Affiliation: University of Maryland
- Role of TWEAK and Fn14 in tumor biologyJeffrey 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...
- The HER2- and Heregulin β1 (HRG)-Inducible TNFR Superfamily Member Fn14 Promotes HRG-Driven Breast Cancer Cell Migration, Invasion, and MMP9 ExpressionKaushal 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...
- 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...
- Differential regulation of polo-like kinase 1, 2, 3, and 4 gene expression in mammalian cells and tissuesJeffrey 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...
- The TWEAK-Fn14 cytokine-receptor axis: discovery, biology and therapeutic targetingJeffrey 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...
- A soluble Fn14-Fc decoy receptor reduces infarct volume in a murine model of cerebral ischemiaManuel 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...
- Full-length, membrane-anchored TWEAK can function as a juxtacrine signaling molecule and activate the NF-kappaB pathwaySharron 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...
- TWEAK binding to the Fn14 cysteine-rich domain depends on charged residues located in both the A1 and D2 modulesSharron 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...
- Soluble tumor necrosis factor-like weak inducer of apoptosis overexpression in HEK293 cells promotes tumor growth and angiogenesis in athymic nude miceDavid 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...
- TWEAK, via its receptor Fn14, is a novel regulator of mesenchymal progenitor cells and skeletal muscle regenerationMahasweta Girgenrath
Boston Biomedical Research Institute, Watertown, MA, USA
EMBO J 25:5826-39. 2006....
- 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 expressionNhan 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...
- TWEAK, a member of the TNF superfamily, is a multifunctional cytokine that binds the TweakR/Fn14 receptorSteven 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...
- Inhibition of TWEAK activity as a new treatment for inflammatory and degenerative diseasesManuel 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...
- The cytokine TWEAK modulates renal tubulointerstitial inflammationAna 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...
- Polo-like kinase 3 functions as a tumor suppressor and is a negative regulator of hypoxia-inducible factor-1 alpha under hypoxic conditionsYali Yang
Department of Environmental Medicine, New York University School of Medicine, Tuxedo, New York 10987, USA
Cancer Res 68:4077-85. 2008....
- The fibroblast growth factor-inducible 14 receptor is highly expressed in HER2-positive breast tumors and regulates breast cancer cell invasive capacityAmanda 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...
- Increased fibroblast growth factor-inducible 14 expression levels promote glioma cell invasion via Rac1 and nuclear factor-kappaB and correlate with poor patient outcomeNhan 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...
- TWEAK-Fn14 pathway inhibition protects the integrity of the neurovascular unit during cerebral ischemiaXiaohui 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...
- Tumor necrosis factor-like weak inducer of apoptosis increases the permeability of the neurovascular unit through nuclear factor-kappa B pathway activationRohini 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...
- Multiple members of the TNF superfamily contribute to IFN-gamma-mediated inhibition of erythropoiesisNadia Felli
Department of Hematology, Oncology and Molecular Medicine, Istituto Superiore di Sanita, Rome, Italy
J Immunol 175:1464-72. 2005....
- Murine FGF-inducible kinase is rapidly degraded via the nuclear ubiquitin-proteosome system when overexpressed in NIH 3T3 cellsGregory 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...
- Fibroblast growth factor-inducible-14 is induced in axotomized neurons and promotes neurite outgrowthKatsuhisa 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...
- The human Fn14 receptor gene is up-regulated in migrating glioma cells in vitro and overexpressed in advanced glial tumorsNhan 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...
- TWEAK is an endothelial cell growth and chemotactic factor that also potentiates FGF-2 and VEGF-A mitogenic activityPatrick 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...
- The Fn14 cytoplasmic tail binds tumour-necrosis-factor-receptor-associated factors 1, 2, 3 and 5 and mediates nuclear factor-kappaB activationSharron 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...
- The Fnk Kinase and Vascular Cell Growth ControlJEFFREY 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. ..
- Role of TWEAK and Fn14 in Vascular BiologyJEFFREY 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. ..
- The Fn14 Receptor and Brain Tumor InvasionJEFFREY 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. ..
- TWEAK-Fn14 Signaling in the Tumor MicroenvironmentJeffrey A Winkles; Fiscal Year: 2010....
- VASCULAR SMOOTH MUSCLE CELL PROLIFERATIONJEFFREY 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...
- FGF SIGNAL TRANSDUCTION IN VASCULAR CELLSJEFFREY 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. ..
- The Fn14 Receptor and Brain Tumor InvasionJeffrey 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. ..