Robert Abraham

Summary

Affiliation: The Burnham Institute
Country: USA

Publications

  1. ncbi request reprint PI 3-kinase related kinases: 'big' players in stress-induced signaling pathways
    Robert T Abraham
    Program in Signal Transduction Research, The Burnham Institute, 10901 North Torrey Pines Road, La Jolla, CA 92130, USA
    DNA Repair (Amst) 3:883-7. 2004
  2. ncbi request reprint Cell biology. Guiding ATM to broken DNA
    Robert T Abraham
    Signal Transduction Program, The Burnham Institute, La Jolla, CA 92037, USA
    Science 308:510-1. 2005
  3. ncbi request reprint Checkpoint signaling: epigenetic events sound the DNA strand-breaks alarm to the ATM protein kinase
    Robert T Abraham
    Program in Signal Transduction Research, The Burnham Institute, 10901 North Torrey Pines Road, La Jolla, CA 92130, USA
    Bioessays 25:627-30. 2003
  4. ncbi request reprint Jurkat T cells and development of the T-cell receptor signalling paradigm
    Robert T Abraham
    Program in Signal Transduction Research at The Burnham Institute, 10901 North Torrey Pines Road, La Jolla, California 92037, USA
    Nat Rev Immunol 4:301-8. 2004
  5. ncbi request reprint Identification of TOR signaling complexes: more TORC for the cell growth engine
    Robert T Abraham
    Program in Signal Transduction Research, Cancer Research Center, The Burnham Institute, 10901 North Torrey Pines Road, La Jolla, CA 92037, USA
    Cell 111:9-12. 2002
  6. ncbi request reprint TOR signaling: an odyssey from cellular stress to the cell growth machinery
    Robert T Abraham
    Signal Transduction Program, The Burnham Institute, 10901 North Torrey Pines Road, La Jolla, California 92037, USA
    Curr Biol 15:R139-41. 2005
  7. ncbi request reprint The ATM-related kinase, hSMG-1, bridges genome and RNA surveillance pathways
    Robert T Abraham
    Program in Signal Transduction Research, The Burnham Institute, 10901 North Torrey Pines Road, La Jolla, CA 92130, USA
    DNA Repair (Amst) 3:919-25. 2004
  8. ncbi request reprint mTOR as a positive regulator of tumor cell responses to hypoxia
    R T Abraham
    Program in Signal Transduction Research, The Burnham Institute, 10901 North Torrey Pines Road, La Jolla, CA 92037, USA
    Curr Top Microbiol Immunol 279:299-319. 2004
  9. pmc Hypoxia-induced assembly of prolyl hydroxylase PHD3 into complexes: implications for its activity and susceptibility for degradation by the E3 ligase Siah2
    Koh Nakayama
    Signal Transduction Program, Burnham Institute for Medical Research, La Jolla, CA 92037, USA
    Biochem J 401:217-26. 2007
  10. ncbi request reprint Part-time cop nabs deviant DNA
    Robert T Abraham
    Nat Med 11:257-8. 2005

Research Grants

  1. Roles of ATM and ATR Kinases in DNA Damage Responses
    Robert Abraham; Fiscal Year: 2004
  2. SIGNAL TRANSDUCTION FROM THE T CELL ANTIGEN RECEPTOR
    Robert Abraham; Fiscal Year: 2003
  3. CELLULAR PHARMACOLOGY OF RAPAMYCIN
    Robert Abraham; Fiscal Year: 2001
  4. CELLULAR PHARMACOLOGY OF RAPAMYCIN
    Robert Abraham; Fiscal Year: 2004

Collaborators

Detail Information

Publications57

  1. ncbi request reprint PI 3-kinase related kinases: 'big' players in stress-induced signaling pathways
    Robert T Abraham
    Program in Signal Transduction Research, The Burnham Institute, 10901 North Torrey Pines Road, La Jolla, CA 92130, USA
    DNA Repair (Amst) 3:883-7. 2004
    ..This overview provides some general insights into the pharmacology, biochemistry, and function of this nonconventional group of protein kinases...
