Peter Vogt

Summary

Affiliation: The Scripps Research Institute
Country: USA

Publications

  1. ncbi request reprint PI3K p110β: more tightly controlled or constitutively active?
    Peter K Vogt
    The Scripps Research Institute, Department of Molecular and Experimental Medicine, 10550 North Torrey Pines Road, La Jolla, CA 92037, USA
    Mol Cell 41:499-501. 2011
  2. pmc Retroviral oncogenes: a historical primer
    Peter K Vogt
    The Scripps Research Institute, La Jolla, California 92037, USA
    Nat Rev Cancer 12:639-48. 2012
  3. pmc PI3K and STAT3: a new alliance
    Peter K Vogt
    The Scripps Research Institute, Department of Molecular and Experimental Medicine, 10550 North Torrey Pines Road, La Jolla, CA 92037, USA
    Cancer Discov 1:481-6. 2011
  4. ncbi request reprint Phosphoinositide 3-kinase: from viral oncoprotein to drug target
    Peter K Vogt
    Department of Molecular and Experimental Medicine, The Scripps Research Institute, 10550 North Torrey Pines Road BCC 239, La Jolla, CA 92037, USA
    Virology 344:131-8. 2006
  5. ncbi request reprint PI 3-kinases: hidden potentials revealed
    Peter K Vogt
    Department of Molecular and Experimental Medicine, The Scripps Research Institute, La Jolla, California 92037, USA
    Cell Cycle 5:946-9. 2006
  6. ncbi request reprint Triple layer control: phosphorylation, acetylation and ubiquitination of FOXO proteins
    Peter K Vogt
    Department of Molecular and Experimental Medicine, The Scripps Research Institute, La Jolla, California 92037, USA
    Cell Cycle 4:908-13. 2005
  7. ncbi request reprint Kinase inhibitors: vice becomes virtue
    Peter K Vogt
    Department of Molecular and Experimental Medicine, The Scripps Research Institute, 10550 North Torrey Pines Road, La Jolla, California 92037, USA
    Cancer Cell 9:327-8. 2006
  8. ncbi request reprint Cancer-specific mutations in phosphatidylinositol 3-kinase
    Peter K Vogt
    Department of Molecular and Experimental Medicine, The Scripps Research Institute, La Jolla, CA 92037, USA
    Trends Biochem Sci 32:342-9. 2007
  9. doi request reprint Drug-resistant phosphatidylinositol 3-kinase: guidance for the preemptive strike
    Peter K Vogt
    Division of Oncovirology, The Scripps Research Institute, La Jolla, CA 92037, USA
    Cancer Cell 14:107-8. 2008
  10. pmc PI 3-kinase and cancer: changing accents
    Peter K Vogt
    Department of Molecular and Experimental Medicine, Division of Oncovirology, The Scripps Research Institute, La Jolla, CA 92037, USA
    Curr Opin Genet Dev 19:12-7. 2009

Collaborators

Detail Information

Publications49

  1. ncbi request reprint PI3K p110β: more tightly controlled or constitutively active?
    Peter K Vogt
    The Scripps Research Institute, Department of Molecular and Experimental Medicine, 10550 North Torrey Pines Road, La Jolla, CA 92037, USA
    Mol Cell 41:499-501. 2011
  2. pmc Retroviral oncogenes: a historical primer
    Peter K Vogt
    The Scripps Research Institute, La Jolla, California 92037, USA
    Nat Rev Cancer 12:639-48. 2012
    ..The MYC, RAS and ERBB oncogenes quickly followed SRC, and these together with PI3K are now recognized as crucial driving forces in human cancer...
  3. pmc PI3K and STAT3: a new alliance
    Peter K Vogt
    The Scripps Research Institute, Department of Molecular and Experimental Medicine, 10550 North Torrey Pines Road, La Jolla, CA 92037, USA
    Cancer Discov 1:481-6. 2011
    ..The new data document an important role of STAT3 in PI3K-driven oncogenic transformation and mark BMX as a promising therapeutic target that could enhance the effectiveness of PI3K inhibitors...
