R khosravi-far

Summary

Affiliation: Harvard Medical School
Location: Boston, USA
URL: http://www.hms.harvard.edu/dms/bbs/fac/Khosravi-Far.html

Publications

  1. ncbi request reprint Harnessing the tumor suppressor function of FOXO as an alternative therapeutic approach in cancer
    Amrik Singh
    Department of Pathology, Harvard Medical School and Beth Israel Deaconess Medical Center, Boston, MA 02115, USA
    Curr Drug Targets 12:1311-21. 2011
  2. pmc FoxO tumor suppressors and BCR-ABL-induced leukemia: a matter of evasion of apoptosis
    Zainab Jagani
    Department of Pathology, Harvard Medical School and Beth Israel Deaconess Medical Center, Boston, MA 02115, USA
    Biochim Biophys Acta 1785:63-84. 2008
  3. pmc c-Fos as a proapoptotic agent in TRAIL-induced apoptosis in prostate cancer cells
    Xiaoping Zhang
    Department of Urology, Massachusetts General Hospital, Boston, MA 02114, USA
    Cancer Res 67:9425-34. 2007
  4. pmc CDIP, a novel pro-apoptotic gene, regulates TNFalpha-mediated apoptosis in a p53-dependent manner
    Lauren Brown
    Cutaneous Biology Research Center, Massachusetts General Hospital and Harvard Medical School, Charlestown, MA 02129, USA
    EMBO J 26:3410-22. 2007
  5. pmc Death receptor ligation triggers membrane scrambling between Golgi and mitochondria
    S Ouasti
    Faculty of Life Sciences, The University of Manchester, Stopford Building, Oxford Road, Manchester, UK
    Cell Death Differ 14:453-61. 2007
  6. pmc Transduction of tumor necrosis factor-related apoptosis-inducing ligand into hematopoietic cells leads to inhibition of syngeneic tumor growth in vivo
    Keli Song
    Department of Pathology, Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, Massachusetts 02215, USA
    Cancer Res 66:6304-11. 2006
  7. ncbi request reprint Activation of extracellular signal-regulated protein kinase 5 downregulates FasL upon osmotic stress
    X Wang
    Faculty of Life Sciences, University of Manchester, Manchester, UK
    Cell Death Differ 13:2099-108. 2006
  8. ncbi request reprint Quest for molecular markers in adult soft tissue tumors
    Keli Song
    Department of Pathology, Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, Massachusetts 02215, USA
    Cancer Biol Ther 5:234-5. 2006
  9. ncbi request reprint Regulation of tumor angiogenesis by thrombospondin-1
    Bin Ren
    Department of Pathology, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA 02215, USA
    Biochim Biophys Acta 1765:178-88. 2006
  10. pmc Tumor necrosis factor-related apoptosis-inducing ligand alters mitochondrial membrane lipids
    Ferry Sandra
    Department of Pathology, Harvard Medical School, Beth Israel Deaconess Medical Center, Boston, Massachusetts 02215, USA
    Cancer Res 65:8286-97. 2005

Research Grants

  1. Tumor Selective Apoptosis by TRAIL
    Roya Khosravi Far; Fiscal Year: 2009
  2. Novel Strategies for Treatment of Myeloproliferative Disorders
    Roya Khosravi Far; Fiscal Year: 2010
  3. Tumor Selective Apoptosis by TRAIL
    Roya Khosravi Far; Fiscal Year: 2010
  4. Tumor Selective Apoptosis by TRAIL
    Roya Khosravi Far; Fiscal Year: 2005
  5. Tumor Selective Apoptosis by TRAIL
    Roya Khosravi Far; Fiscal Year: 2009
  6. Novel Strategies for Treatment of Myeloproliferative Disorders
    Roya Khosravi Far; Fiscal Year: 2009
  7. Tumor Selective Apoptosis by TRAIL
    Roya Khosravi Far; Fiscal Year: 2009
  8. Tumor Selective Apoptosis by TRAIL
    Roya Khosravi Far; Fiscal Year: 2007
  9. Tumor Selective Apoptosis by TRAIL
    Roya Khosravi Far; Fiscal Year: 2006

Collaborators

Detail Information

Publications64

  1. ncbi request reprint Harnessing the tumor suppressor function of FOXO as an alternative therapeutic approach in cancer
    Amrik Singh
    Department of Pathology, Harvard Medical School and Beth Israel Deaconess Medical Center, Boston, MA 02115, USA
    Curr Drug Targets 12:1311-21. 2011
    ..This review will discuss our current understanding of mechanisms for FOXO regulation and the potential implications for therapeutically restoring FOXO transcriptional activity...