  2. ncbi request reprint Cell biology. Guiding ATM to broken DNA
    Robert T Abraham
    Signal Transduction Program, The Burnham Institute, La Jolla, CA 92037, USA
    Science 308:510-1. 2005
  3. ncbi request reprint Checkpoint signaling: epigenetic events sound the DNA strand-breaks alarm to the ATM protein kinase
    Robert T Abraham
    Program in Signal Transduction Research, The Burnham Institute, 10901 North Torrey Pines Road, La Jolla, CA 92130, USA
    Bioessays 25:627-30. 2003
    ..The new findings underscore the critical importance of epigenetic events in genome function and surveillance in mammalian cells...
  4. ncbi request reprint Jurkat T cells and development of the T-cell receptor signalling paradigm
    Robert T Abraham
    Program in Signal Transduction Research at The Burnham Institute, 10901 North Torrey Pines Road, La Jolla, California 92037, USA
    Nat Rev Immunol 4:301-8. 2004
  5. ncbi request reprint Identification of TOR signaling complexes: more TORC for the cell growth engine
    Robert T Abraham
    Program in Signal Transduction Research, Cancer Research Center, The Burnham Institute, 10901 North Torrey Pines Road, La Jolla, CA 92037, USA
    Cell 111:9-12. 2002
    ..The recent identification of novel TOR-interacting proteins has provided crucial insights into TOR regulation and function...
  6. ncbi request reprint TOR signaling: an odyssey from cellular stress to the cell growth machinery
    Robert T Abraham
    Signal Transduction Program, The Burnham Institute, 10901 North Torrey Pines Road, La Jolla, California 92037, USA
    Curr Biol 15:R139-41. 2005
    ..Two recent reports have illuminated a mechanism whereby hypoxic stress dampens TOR signaling in metazoan cells...
  7. ncbi request reprint The ATM-related kinase, hSMG-1, bridges genome and RNA surveillance pathways
    Robert T Abraham
    Program in Signal Transduction Research, The Burnham Institute, 10901 North Torrey Pines Road, La Jolla, CA 92130, USA
    DNA Repair (Amst) 3:919-25. 2004
    ..In this review, we introduce a model in which hSMG-1 teams with ATM and ATR to insure the overall quality of the transcriptome in human cells...
  8. ncbi request reprint mTOR as a positive regulator of tumor cell responses to hypoxia
    R T Abraham
    Program in Signal Transduction Research, The Burnham Institute, 10901 North Torrey Pines Road, La Jolla, CA 92037, USA
    Curr Top Microbiol Immunol 279:299-319. 2004
    ..Here we review evidence that mTOR functions as a positive regulator of HIF-1-dependent responses to hypoxic stress in human cancer cells...
  9. pmc Hypoxia-induced assembly of prolyl hydroxylase PHD3 into complexes: implications for its activity and susceptibility for degradation by the E3 ligase Siah2
    Koh Nakayama
    Signal Transduction Program, Burnham Institute for Medical Research, La Jolla, CA 92037, USA
    Biochem J 401:217-26. 2007
    ..These findings provide new insight into the mechanism underlying the regulation of PHD3 availability and activity in hypoxia by the E3 ligase Siah2...
  10. ncbi request reprint Part-time cop nabs deviant DNA
    Robert T Abraham
    Nat Med 11:257-8. 2005
  11. ncbi request reprint MAPKAP kinase-2: three's company at the G(2) checkpoint
    Robert T Abraham
    Signal Transduction Program, The Burnham Institute, 10901 North Torrey Pines Road, La Jolla, CA 92037, USA
    Mol Cell 17:163-4. 2005
    ..Elegant studies in fission yeast by and in mammalian cells by offer new insights into the mechanism through which stress-induced p38 activation inhibits mitotic entry in eukaryotic cells...
  12. pmc Functional analysis of human microtubule-based motor proteins, the kinesins and dyneins, in mitosis/cytokinesis using RNA interference
    Changjun Zhu
    The Burnham Institute, La Jolla, CA 92037, USA
    Mol Biol Cell 16:3187-99. 2005
    ..Using immunofluorescence analysis, time-lapse microscopy, and rescue experiments, we investigate the roles of these 12 kinesins in detail...