  4. ncbi request reprint Phosphoinositide 3-kinase: from viral oncoprotein to drug target
    Peter K Vogt
    Department of Molecular and Experimental Medicine, The Scripps Research Institute, 10550 North Torrey Pines Road BCC 239, La Jolla, CA 92037, USA
    Virology 344:131-8. 2006
    ..Mutated p110alpha proteins are ideal drug targets. Identification of small molecule inhibitors that specifically target these mutant proteins is a realistic and urgent goal...
  5. ncbi request reprint PI 3-kinases: hidden potentials revealed
    Peter K Vogt
    Department of Molecular and Experimental Medicine, The Scripps Research Institute, La Jolla, California 92037, USA
    Cell Cycle 5:946-9. 2006
    ..Although these non-alpha isoforms of PI 3-kinase have not been found mutated in human cancer, deregulated expression could contribute to cellular oncogenic properties and deserves increased attention...
  6. ncbi request reprint Triple layer control: phosphorylation, acetylation and ubiquitination of FOXO proteins
    Peter K Vogt
    Department of Molecular and Experimental Medicine, The Scripps Research Institute, La Jolla, California 92037, USA
    Cell Cycle 4:908-13. 2005
    ..The nuclear-cytoplasmic "FOXO shuttle" is driven by stress signals that result in nuclear import and FOXO transcriptional activity and growth signals that initiate nuclear export and proteasomal degradation of FOXO...
  7. ncbi request reprint Kinase inhibitors: vice becomes virtue
    Peter K Vogt
    Department of Molecular and Experimental Medicine, The Scripps Research Institute, 10550 North Torrey Pines Road, La Jolla, California 92037, USA
    Cancer Cell 9:327-8. 2006
    ..The new PI3K inhibitor achieves the effects of combination therapy as a single agent by fortuitously hitting two critical targets...
  8. ncbi request reprint Cancer-specific mutations in phosphatidylinositol 3-kinase
    Peter K Vogt
    Department of Molecular and Experimental Medicine, The Scripps Research Institute, La Jolla, CA 92037, USA
    Trends Biochem Sci 32:342-9. 2007
    ..The mutated p110 alpha proteins are promising cancer targets. Although identification of mutant-specific small-molecule inhibitors seems technically challenging, the therapeutic benefits from such inhibitors could be extremely important...
  9. doi request reprint Drug-resistant phosphatidylinositol 3-kinase: guidance for the preemptive strike
    Peter K Vogt
    Division of Oncovirology, The Scripps Research Institute, La Jolla, CA 92037, USA
    Cancer Cell 14:107-8. 2008
    ..Information on these critical residues provides a road map for generating novel PI3K inhibitors that can overcome the anticipated resistance mutations...
  10. pmc PI 3-kinase and cancer: changing accents
    Peter K Vogt
    Department of Molecular and Experimental Medicine, Division of Oncovirology, The Scripps Research Institute, La Jolla, CA 92037, USA
    Curr Opin Genet Dev 19:12-7. 2009
    ..The oncogenic activities of p110beta include a non-catalytic function, a finding that will have immediate consequences for drug development...
  11. ncbi request reprint Fortuitous convergences: the beginnings of JUN
    Peter K Vogt
    Division of Oncovirology, The Scripps Research Institute, 10550 N Torrey Pines Road BCC239, La Jolla, California 92037, USA
    Nat Rev Cancer 2:465-9. 2002
  12. doi request reprint Akt demoted in glioblastoma
    Peter K Vogt
    The Scripps Research Institute, Department of Molecular and Experimental Medicine, 10550 North Torrey Pines Road, La Jolla, CA 92037, USA
    Sci Signal 2:pe26. 2009
    ..Although PKCalpha (protein kinase Calpha) has been identified as an essential component, the detailed wiring of this previously unexplored noncanonical pathway remains to be worked out...
  13. pmc Phosphatidylinositol 3-kinase: the oncoprotein
    Peter K Vogt
    Department of Molecular and Experimental Medicine, The Scripps Research Institute, La Jolla, CA 92037, USA
    Curr Top Microbiol Immunol 347:79-104. 2010
    ..TOR is an integrator of growth and of metabolic inputs. In complex with the raptor protein (TORC1), it controls cap-dependent translation, and this function is essential for PI3K-initiated oncogenesis...
