red Cross, Rockville, Maryland 20855, USA
    Cell Cycle 3:678-84. 2004
    ..Furthermore, our studies indicate that the downregulation of endogenous Fnk activity in stressed cells may occur, at least in part, by Fnk nuclear translocation and proteosomal degradation...
  22. ncbi request reprint Fibroblast growth factor-inducible-14 is induced in axotomized neurons and promotes neurite outgrowth
    Katsuhisa Tanabe
    Department of Neurology, Yale University School of Medicine, New Haven, Connecticut 06510, USA
    J Neurosci 23:9675-86. 2003
    ..The neurite outgrowth-promoting effect of Fn14 is enhanced by Rac1 activation and suppressed by Rac1 inactivation. These findings suggest that Fn14 contributes to nerve regeneration via a Rac1 GTPase-dependent mechanism...
  23. pmc The human Fn14 receptor gene is up-regulated in migrating glioma cells in vitro and overexpressed in advanced glial tumors
    Nhan L Tran
    Neuro Oncology Research, Barrow Neurological Institute, Phoenix, Arizona, USA
    Am J Pathol 162:1313-21. 2003
    ..These results suggest a positive role for TWEAK and Fn14 in glioma progression and indicate that Fn14 gene expression may serve as a marker for invasive glioma cells...
  24. ncbi request reprint TWEAK is an endothelial cell growth and chemotactic factor that also potentiates FGF-2 and VEGF-A mitogenic activity
    Patrick J Donohue
    Department of Vascular Biology, Jerome H Holland Laboratory for the Biomedical Sciences, American Red Cross, 15601 Crabbs Branch Way, Rockville, MD 20855, USA
    Arterioscler Thromb Vasc Biol 23:594-600. 2003
    ..We also determined whether a soluble Fn14-Fc fusion protein could inhibit TWEAK biologic activity on ECs and investigated TWEAK signal transduction in ECs...
  25. pmc The Fn14 cytoplasmic tail binds tumour-necrosis-factor-receptor-associated factors 1, 2, 3 and 5 and mediates nuclear factor-kappaB activation
    Sharron A N Brown
    Vascular Biology Department, Jerome H Holland Laboratory for the Biomedical Sciences, American Red Cross, 15601 Crabbs Branch Way, Rockville, MD 20855, USA
    Biochem J 371:395-403. 2003
    ..These results indicate that Fn14 is a functional TWEAK receptor that can associate with four distinct TRAF family members and stimulate the NF-kappaB transcription factor signalling pathway...

Research Grants24

  1. The Fnk Kinase and Vascular Cell Growth Control
    JEFFREY WINKLES; Fiscal Year: 2004
    ..It is anticipated that these studies will provide important information on the biological functions of the Fnk protein and its potential role in vascular cell growth control in vivo. ..
  2. Role of TWEAK and Fn14 in Vascular Biology
    JEFFREY WINKLES; Fiscal Year: 2005
    ..It is anticipated that these studies will provide important information on the functions of the TWEAK and Fn14 proteins and their role in vascular cell biology. ..
  3. The Fn14 Receptor and Brain Tumor Invasion
    JEFFREY WINKLES; Fiscal Year: 2007
    ..The proposed studies will examine whether a protein named Fn14 contributes to tumor cell invasiveness and whether it could be a novel molecular target for anti-invasive therapy in humans. ..
  4. TWEAK-Fn14 Signaling in the Tumor Microenvironment
    Jeffrey A Winkles; Fiscal Year: 2010
    ....
  5. VASCULAR SMOOTH MUSCLE CELL PROLIFERATION
    JEFFREY WINKLES; Fiscal Year: 1993
    ..Results obtained from the research program described in this proposal may aid in the rational design of specific therapeutic approaches to the problem of SMC hyperplasia...
  6. FGF SIGNAL TRANSDUCTION IN VASCULAR CELLS
    JEFFREY WINKLES; Fiscal Year: 2000
    ..It is anticipated that these studies will provide novel information on the mechanism of growth factor signal transduction and may also identify a new therapeutic target for vascular cell antiproliferative therapy. ..
  7. The Fn14 Receptor and Brain Tumor Invasion
    Jeffrey A Winkles; Fiscal Year: 2011
    ..The proposed studies will examine whether a protein named Fn14 contributes to tumor cell invasiveness and whether it could be a novel molecular target for anti-invasive therapy in humans. ..