  13. pmc Interaction between human MCM7 and Rad17 proteins is required for replication checkpoint signaling
    Cheng Chung Tsao
    Program in Signal Transduction Research, Cancer Research Center, The Burnham Institute, La Jolla, CA 92037, USA
    EMBO J 23:4660-9. 2004
    ..These results demonstrate that hMCM7 plays a direct role in the transmission of DNA damage signals from active replication forks to the S-phase checkpoint machinery in human cells...
  14. pmc ATR functions as a gene dosage-dependent tumor suppressor on a mismatch repair-deficient background
    Yanan Fang
    Department of Pharmacology and Cancer Biology, Duke University Medical Center, Durham, NC 27710, USA
    EMBO J 23:3164-74. 2004
    ..These results demonstrate that MMR proteins and ATR functionally interact during the cellular response to genotoxic stress, and that ATR serves as a haploinsufficient tumor suppressor in MMR-deficient cells...
  15. ncbi request reprint Dynamic recruitment of PAK1 to the immunological synapse is mediated by PIX independently of SLP-76 and Vav1
    Hyewon Phee
    Department of Medicine, Howard Hughes Medical Institute, Rosalind Russell Medical Research Center for Arthritis, University of California San Francisco, 94143, USA
    Nat Immunol 6:608-17. 2005
    ..These data indicate that a pathway involving the GIT-PIX-PAK1 complex has a crucial function in PAK1 activation by recruiting PAK1 to the immunological synapse...
  16. ncbi request reprint Phosphorylation of mammalian target of rapamycin (mTOR) at Ser-2448 is mediated by p70S6 kinase
    Gary G Chiang
    Program in Signal Transduction Research, The Burnham Institute, La Jolla, California 92037, USA
    J Biol Chem 280:25485-90. 2005
    ..Taken together, these results suggest that p70S6 kinase is a major effector of mTOR phosphorylation at Ser-2448 in response to both mitogen- and nutrient-derived stimuli...
  17. pmc A protective role for the human SMG-1 kinase against tumor necrosis factor-alpha-induced apoptosis
    Vasco Oliveira
    Department of Experimental Therapeutics, H Lee Moffitt Cancer Center and Research Institute, University of South Florida, Tampa, Florida 33612, USA
    J Biol Chem 283:13174-84. 2008
    ..These results suggest that hSMG-1 plays an important role in cell survival during TNFalpha-induced stress...
  18. pmc A retroinhibition approach reveals a tumor cell-autonomous response to rapamycin in head and neck cancer
    Panomwat Amornphimoltham
    Oral and Pharyngeal Cancer Branch, National Institute of Craniofacial and Dental Research, NIH, Bethesda, Maryland 20892 4330, USA
    Cancer Res 68:1144-53. 2008
    ..These findings indicate that HNSCC cells are the primary target of rapamycin in vivo, and provide evidence that its antiangiogenic effects may represent a downstream consequence of mTOR inhibition in HNSCC cells...
  19. ncbi request reprint Discovery of lactoquinomycin and related pyranonaphthoquinones as potent and allosteric inhibitors of AKT/PKB: mechanistic involvement of AKT catalytic activation loop cysteines
    Lourdes Toral-Barza
    Oncology Research, Wyeth Research, Pearl River, NY 10965, USA
    Mol Cancer Ther 6:3028-38. 2007
    ..Moreover, lactoquinomycin reduced cellular mammalian target of rapamycin signaling and cap-dependent mRNA translation initiation. Our results highlight T-loop targeting as a new strategy for the generation of selective AKT inhibitors...
  20. ncbi request reprint The phosphatidylinositol 3-kinase inhibitor, PX-866, is a potent inhibitor of cancer cell motility and growth in three-dimensional cultures
    Amy L Howes
    Burnham Institute for Medical Research, 10901 North Torrey Pines Road, La Jolla, CA 92037, USA
    Mol Cancer Ther 6:2505-14. 2007
    ..In addition, we propose that the use of three-dimensional tumor models is more predictive of in vivo growth inhibition by PI3K inhibitors in cancer cell lines lacking phosphatase and tensin homologue activity or expression...