  2. pmc FoxO tumor suppressors and BCR-ABL-induced leukemia: a matter of evasion of apoptosis
    Zainab Jagani
    Department of Pathology, Harvard Medical School and Beth Israel Deaconess Medical Center, Boston, MA 02115, USA
    Biochim Biophys Acta 1785:63-84. 2008
    ....
  3. pmc c-Fos as a proapoptotic agent in TRAIL-induced apoptosis in prostate cancer cells
    Xiaoping Zhang
    Department of Urology, Massachusetts General Hospital, Boston, MA 02114, USA
    Cancer Res 67:9425-34. 2007
    ..Strategies to activate c-Fos or inhibit c-FLIP(L) may potentiate TRAIL-based proapoptotic therapies...
  4. pmc CDIP, a novel pro-apoptotic gene, regulates TNFalpha-mediated apoptosis in a p53-dependent manner
    Lauren Brown
    Cutaneous Biology Research Center, Massachusetts General Hospital and Harvard Medical School, Charlestown, MA 02129, USA
    EMBO J 26:3410-22. 2007
    ....
  5. pmc Death receptor ligation triggers membrane scrambling between Golgi and mitochondria
    S Ouasti
    Faculty of Life Sciences, The University of Manchester, Stopford Building, Oxford Road, Manchester, UK
    Cell Death Differ 14:453-61. 2007
    ..Thus, our work unveils that Fas ligand-mediated apoptosis induces scrambling of mitochondrial and secretory organelles via a global alteration of membrane traffic that is modulated by apical caspases...
  6. pmc Transduction of tumor necrosis factor-related apoptosis-inducing ligand into hematopoietic cells leads to inhibition of syngeneic tumor growth in vivo
    Keli Song
    Department of Pathology, Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, Massachusetts 02215, USA
    Cancer Res 66:6304-11. 2006
    ..This approach may be used further to identify important molecules that regulate the sensitivity of tumor cells to TRAIL-induced cell death in vivo...
  7. ncbi request reprint Activation of extracellular signal-regulated protein kinase 5 downregulates FasL upon osmotic stress
    X Wang
    Faculty of Life Sciences, University of Manchester, Manchester, UK
    Cell Death Differ 13:2099-108. 2006
    ..Based on these results, we conclude that the ERK5 signaling pathway promotes cell survival by downregulating FasL expression via a mechanism that implicates PKB-dependent inhibition of Foxo3a downstream of phosphoinositide 3 kinase...
  8. ncbi request reprint Quest for molecular markers in adult soft tissue tumors
    Keli Song
    Department of Pathology, Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, Massachusetts 02215, USA
    Cancer Biol Ther 5:234-5. 2006
  9. ncbi request reprint Regulation of tumor angiogenesis by thrombospondin-1
    Bin Ren
    Department of Pathology, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA 02215, USA
    Biochim Biophys Acta 1765:178-88. 2006
    ..An understanding of the molecular basis of TSP-1-mediated inhibition of angiogenesis and tumor progression will aid in the development of novel therapeutics for the treatment of cancer...
  10. pmc Tumor necrosis factor-related apoptosis-inducing ligand alters mitochondrial membrane lipids
    Ferry Sandra
    Department of Pathology, Harvard Medical School, Beth Israel Deaconess Medical Center, Boston, Massachusetts 02215, USA
    Cancer Res 65:8286-97. 2005
    ..We also show that preservation of phosphatidylcholine homeostasis by inhibition of lipid-degrading enzymes almost completely impedes the activation of pro-caspase-9 while scarcely changing the activation of caspase-8...