  14. pmc Y box-binding protein 1 induces resistance to oncogenic transformation by the phosphatidylinositol 3-kinase pathway
    Andreas G Bader
    Department of Molecular and Experimental Medicine, The Scripps Research Institute, 10550 North Torrey Pines Road, La Jolla, CA 92037, USA
    Proc Natl Acad Sci U S A 100:12384-9. 2003
    ..These results suggest that YB-1 acts like a rapamycin mimic, inhibiting translational events that are required in phosphatidylinositol 3-kinase-driven oncogenic transformation...
  15. ncbi request reprint MafA has strong cell transforming ability but is a weak transactivator
    Makoto Nishizawa
    Department of Molecular and Experimental Medicine, BCC239, The Scripps Research Institute, La Jolla, CA, 92037, USA
    Oncogene 22:7882-90. 2003
    ..These regulatable constructs permit a kinetic characterization of target gene responses and facilitate discrimination between direct and indirect targets...
  16. pmc Phosphatidylinositol 3-kinase mutations identified in human cancer are oncogenic
    Sohye Kang
    Department of Molecular and Experimental Medicine, The Scripps Research Institute, La Jolla, CA 92037, USA
    Proc Natl Acad Sci U S A 102:802-7. 2005
    ..The oncogenic transforming activity makes the mutated PI3-kinase proteins promising targets for small molecule inhibitors that could be developed into effective and highly specific anticancer drugs...
  17. pmc Proteasomal degradation of the FoxO1 transcriptional regulator in cells transformed by the P3k and Akt oncoproteins
    Masahiro Aoki
    Department of Molecular and Experimental Medicine, The Scripps Research Institute, 10550 North Torrey Pines Road, La Jolla, CA 92037, USA
    Proc Natl Acad Sci U S A 101:13613-7. 2004
    ..The FoxG1 oncoprotein also inhibits transcriptional activation by FoxO1. Inhibition of FoxO1, albeit by different mechanisms, appears to be a common denominator of the PI3K and FoxG1 oncogenic pathways...
  18. pmc Akt-mediated regulation of NFkappaB and the essentialness of NFkappaB for the oncogenicity of PI3K and Akt
    Dong Bai
    The Scripps Research Institute, Department of Molecular and Experimental Medicine, 10550 N Torrey Pines Road, La Jolla, CA 92037, USA
    Int J Cancer 125:2863-70. 2009
    ..The data further support the conclusion that NFkappaB activity is essential for PI3K- and Akt-induced oncogenic transformation...
  19. pmc Oncogenic transformation induced by the p110beta, -gamma, and -delta isoforms of class I phosphoinositide 3-kinase
    Sohye Kang
    Department of Molecular and Experimental Medicine, The Scripps Research Institute, 10550 North Torrey Pines Road, BCC 239, La Jolla, CA 92037, USA
    Proc Natl Acad Sci U S A 103:1289-94. 2006
    ....
  20. pmc Small-molecule antagonists of Myc/Max dimerization inhibit Myc-induced transformation of chicken embryo fibroblasts
    Thorsten Berg
    Department of Molecular and Experimental Medicine, The Scripps Research Institute, 10550 North Torrey Pines Road, La Jolla, CA 92037, USA
    Proc Natl Acad Sci U S A 99:3830-5. 2002
    ..Our work provides proof of principle for the identification of small molecule inhibitors of protein-protein interactions by using high-throughput screens of combinatorial chemical libraries...
  21. ncbi request reprint The C-terminal region of cellular Qin oligomerizes: correlation with oncogenic transformation and transcriptional repression
    Corinna K Sonderegger
    Department of Molecular and Experimental Medicine, The Scripps Research Institute, La Jolla, CA 92037, USA
    Oncogene 22:1908-15. 2003
    ..A 60 amino-acid region within the oligomerization domain is necessary and sufficient for transcriptional repression induced by Qin...
  22. ncbi request reprint Artificial oncoproteins: modified versions of the yeast bZip protein GCN4 induce cellular transformation
    Makoto Nishizawa
    Department of Molecular and Experimental Medicine, The Scripps Research Institute, La Jolla, CA 92037, USA
    Oncogene 22:7931-41. 2003
    ..We have further constructed a regulatable GCN4-VP16 protein that will permit a kinetic characterization of target gene responses and will facilitate discrimination between direct and indirect targets...