  21. ncbi request reprint SKAP55 modulates T cell antigen receptor-induced activation of the Ras-Erk-AP1 pathway by binding RasGRP1
    KARENA A KOSCO
    Program on Inflammatory Disease Research, Infectious and Inflammatory Disease Center, The Burnham Institute for Medical Research, 10901 North Torrey Pines Road, La Jolla, CA 92037, USA
    Mol Immunol 45:510-22. 2008
    ..The binding of RasGRP1 to SKAP55 required the C-terminus of SKAP55 and was enhanced by tyrosine phosphorylation of SKAP55. These results suggest that SKAP55 modulates signal transduction from the TCR to Ras by binding to RasGRP1...
  22. ncbi request reprint The mammalian target of rapamycin signaling pathway: twists and turns in the road to cancer therapy
    Robert T Abraham
    Department of Oncology Discovery, Wyeth, Pearl River, New York 10960, USA
    Clin Cancer Res 13:3109-14. 2007
    ..This article highlights recent advances in our understanding of the mTOR signaling pathway and the implications of these findings for the clinical application of mTOR inhibitors in cancer patients...
  23. ncbi request reprint The FRB domain of mTOR: NMR solution structure and inhibitor design
    Marilisa Leone
    Cancer Research Center, Burnham Institute for Medical Research, 10901 North Torrey Pines Road, La Jolla, California 92037, USA
    Biochemistry 45:10294-302. 2006
    ..As such, these ligands could be useful in deciphering the complex regulation of mTOR in the cell and in validating the FRB domain as a possible target for the development of novel therapeutic compounds...
  24. pmc The functional role of Cdc6 in S-G2/M in mammalian cells
    Eric Lau
    The Burnham Institute, La Jolla, California 92037, USA
    EMBO Rep 7:425-30. 2006
    ..These results show that Cdc6 is not only required for G1 origin licensing, but is also crucial for proper S-phase DNA replication that is essential for DNA segregation during mitosis...
  25. doi request reprint Moving out: mobilizing activated T cells from lymphoid tissues
    Gabriel Berstein
    Nat Immunol 9:455-7. 2008
  26. ncbi request reprint Genotoxic stress targets human Chk1 for degradation by the ubiquitin-proteasome pathway
    You Wei Zhang
    Signal Transduction Program, The Burnham Institute, La Jolla, California 92037, USA
    Mol Cell 19:607-18. 2005
    ..Proteolysis of activated Chk1 may promote checkpoint termination under normal conditions, and may play an important role in the cytotoxic effects of CPT and related anticancer drugs...
  27. ncbi request reprint Antitumor activity of rapamycin in a transgenic mouse model of ErbB2-dependent human breast cancer
    Mei Liu
    Program in Signal Transduction Research, The Burnham Institute, La Jolla, California 92037, USA
    Cancer Res 65:5325-36. 2005
    ....
  28. doi request reprint A new pharmacologic action of CCI-779 involves FKBP12-independent inhibition of mTOR kinase activity and profound repression of global protein synthesis
    Boris Shor
    Discovery Oncology, Wyeth Research, Pearl River, NY 10965, USA
    Cancer Res 68:2934-43. 2008
    ..This distinctive high-dose drug effect could be directly related to the antitumor activities of CCI-779 and other rapalogues in human cancer patients...
  29. ncbi request reprint Differential effects of rapamycin on mammalian target of rapamycin signaling functions in mammalian cells
    Aimee L Edinger
    Abramson Family Cancer Research Institute, University of Pennsylvania, Philadelphia, Pennsylvania, USA
    Cancer Res 63:8451-60. 2003
    ..These results indicate that rapamycin exerts variable inhibitory actions on mTOR signaling functions and suggest that direct inhibitors of the mTOR kinase domain will display substantially broader anticancer activities than rapamycin...
  30. ncbi request reprint Determination of the catalytic activities of mTOR and other members of the phosphoinositide-3-kinase-related kinase family
    Gary G Chiang
    Program in Signal Transduction Research, The Burnham Institute, La Jolla, CA, USA
    Methods Mol Biol 281:125-41. 2004
    ..Here we describe, in detail, the determination of PIKK catalytic activity with a standardized immune-complex kinase assay protocol...