  11. ncbi request reprint Diversity of the protein disulfide isomerase family: identification of breast tumor induced Hag2 and Hag3 as novel members of the protein family
    Staffan Persson
    Department of Plant Biochemistry, Lund University, SE 22100 Lund, Sweden
    Mol Phylogenet Evol 36:734-40. 2005
  12. pmc Death receptor signals to mitochondria
    Roya Khosravi-Far
    Department of Pathology, Harvard Medical School, Beth Israel Deaconess Medical Center, 99 Brookline Ave, Boston, Massachusetts 02215, USA
    Cancer Biol Ther 3:1051-7. 2004
    ..Here, we review our current knowledge about the layers of complexity that are posed by the interactions between death receptor-induced pathways and how they influence mitochondria to regulate cellular life and death decisions...
  13. pmc Pro-apoptotic Bid induces membrane perturbation by inserting selected lysolipids into the bilayer
    Alexander Goonesinghe
    School of Biological Sciences, The University of Manchester, Stopford Building, Oxford Road, Manchester M13 9PT, UK
    Biochem J 387:109-18. 2005
    ..A Bid mutant that is not pro-apoptotic in vivo is defective in lysophosphatidylcholine-mediated membrane perturbation in vitro. Our results thus provide a biochemical explanation for the pro-apoptotic action of f.l. Bid...
  14. pmc Fas-associated protein with death domain (FADD)-independent recruitment of c-FLIPL to death receptor 5
    Tai Guang Jin
    Department of Pathology, Beth Israel Deaconess Medical Center and Harvard Medical School, 99 Brookline Avenue, Boston, MA 02215, USA
    J Biol Chem 279:55594-601. 2004
    ....
  15. pmc Neuropilin-1 modulates p53/caspases axis to promote endothelial cell survival
    Ling Wang
    Department of Biochemistry and Molecular Biology, Mayo Clinic College of Medicine, Rochester, Minnesota, United States of America
    PLoS ONE 2:e1161. 2007
    ....
  16. doi request reprint The mitochondrial death pathway
    Anas Chalah
    Department of Pathology, Harvard Medical School, Beth Israel Deaconess Medical Center, 99 Brookline Avenue, Boston, MA 02215, USA
    Adv Exp Med Biol 615:25-45. 2008
    ..This chapter focuses mainly on the role the mitochondria in mammalian cell death and cancer progression and therapy...
  17. doi request reprint Apoptotic pathways in tumor progression and therapy
    Armelle Melet
    Department of Pathology, Harvard Medical School, Beth Israel Deaconess Medical Center, 99 Brookline Avenue, Boston, MA 02215, USA
    Adv Exp Med Biol 615:47-79. 2008
    ..Here, we review our current knowledge of apoptosis regulation in cancer progression and therapy, as well as the new molecular targeted molecules that are being developed to reinstate cancer cell death...
  18. pmc Priming of the vascular endothelial growth factor signaling pathway by thrombospondin-1, CD36, and spleen tyrosine kinase
    Shideh Kazerounian
    Division of Experimental Pathology, Department of Pathology, Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, MA, USA
    Blood 117:4658-66. 2011
    ..Together, these studies introduce a new signaling pathway for TSP-1, CD36, and Syk, and address the role of these proteins in regulating the angiogenic switch...
  19. pmc Apoptotic cell signaling in cancer progression and therapy
    Jessica Plati
    Department of Pathology, Harvard Medical School, Beth Israel Deaconess Medical Center, 330 Brookline Ave, Boston, MA 02215, USA
    Integr Biol (Camb) 3:279-96. 2011
    ..In addition, therapeutic strategies aimed at modulating the activity of BCL-2 family proteins, IAPs, and c-FLIP for the targeted induction of apoptosis are briefly discussed...
  20. pmc Bortezomib treatment causes remission in a Ph+ALL patient and reveals FoxO as a theranostic marker
    Rajan Dewar
    Department of Pathology, Harvard Medical School and Beth Israel Deaconess Medical Center, Boston MA, USA
    Cancer Biol Ther 11:552-8. 2011
    ..Additionally, proteasomal inhibition by bortezomib may be a promising therapeutic option in Philadelphia-positive ALL, where FoxO3 is downregulated...