  23. pmc Cancer-derived mutations in the regulatory subunit p85alpha of phosphoinositide 3-kinase function through the catalytic subunit p110alpha
    Minghao Sun
    Department of Molecular and Experimental Medicine, The Scripps Research Institute, La Jolla, CA 92037, USA
    Proc Natl Acad Sci U S A 107:15547-52. 2010
    ....
  24. pmc Discovery of inhibitors of aberrant gene transcription from Libraries of DNA binding molecules: inhibition of LEF-1-mediated gene transcription and oncogenic transformation
    James S Stover
    Department of Chemistry, The Skaggs Institute for Chemical Biology, The Scripps Research Institute, 10550 North Torrey Pines Road, La Jolla, California 92037, USA
    J Am Chem Soc 131:3342-8. 2009
    ....
  25. pmc Posttranslational regulation of Myc by promyelocytic leukemia zinc finger protein
    Jin Shi
    Department of Molecular and Experimental Medicine, The Scripps Research Institute, La Jolla, CA 92037, USA
    Int J Cancer 125:1558-65. 2009
    ..In support of this suggestion, a specific inhibitor of Myc is able to revert the transformed phenotype of PLZF mutant-expressing cells...
  26. pmc Stabilizers of the Max homodimer identified in virtual ligand screening inhibit Myc function
    Hao Jiang
    Department of Molecular and Experimental Medicine, The Scripps Research Institute, 10550 North Torrey Pines Road, La Jolla, CA 92037, USA
    Mol Pharmacol 76:491-502. 2009
    ..The Max-Max stabilizer can be considered a lead compound for the development of inhibitors of the Myc network...
  27. ncbi request reprint An essential role for protein synthesis in oncogenic cellular transformation
    Andreas G Bader
    Division of Oncovirology, Department of Molecular and Experimental Medicine, The Scripps Research Institute, 10550 North Torrey Pines Road, La Jolla CA 92037, USA
    Oncogene 23:3145-50. 2004
    ..Here we review the components of the PI 3-kinase signaling pathway and the mRNA-binding protein YB-1, exploring their roles in protein synthesis and oncogenic cell transformation...
  28. pmc Inhibition of protein synthesis by Y box-binding protein 1 blocks oncogenic cell transformation
    Andreas G Bader
    Department of Molecular and Experimental Medicine, The Scripps Research Institute, 10550 North Torrey Pines Rd, BCC239, La Jolla, CA 92037, USA
    Mol Cell Biol 25:2095-106. 2005
    ..Potential functions of the C-terminal region are discussed...
  29. ncbi request reprint Binding of the corepressor TLE1 to Qin enhances Qin-mediated transformation of chicken embryo fibroblasts
    Corinna K Sonderegger
    Department of Molecular and Experimental Medicine, The Scripps Research Institute, La Jolla, CA 92037, USA
    Oncogene 22:1749-57. 2003
    ..Expression of TLE1 in CEF by the retroviral vector RCAS enhances cell growth and induces formation of agar colonies...
  30. pmc Cancer-specific mutations in PIK3CA are oncogenic in vivo
    Andreas G Bader
    Department of Molecular and Experimental Medicine, The Scripps Research Institute, 10550 North Torrey Pines Road, La Jolla, CA 92037, USA
    Proc Natl Acad Sci U S A 103:1475-9. 2006
    ..The in vivo oncogenicity of PIK3CA mutants in an avian species strongly suggests a critical role for these mutated proteins in human malignancies...
  31. ncbi request reprint Oncogenic transformation by beta-catenin: deletion analysis and characterization of selected target genes
    Masahiro Aoki
    Department of Molecular and Experimental Medicine, The Scripps Research Institute, La Jolla, California, CA 92037, USA
    Oncogene 21:6983-91. 2002
    ..A new target gene, coding for inositol hexakisphosphate kinase 2 (IP6K2) was identified. Its expression showed concordance with the transforming activity of beta-catenin constructs...