  31. pmc The rapamycin-binding domain governs substrate selectivity by the mammalian target of rapamycin
    Lloyd P McMahon
    Department of Pharmacology, University of Virginia School of Medicine, Charlottesville, Virginia 22908, USA
    Mol Cell Biol 22:7428-38. 2002
    ..The findings also impose new limitations on interpreting results from experiments in which rapamycin and/or rapamycin-resistant forms of mTOR are used to investigate mTOR function in cells...
  32. pmc Regulation of hypoxia-inducible factor 1alpha expression and function by the mammalian target of rapamycin
    Christine C Hudson
    Department of Pharmacology and Cancer Biology, Duke University Medical Center, Durham, North Carolina 27710, USA
    Mol Cell Biol 22:7004-14. 2002
    ..These studies position mTOR as an upstream activator of HIF-1 function in cancer cells and suggest that the antitumor activity of rapamycin is mediated, in part, through the inhibition of cellular responses to hypoxic stress...
  33. pmc Pleiotropic defects in TCR signaling in a Vav-1-null Jurkat T-cell line
    Youjia Cao
    Department of Pharmacology and Cancer Biology and Department of Immunology, Duke University Medical Center, Durham, NC 27710, USA
    EMBO J 21:4809-19. 2002
    ..Vav1 cells. Finally, evidence is presented to suggest that the alternative Vav family members, Vav-2 and Vav-3, are activated during TCR ligation, and partially compensate for the loss of Vav-1 in Jurkat T cells...
  34. pmc Distinct requirements for Ras oncogenesis in human versus mouse cells
    Nesrin M Hamad
    Department of Pharmacology, Division of Neurology, Duke University Medical Center, Durham North Carolina 27710, USA
    Genes Dev 16:2045-57. 2002
    ..Thus, oncogenic Ras may transform murine and human cells by distinct mechanisms, and the RalGEF pathway--previously deemed to play a secondary role in Ras transformation--could represent a new target for anti-cancer therapy...
  35. ncbi request reprint Activation of ZAP-70 through specific dephosphorylation at the inhibitory Tyr-292 by the low molecular weight phosphotyrosine phosphatase (LMPTP)
    Nunzio Bottini
    Program of Signal Transduction, La Jolla Cancer Research Center, The Burnham Institute, La Jolla, California 92037, USA
    J Biol Chem 277:24220-4. 2002
    ..The ZAP-70 Y292F mutant was not affected by LMPTP. Our results indicate that LMPTP, like CD45, dephosphorylates a negative regulatory tyrosine site in a protein-tyrosine kinase and thereby strengthens T cell receptor signaling...
  36. pmc Translocation of PKC[theta] in T cells is mediated by a nonconventional, PI3-K- and Vav-dependent pathway, but does not absolutely require phospholipase C
    Martin Villalba
    Division of Cell Biology, La Jolla Institute for Allergy and Immunology, San Diego, CA 92121, USA
    J Cell Biol 157:253-63. 2002
    ..These results provide evidence that a nonconventional PI3-K- and Vav-dependent pathway mediates the selective membrane recruitment and, possibly, activation of PKCtheta in T cells...
  37. pmc Hypoxia links ATR and p53 through replication arrest
    Ester M Hammond
    Center for Clinical Sciences Research, Department of Radiation Oncology, Stanford University, Stanford, CA 94303 5152, USA
    Mol Cell Biol 22:1834-43. 2002
    ....
  38. ncbi request reprint Novel pyrrolo-quinoline derivatives as potent inhibitors for PI3-kinase related kinases
    Hairuo Peng
    School of Chemistry and Biochemistry, Georgia Institute of Technology, Atlanta, GA 30332, USA
    Bioorg Med Chem 10:167-74. 2002
    ....
  39. ncbi request reprint Tyrosine phosphorylation of VHR phosphatase by ZAP-70
    Andres Alonso
    Program of Signal Transduction, The Burnham Institute, 10901 North Torrey Pines Road, La Jolla, CA 92037, USA
    Nat Immunol 4:44-8. 2003
    ..These results suggest that VHR is a target for ZAP-70 and tempers activation of the Erk2 pathway in a ZAP-70-controlled manner...