  21. pmc Discovery of a small-molecule type II inhibitor of wild-type and gatekeeper mutants of BCR-ABL, PDGFRalpha, Kit, and Src kinases: novel type II inhibitor of gatekeeper mutants
    Ellen Weisberg
    Department of Medical Oncology Hematologic Neoplasia, Dana Farber Cancer Institute, Boston, MA
    Blood 115:4206-16. 2010
    ..The distinctive ability of HG-7-85-01 to simultaneously inhibit both wild-type and mutant forms of several kinases of clinical relevance is an important step in the development of the next generation of tyrosine kinase inhibitors...
  22. pmc Protein phosphatase 2A reactivates FOXO3a through a dynamic interplay with 14-3-3 and AKT
    Amrik Singh
    Department of Pathology, Beth Israel Deaconess Medical Center, and Harvard Medical School, Boston, MA 02215, USA
    Mol Biol Cell 21:1140-52. 2010
    ....
  23. pmc Proteasome inhibition causes regression of leukemia and abrogates BCR-ABL-induced evasion of apoptosis in part through regulation of forkhead tumor suppressors
    Zainab Jagani
    Department of Pathology, Harvard Medical School and Beth Israel Deaconess Medical Center, Boston, Massachusetts 02215, USA
    Cancer Res 69:6546-55. 2009
    ..Our data delineate the involvement of FoxO proteins in BCR-ABL-induced evasion of apoptosis and provide evidence that bortezomib is a candidate therapeutic in the treatment of BCR-ABL-induced leukemia...
  24. pmc A double hit to kill tumor and endothelial cells by TRAIL and antiangiogenic 3TSR
    Bin Ren
    Department of Pathology, Division of Cancer Biology and Angiogenesis, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, Massachusetts, USA
    Cancer Res 69:3856-65. 2009
    ....
  25. pmc Fas death receptor enhances endocytic membrane traffic converging into the Golgi region
    Mauro Degli Esposti
    Faculty of Life Sciences, The University of Manchester, M139PT Manchester, United Kingdom
    Mol Biol Cell 20:600-15. 2009
    ..Hence, T lymphocytes show a diversion in the traffic of endocytic membranes after Fas stimulation that seems to resemble the polarization of membrane traffic after their activation...
  26. ncbi request reprint Analysis of TNF-related apoptosis-inducing ligand in vivo through bone marrow transduction and transplantation
    Keli Song
    Department of Pathology, Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, Massachusetts, USA
    Methods Enzymol 446:315-31. 2008
    ....
  27. doi request reprint Methods in enzymolology book on cell death
    Roya Khosravi-Far
    Methods Enzymol 446:xxi-xxii. 2008
  28. pmc Tumor necrosis factor (TNF)-related apoptosis-inducing ligand (TRAIL) induced mitochondrial pathway to apoptosis and caspase activation is potentiated by phospholipid scramblase-3
    Kenneth Ndebele
    Department of Pathology, Harvard Medical School, Beth Israel Deaconess Medical Center, 99 Brookline Ave, Boston, MA 02215, USA
    Apoptosis 13:845-56. 2008
    ..Moreover, we show that knock-down of endogenous PLS3 suppresses TRAIL-induced changes in cardiolipin. Finally, we demonstrate that TRAIL-induced activation of PKC-delta mediates regulation of the PLS3-induced changes in cardiolipin...
  29. pmc Dysregulation of apoptotic signaling in cancer: molecular mechanisms and therapeutic opportunities
    Jessica Plati
    Department of Pathology, Harvard Medical School, Beth Israel Deaconess Medical Center, Boston, Massachusetts 02215, USA
    J Cell Biochem 104:1124-49. 2008
    ..We will also discuss several therapeutic strategies that aim to reestablish the apoptotic response, and thereby eradicate cancer cells, including those that demonstrate resistance to traditional therapies...
  30. pmc Endosomal compartment contributes to the propagation of CD95/Fas-mediated signals in type II cells
    Paola Matarrese
    Department of Drug Research and Evaluation, Section of Cell Aging and Degeneration, Istituto Superiore di Sanita, Viale Regina Elena 299, 00161 Rome, Italy
    Biochem J 413:467-78. 2008
    ..Altogether, these findings suggest a key role of endocytosis in the propagation and amplification of the CD95/Fas-activated signalling leading to type II cell demise...