  32. ncbi request reprint Partial oncogenic transformation of chicken embryo fibroblasts by Jun dimerization protein 2, a negative regulator of TRE- and CRE-dependent transcription
    Erik Blazek
    Department of Molecular and Experimental Medicine, The Scripps Research Institute, La Jolla, CA 92037, USA
    Oncogene 22:2151-9. 2003
    ....
  33. ncbi request reprint Oncogenic PI3K deregulates transcription and translation
    Andreas G Bader
    Department of Molecular and Experimental Medicine, The Scripps Research Institute, 10550 North Torrey Pines Road, La Jolla, California 92037, USA
    Nat Rev Cancer 5:921-9. 2005
    ....
  34. ncbi request reprint Mutated PI 3-kinases: cancer targets on a silver platter
    Sohye Kang
    Department of Molecular and Experimental Medicine, The Scripps Research Institute, La Jolla, California 92037, USA
    Cell Cycle 4:578-81. 2005
    ..The mutated p110alpha proteins are ideal targets for specific small molecule inhibitors that discriminate between the oncogenic and the wild-type forms of the enzyme. Such inhibitors could become highly effective anti-cancer drugs...
  35. doi request reprint Biochemical and biological characterization of tumor-associated mutations of p110alpha
    Adam Denley
    Department of Molecular and Experimental Medicine, The Scripps Research Institute, La Jolla, California, USA
    Methods Enzymol 438:291-305. 2008
    ..Loss of Ras function can interfere with PI3K signaling. Various lines of evidence suggest complementary roles for PI3K and MAPK signaling in oncogenesis...
  36. ncbi request reprint Jun: stealth, stability, and transformation
    Peter K Vogt
    Department of Molecular and Experimental Medicine, The Scripps Research Institute, La Jolla, California 92037, USA
    Mol Cell 19:432-3. 2005
    ..2005)...
  37. pmc Requirement of phosphatidylinositol(3,4,5)trisphosphate in phosphatidylinositol 3-kinase-induced oncogenic transformation
    Adam Denley
    Department of Molecular and Experimental Medicine, The Scripps Research Institute, La Jolla, CA 92037, USA
    Mol Cancer Res 7:1132-8. 2009
    ..We conclude that PIP3 is an essential component of PI3K-mediated oncogenesis and that inability to generate PIP3 abolishes oncogenic potential...
  38. pmc Rare cancer-specific mutations in PIK3CA show gain of function
    Marco Gymnopoulos
    Department of Molecular and Experimental Medicine, The Scripps Research Institute, La Jolla, CA 92037, USA
    Proc Natl Acad Sci U S A 104:5569-74. 2007
    ..Engineered mutants that exchange acidic or neutral residues for basic residues on the critical surfaces show a gain of function...
  39. ncbi request reprint v-Jun targets showing an expression pattern that correlates with the transformed cellular phenotype
    Jason S Iacovoni
    Department of Molecular and Experimental Medicine, The Scripps Research Institute, 10550 North Torrey Pines Road, La Jolla, CA 92037, USA
    Oncogene 23:5703-6. 2004
    ..With these cells, we find that the upregulated target Sprr1a has an expression pattern that correlates with the transformed phenotype...
  40. ncbi request reprint A credit-card library approach for disrupting protein-protein interactions
    Yang Xu
    Department of Chemistry and Immunology, The Skaggs Institute for Chemical Biology, The Scripps Research Institute, 10550 North Torrey Pines Road, La Jolla CA 92037, USA
    Bioorg Med Chem 14:2660-73. 2006
    ..Finally, this strategy for disrupting protein-protein interactions should prove applicable to other families of proteins...
  41. pmc Small molecule inhibitors of Myc/Max dimerization and Myc-induced cell transformation
    Jin Shi
    Department of Molecular and Experimental Medicine, The Skaggs Institute for Chemical Biology, The Scripps Research Institute, 10550 N Torrey Pines Road, La Jolla, CA 92037, USA
    Bioorg Med Chem Lett 19:6038-41. 2009
    ..The preparation and evaluation of a series of inhibitors of Myc/Max dimerization and Myc-induced cell transformation are described providing mycmycin-1 (3) and mycmycin-2 (4)...