  40. ncbi request reprint Mechanism of recruitment of WASP to the immunological synapse and of its activation following TCR ligation
    Yoji Sasahara
    Division of Immunology, Children s Hospital and Department of Pediatrics, Harvard Medical School, Boston, MA 02115, USA
    Mol Cell 10:1269-81. 2002
    ..These results suggest that the ZAP-70-CrkL-WIP pathway and PKCtheta link TCR to WASP activation...
  41. pmc Differential regulation of TCR-mediated gene transcription by Vav family members
    Shaheen Zakaria
    Division of Oncology Research, Mayo Clinic College of Medicine, Rochester, MN 55905, USA
    J Exp Med 199:429-34. 2004
    ..These data indicate that, although both Vav proteins are biochemically coupled to the TCR, they regulate distinct molecular pathways leading to defined gene transcriptional events...
  42. ncbi request reprint SLP-76 coordinates Nck-dependent Wiskott-Aldrich syndrome protein recruitment with Vav-1/Cdc42-dependent Wiskott-Aldrich syndrome protein activation at the T cell-APC contact site
    Rong Zeng
    Department of Pathology, University of Chicago, Chicago, IL 60637, USA
    J Immunol 171:1360-8. 2003
    ..Taken together, these findings reconstruct the signaling pathway leading from TCR ligation to localized WASP activation...
  43. pmc Requirement of protein phosphatase 5 in DNA-damage-induced ATM activation
    Ambereen Ali
    Department of Pharmacology and Cancer Biology, Duke University Medical Center, Durham, North Carolina 27710, USA
    Genes Dev 18:249-54. 2004
    ..Together our findings indicate that PP5 plays an essential role in the activation and checkpoint signaling functions of ATM in cells that have suffered DNA double-strand breaks...
  44. ncbi request reprint The mRNA surveillance protein hSMG-1 functions in genotoxic stress response pathways in mammalian cells
    Kathryn M Brumbaugh
    Program in Signal Transduction Research, The Burnham Institute, La Jolla, CA 92037, USA
    Mol Cell 14:585-98. 2004
    ..Finally, NMD is suppressed in hSMG-1- but not ATM-deficient cells. These results indicate that hSMG-1 plays important roles in the maintenance of both genome and transcriptome integrity in human cells...
  45. ncbi request reprint Vav-1 and the IKK alpha subunit of I kappa B kinase functionally associate to induce NF-kappa B activation in response to CD28 engagement
    Enza Piccolella
    Department of Cellular and Developmental Biology, University of Rome La Sapienza, Rome, Italy
    J Immunol 170:2895-903. 2003
    ..Taken together, these data evidence that Vav-1 plays a key role in the control of NF-kappa B pathway by targeting IKK alpha in the T cell membrane and favoring its activation in response to CD28 stimulation...
  46. ncbi request reprint Antigen receptors rap to integrin receptors
    Robert T Abraham
    Nat Immunol 3:212-3. 2002
  47. ncbi request reprint Isoform-specific phosphoinositide 3-kinase inhibitors from an arylmorpholine scaffold
    Zachary A Knight
    Program in Chemistry and Chemical Biology, University of California San Francisco, San Francisco, CA 94143, USA
    Bioorg Med Chem 12:4749-59. 2004
    ..13 microM, p110delta=0.63 microM). We also identify trends that suggest certain PI3-K isoforms may be more sensitive to potent inhibition by arylmorpholines, thereby guiding future drug design based on this pharmacophore...
  48. ncbi request reprint Protein tyrosine phosphorylation in T cell signaling
    Tomas Mustelin
    Program of Signal Transduction, Cancer Research Center, The Burnham Institute, La Jolla, CA 92037, USA
    Front Biosci 7:d918-69. 2002
    ..Finally, we briefly review the key substrates for tyrosine phosphorylation and their role in coupling the kinases and phosphatases to gene transcription and other aspects of the T lymphocyte response to antigen...