  31. ncbi request reprint Persistent c-FLIP(L) expression is necessary and sufficient to maintain resistance to tumor necrosis factor-related apoptosis-inducing ligand-mediated apoptosis in prostate cancer
    Xiaoping Zhang
    Division of Urologic Surgery and Department of Pathology, Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, Massachusetts 02215, USA
    Cancer Res 64:7086-91. 2004
    ..Therefore, persistent expression of c-FLIP(L) is necessary and sufficient to regulate sensitivity to TRAIL-mediated apoptosis in prostate cancer cells...
  32. pmc Severe hepatic injury in interleukin 18 (IL-18) transgenic mice: a key role for IL-18 in regulating hepatocyte apoptosis in vivo
    S Finotto
    Laboratory of Immunology, I Medical Clinic, University of Mainz, Germany
    Gut 53:392-400. 2004
    ..Interleukin 18 (IL-18) is a cytokine with pleiotropic activity that augments T helper 1 responses and cytotoxic activity of natural killer cells...
  33. ncbi request reprint Ras interaction with two distinct binding domains in Raf-1 may be required for Ras transformation
    J K Drugan
    Department of Biochemistry and Biophysics, University of North Carolina, Chapel Hill 27599, USA
    J Biol Chem 271:233-7. 1996
    ..Finally, since Ha-Ras T35A and E37G mutations prevent Ras interaction with full-length Raf-1, we suggest that Raf-Cys is a cryptic binding site that is unmasked upon Ras interaction with Raf-1-(55-131)...
  34. ncbi request reprint Prenylation analysis of bacterially expressed and insect cell-expressed Ras and Ras-related proteins
    R Khosravi-Far
    Department of Pharmacology, School of Medicine, University of North Carolina at Chapel Hill 27599, USA
    Methods Enzymol 255:46-60. 1995
  35. ncbi request reprint Transcripts of a maize chlorotic mottle virus cDNA clone replicate in maize protoplasts and infect maize plants
    K Scheets
    Department of Plant Pathology, Oklahoma State University, Stillwater 74078
    Virology 193:1006-9. 1993
    ..The transcripts one nucleotide longer or shorter than uncapped pMCM41 transcripts were not able to infect maize plants...
  36. ncbi request reprint The Ras signal transduction pathway
    R Khosravi-Far
    Department of Pharmacology, School of Medicine, Lineberger Comprehensive Cancer Center, University of North Carolina at Chapel Hill 27599 7365
    Cancer Metastasis Rev 13:67-89. 1994
    ..The brisk pace at which the key components of Ras-mediated signal transduction pathways are being identified hold great promise that new targets for therapeutic intervention in cancer may now be identified...
  37. pmc Dbl and Vav mediate transformation via mitogen-activated protein kinase pathways that are distinct from those activated by oncogenic Ras
    R Khosravi-Far
    Department of Cellular Biology, University of North Carolina at Chapel Hill 27599
    Mol Cell Biol 14:6848-57. 1994
    ..Taken together, our observations indicate that Vav and Dbl transformation is not a consequence of Ras activation and instead may involve the constitutive activation of MAPKs...
  38. ncbi request reprint Guanine nucleotide exchange factors: activators of the Ras superfamily of proteins
    L A Quilliam
    School of Medicine, University of North Carolina at Chapel Hill, Department of Pharmacology, USA
    Bioessays 17:395-404. 1995
    ..Additionally, we describe mechanisms of GEF activation of Ras in signal transduction and address the potential that deregulated GEFs might contribute to malignant transformation through chronic Ras protein activation...
  39. pmc Activation of Rac1, RhoA, and mitogen-activated protein kinases is required for Ras transformation
    R Khosravi-Far
    Curriculum in Genetics and Molecular Biology, University of North Carolina at Chapel Hill, Chapel Hill 27599, USA
    Mol Cell Biol 15:6443-53. 1995
    ....
  40. pmc Rab1b regulates vesicular transport between the endoplasmic reticulum and successive Golgi compartments
    H Plutner
    Department of Molecular and Cellular Biology, Scripps Research Institute, La Jolla, California 92037
    J Cell Biol 115:31-43. 1991
    ..We suggest that rab1b may provide a common link between upstream and downstream components of the vesicular fission and fusion machinery functioning in early compartments of the secretory pathway...
  41. pmc Isoprenoid modification of rab proteins terminating in CC or CXC motifs
    R Khosravi-Far
    La Jolla Cancer Research Foundation, CA 92037
    Proc Natl Acad Sci U S A 88:6264-8. 1991
    ..Therefore, rab proteins may be modified by a prenyltransferase(s) distinct from the prenyltransferases that modify carboxyl-terminal CAAX proteins...
  42. ncbi request reprint Alternate mechanisms of ras activation are complementary and favor and formation of ras-GTP
    G Patel
    La Jolla Cancer Research Foundation, California 92037
    Oncogene 7:283-8. 1992
    ....
  43. pmc GTP-binding mutants of rab1 and rab2 are potent inhibitors of vesicular transport from the endoplasmic reticulum to the Golgi complex
    E J Tisdale
    Department of Cell Biology, Scripps Research Institute, La Jolla, California 92037
    J Cell Biol 119:749-61. 1992
    ..We suggest that at least three members of the rab family (rab1a, rab1b, and rab2) use GTP hydrolysis to regulate components of the transport machinery involved in vesicle traffic between early compartments of the secretory pathway...
  44. ncbi request reprint Protein prenylation: key to ras function and cancer intervention?
    R Khosravi-Far
    La Jolla Cancer Research Foundation, La Jolla, California 92037
    Cell Growth Differ 3:461-9. 1992
  45. ncbi request reprint Ras (CXXX) and Rab (CC/CXC) prenylation signal sequences are unique and functionally distinct
    R Khosravi Far
    Department of Pharmacology, Lineberger Cancer Center, University of North Carolina, Chapel Hill 27599
    J Biol Chem 267:24363-8. 1992
    ..Finally, competition studies demonstrate that a common geranylgeranyl transferase activity is responsible for the modification of Rab proteins terminating in CC or CXC motifs...
  46. ncbi request reprint Guanine nucleotide exchange factors: activators of Ras superfamily proteins
    A F Overbeck
    Department of Pharmacology, University of North Carolina at Chapel Hill, USA
    Mol Reprod Dev 42:468-76. 1995
    ..Our results suggest that Dbl oncogenes cause transformation via a Ras-independent activation of MAP kinases and Rho family proteins...
  47. ncbi request reprint The mitogen-activated protein kinase phosphatases PAC1, MKP-1, and MKP-2 have unique substrate specificities and reduced activity in vivo toward the ERK2 sevenmaker mutation
    Y Chu
    Labortory of Pathology, NCI, National Institutes of Health, Bethesda, Maryland 20892, USA
    J Biol Chem 271:6497-501. 1996
    ..A hyperactive allele of ERK2 (D319N), analogous to the Drosophila sevenmaker gain-of-function mutation, has significantly reduced sensitivity to all three MAP kinase phosphatases in vivo...
  48. pmc Development of human protein reference database as an initial platform for approaching systems biology in humans
    Suraj Peri
    McKusick Nathans Institute of Genetic Medicine, Johns Hopkins University, Baltimore, Maryland 21287, USA
    Genome Res 13:2363-71. 2003
    ..hprd.org to the academic community. This unified bioinformatics platform will be useful in cataloging and mining the large number of proteomic interactions and alterations that will be discovered in the postgenomic era...
  49. pmc Cytokines and BCR-ABL mediate suppression of TRAIL-induced apoptosis through inhibition of forkhead FOXO3a transcription factor
    Saghi Ghaffari
    Whitehead Institute for Biomedical Research, Cambridge, MA 02142, USA
    Proc Natl Acad Sci U S A 100:6523-8. 2003
    ..BCR-ABL-induced inhibition of TRAIL transcription in hematopoietic cells may provide a novel mechanism for tumorigenicity in chronic myeloid leukemia...