  49. ncbi request reprint Targeting the mTOR signaling network in cancer
    Gary G Chiang
    Program in Signal Transduction, Burnham Institute for Medical Research, 10901 N Torrey Pines Road, La Jolla, CA 92037, USA
    Trends Mol Med 13:433-42. 2007
    ..In this review, we discuss the regulatory pathways that govern mTOR activity, and highlight clinical results obtained with the first generation of mTOR inhibitors to reach the oncology clinics...
  50. ncbi request reprint Mammalian target of rapamycin as a therapeutic target in oncology
    Robert T Abraham
    Oncology Discovery Research, Wyeth, 401 N Middletown Road, Pearl River, NY 10965, USA
    Expert Opin Ther Targets 12:209-22. 2008
    ..The mammalian target of rapamycin (mTOR) has emerged as a validated therapeutic target in cancer and mTOR inhibitors alter tumor cell responses to mitogenic signals and microenvironmental stress...
  51. ncbi request reprint Checkpoint signalling: focusing on 53BP1
    Robert T Abraham
    Nat Cell Biol 4:E277-9. 2002
  52. ncbi request reprint Rap1 redux
    Robert T Abraham
    Nat Immunol 4:725-7. 2003
  53. ncbi request reprint Characterization of the cytotoxic activities of novel analogues of the antitumor agent, lavendamycin
    Yanan Fang
    Department of Pharmacology and Cancer Biology, Duke University, Durham, North Carolina 27710, USA
    Mol Cancer Ther 2:517-26. 2003
    ..Finally, MB-97 showed significant cytotoxic activity in the National Cancer Institute's panel of 60 cancer cell lines and antitumor activity in vivo in hollow fiber tumorigenesis assays...
  54. ncbi request reprint Signalomic signatures enlighten drug profiling
    Robert T Abraham
    Nat Chem Biol 2:295-6. 2006
  55. ncbi request reprint A new link between the c-Abl tyrosine kinase and phosphoinositide signalling through PLC-gamma1
    Rina Plattner
    Department of Pharmacology and Cancer Biology Duke University Medical Center Durham, NC 27710, USA
    Nat Cell Biol 5:309-19. 2003
    ..After activation, c-Abl phosphorylates PLC-gamma1 and negatively modulates its function in vivo. These findings uncover a newly discovered functional interdependence between non-receptor Tyr kinase and lipid signalling pathways...
  56. pmc The phosphatidylinositol-3-kinase inhibitor PX-866 overcomes resistance to the epidermal growth factor receptor inhibitor gefitinib in A-549 human non-small cell lung cancer xenografts
    Nathan T Ihle
    Arizona Cancer Center, University of Arizona, Tucson, USA
    Mol Cancer Ther 4:1349-57. 2005
    ..Thus, PX-866, by inhibiting PI3-K signaling, may have clinical use in increasing the response to EGFR inhibitors such as gefitinib in patients with NSCLC and possibly in other cancers who do not respond to EGFR inhibition...
  57. ncbi request reprint Turning the replication checkpoint on and off
    You Wei Zhang
    Molecular and Cellular Biology, The Salk Institute, La Jolla, California, USA
    Cell Cycle 5:125-8. 2006
    ..This review provides an overview of the study's major findings, together with their implications for both replication checkpoint function and tumor responsiveness to CPT and related anticancer drugs...

Research Grants12

  1. Roles of ATM and ATR Kinases in DNA Damage Responses
    Robert Abraham; Fiscal Year: 2004
    ....
  2. SIGNAL TRANSDUCTION FROM THE T CELL ANTIGEN RECEPTOR
    Robert Abraham; Fiscal Year: 2003
    ..However, experiments in fibroblasts stimulated with PDGF indicate that phosphorylation at residue 783 is necessary for increased enzymatic activity, while phosphorylation at Y771 results in inhibition of activity. ..
  3. CELLULAR PHARMACOLOGY OF RAPAMYCIN
    Robert Abraham; Fiscal Year: 2001
    ....
  4. CELLULAR PHARMACOLOGY OF RAPAMYCIN
    Robert Abraham; Fiscal Year: 2004
    ..abstract_text> ..