  50. ncbi request reprint Cloning and characterization of PAK5, a novel member of mammalian p21-activated kinase-II subfamily that is predominantly expressed in brain
    Akhilesh Pandey
    Center for Experimental Bioinformatics, University of Southern Denmark, Campusvej 55, DK 5230 Odense M, Denmark
    Oncogene 21:3939-48. 2002
    ..The expression pattern of PAK5 is distinct from that of PAK4 and PAK6, suggesting a functional division among PAK-II subfamily kinases based on differential tissue distribution...
  51. ncbi request reprint The complexity of TNF-related apoptosis-inducing ligand
    K Abe
    Department of Pathology, Beth Israel Deaconess Medical Center and Harvard Medical School, 99 Brookline Ave, RN 270F, Boston, MA 02215, USA
    Ann N Y Acad Sci 926:52-63. 2000
    ..This review will focus on the complexity of TRAIL and the role of c-FLIP in mediating TRAIL function...
  52. ncbi request reprint Role of protein kinase Czeta in Ras-mediated transcriptional activation of vascular permeability factor/vascular endothelial growth factor expression
    S Pal
    Department of Pathology, Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, Massachusetts 02215, USA
    J Biol Chem 276:2395-403. 2001
    ..Taken together, these data elucidate the signaling mechanism of Ras-mediated VPF/VEGF transcriptional activation through PKCzeta and also provide insight into PKCzeta and Sp1-dependent transcriptional regulation of VPF/VEGF...
  53. ncbi request reprint Differential contribution of the ERK and JNK mitogen-activated protein kinase cascades to Ras transformation of HT1080 fibrosarcoma and DLD-1 colon carcinoma cells
    R Plattner
    Department of Microbiology and Molecular Genetics, University of California, Irvine 92697 4025, USA
    Oncogene 18:1807-17. 1999
    ..These results emphasize that cell type differences exist in the signaling pathways by which oncogenic Ras causes transformation...
  54. ncbi request reprint Rho family proteins and Ras transformation: the RHOad less traveled gets congested
    I M Zohn
    Department of Pharmacology, MIT, Cambridge, Massachusetts 02139, USA
    Oncogene 17:1415-38. 1998
    ..These efforts may reveal novel targets for the development of anti-Ras and anti-cancer drugs...
  55. ncbi request reprint Increasing complexity of Ras signaling
    S L Campbell
    Department of Biochemistry and Biophysics, MIT, Cambridge, Massachusetts 02139, USA
    Oncogene 17:1395-413. 1998
    ....
  56. ncbi request reprint Increasing complexity of Ras signal transduction: involvement of Rho family proteins
    R Khosravi-Far
    Department of Biology, Massachusetts Institute of Technology, Cambridge 02139, USA
    Adv Cancer Res 72:57-107. 1998
  57. pmc Daxx, a novel Fas-binding protein that activates JNK and apoptosis
    X Yang
    Department of Biology, Massachusetts Institute of Technology, Cambridge 02139, USA
    Cell 89:1067-76. 1997
    ..The Daxx apoptotic pathway is sensitive to both Bcl-2 and dominant-negative JNK pathway components and acts cooperatively with the FADD pathway. Thus, Daxx and FADD define two distinct apoptotic pathways downstream of Fas...
  58. pmc Lck regulates Vav activation of members of the Rho family of GTPases
    J Han
    Department of Biochemistry and Molecular Biology, Norris Comprehensive Cancer Center, School of Medicine, University of Southern California, Los Angeles 90033, USA
    Mol Cell Biol 17:1346-53. 1997
    ..Further, we present data indicating that the Lck kinase activates the guanine nucleotide exchange factor and transforming activity of Vav...
  59. pmc Transformation by Rho exchange factor oncogenes is mediated by activation of an integrin-dependent pathway
    M A Schwartz
    Department of Vascular Biology, The Scripps Research Institute, La Jolla, CA 92037, USA
    EMBO J 15:6525-30. 1996
    ..These results show, therefore, that anchorage-independent growth results from constitutive activation of integrin-dependent signaling events. They also support the view that Rho is a functionally important mediator of integrin signaling...
  60. ncbi request reprint Expression cloning of lsc, a novel oncogene with structural similarities to the Dbl family of guanine nucleotide exchange factors
    I P Whitehead
    Department of Medical Genetics, University of British Columbia, Vancouver, British Columbia V6T 1Z1, Canada
    J Biol Chem 271:18643-50. 1996
    ..Lsc is a member of a growing family of proteins that may function as activators of Rho family GTPases in a developmental or tissue-specific manner...
  61. pmc Oncogenic Ras activation of Raf/mitogen-activated protein kinase-independent pathways is sufficient to cause tumorigenic transformation
    R Khosravi-Far
    Department of Pharmacology, University of North Carolina at Chapel Hill, 27599 7365, USA
    Mol Cell Biol 16:3923-33. 1996
    ..Finally, cotransfection of H-Ras(12V, 37G) and H-Ras(12V, 40C) resulted in synergistic cooperation of their focus-forming activities, indicating that Ras activates at least two Raf-independent, Ras effector-mediated signaling events...
  62. pmc Combination of bortezomib and mitotic inhibitors down-modulate Bcr-Abl and efficiently eliminates tyrosine-kinase inhibitor sensitive and resistant Bcr-Abl-positive leukemic cells
    Octavian Bucur
    Department of Pathology, Harvard Medical School and Beth Israel Deaconess Medical Center, Boston, Massachusetts, United States of America Institute of Biochemistry of the Romanian Academy, Bucharest, Romania
    PLoS ONE 8:e77390. 2013
    ..These results open novel possibilities for the treatment of Bcr-Abl-positive leukemias, especially in the imatinib, dasatinib and nilotinib-resistant CML cases. ..
  63. pmc killerFLIP: a novel lytic peptide specifically inducing cancer cell death
    B Pennarun
    Department of Pathology, Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, MA, USA
    Cell Death Dis 4:e894. 2013
    ..Thus, we report the discovery of a promising synthetic peptide with novel anticancer activity in vitro and in vivo. ..

Research Grants11

  1. Tumor Selective Apoptosis by TRAIL
    Roya Khosravi Far; Fiscal Year: 2009
    ..These studies will be performed in vitro using Bcr-Abl transformed cells and in an in vivo model for Bcr-Abl-induced leukemia. ..
  2. Novel Strategies for Treatment of Myeloproliferative Disorders
    Roya Khosravi Far; Fiscal Year: 2010
    ....
  3. Tumor Selective Apoptosis by TRAIL
    Roya Khosravi Far; Fiscal Year: 2010
    ..These agents could provide significant enhancements in the current therapeutic strategies in hematological malignancies and other tumors that show resistance to apoptosis-inducing therapeutics. ..
  4. Tumor Selective Apoptosis by TRAIL
    Roya Khosravi Far; Fiscal Year: 2005
    ..These studies will be performed in vitro using Bcr-Abl transformed cells and in an in vivo model for Bcr-Abl-induced leukemia. ..
  5. Tumor Selective Apoptosis by TRAIL
    Roya Khosravi Far; Fiscal Year: 2009
    ..These agents could provide significant enhancements in the current therapeutic strategies in hematological malignancies and other tumors that show resistance to apoptosis-inducing therapeutics. ..
  6. Novel Strategies for Treatment of Myeloproliferative Disorders
    Roya Khosravi Far; Fiscal Year: 2009
    ....
  7. Tumor Selective Apoptosis by TRAIL
    Roya Khosravi Far; Fiscal Year: 2009
    ..These studies will be performed in vitro using Bcr-Abl transformed cells and in an in vivo model for Bcr-Abl-induced leukemia. ..
  8. Tumor Selective Apoptosis by TRAIL
    Roya Khosravi Far; Fiscal Year: 2007
    ..These studies will be performed in vitro using Bcr-Abl transformed cells and in an in vivo model for Bcr-Abl-induced leukemia. ..
  9. Tumor Selective Apoptosis by TRAIL
    Roya Khosravi Far; Fiscal Year: 2006
    ..These studies will be performed in vitro using Bcr-Abl transformed cells and in an in vivo model for Bcr-Abl-induced leukemia. ..