  42. pmc Helical domain and kinase domain mutations in p110alpha of phosphatidylinositol 3-kinase induce gain of function by different mechanisms
    Li Zhao
    Department of Molecular and Experimental Medicine, The Scripps Research Institute, La Jolla, CA 92037
    Proc Natl Acad Sci U S A 105:2652-7. 2008
    ..This synergism also supports the conclusion that the helical and kinase domain mutations operate by two different and independent mechanisms...
  43. pmc Disruption of angiogenesis and tumor growth with an orally active drug that stabilizes the inactive state of PDGFRbeta/B-RAF
    Eric A Murphy
    Department of Pathology, Moores Cancer Center, University of California, San Diego, La Jolla, CA 92093, USA
    Proc Natl Acad Sci U S A 107:4299-304. 2010
    ..Our lead compound was selected as an orally active molecule with favorable pharmacokinetic properties which demonstrated target inhibition in vivo leading to suppression of murine orthotopic tumors in both the kidney and pancreas...
  44. pmc Phosphatidylinositol 4,5-bisphosphate-specific AKT1 is oncogenic
    Nadine Dannemann
    The Scripps Research Institute, Molecular and Experimental Medicine, La Jolla, California 92037, USA
    Int J Cancer 127:239-44. 2010
    ..Gain-of-function mutants of AKT1 may not be affected by PI3K inhibitors that are currently in development. Therefore, AKT1 remains a distinct and important cancer target...
  45. ncbi request reprint A downstream kinase of the mammalian target of rapamycin, p70S6K1, regulates human double minute 2 protein phosphorylation and stability
    Jing Fang
    Department of Microbiology, Immunology and Cell Biology, Mary Babb Randolph Cancer Center, West Virginia University, Morgantown, West Virginia 26506 9300, USA
    J Cell Physiol 209:261-5. 2006
    ..Overexpression of p70S6K1 enhanced HDM2 phosphorylation and led to an increase in HDM2 protein turnover. Our results suggest that p70S6K1 regulates turnover of HDM2 protein for cancer development...
  46. pmc Reversion of the Jun-induced oncogenic phenotype by enhanced synthesis of sialosyllactosylceramide (GM3 ganglioside)
    Yutaka Miura
    Pacific Northwest Research Institute, 720 Broadway, Seattle, WA 98122 4302, USA
    Proc Natl Acad Sci U S A 101:16204-9. 2004
    ..The amounts of this complex are greatly reduced in transformed cells. Expression of GM3 and consequent reversion of the transformed phenotype results in increased levels of that microdomain complex...
  47. ncbi request reprint Disruption of the MYC transcriptional function by a small-molecule antagonist of MYC/MAX dimerization
    Xiaohong Lu
    Northern Institute for Cancer Research, Newcastle University, Newcastle upon Tyne, NE2 4HH, UK
    Oncol Rep 19:825-30. 2008
    ....
  48. pmc Identification of novel mammalian growth regulatory factors by genome-scale quantitative image analysis
    Josephine N Harada
    Genomics Institute of the Novartis Research Foundation, San Diego, California 92121, USA
    Genome Res 15:1136-44. 2005
    ..Taken together, our findings offer new insight into the regulation of cellular growth and proliferation, and demonstrate the value and feasibility of assessing cellular phenotypes through genome-level computational image analysis...
  49. pmc The classic: integration of deoxyribonucleic acid specific for Rous sarcoma virus after infection of permissive and nonpermissive hosts: (RNA tumor viruses/reassociation kinetics/duck cells). 1973
    Harold E Varmus
    Clin Orthop Relat Res 466:2031-8. 2008

Research Grants28

  1. TARGET-GUIDED DEVELOPMENT OF SPECIFIC AKT INHIBITORS
    Peter Vogt; Fiscal Year: 2007
    ..4) Investigate the structure-activity relationship through in situ click chemistry and optimize inhibitors for potency, selectivity and cell-based activity ..
  2. Controlling the Max Network
    Peter Vogt; Fiscal Year: 2007
    ..The proposed work on stabilizers in the Myc-Max network could open the door to a new way of influencing and directing cell growth. ..
  3. P3K, RETROVIRAL ONCOGENE AND HOMOLOG OF PI 3-KINASE
    Peter Vogt; Fiscal Year: 2007
    ..The studies on TOR and YB-1 are complementary. They illuminate a critical phase in Akt-induced transformation from different angles. ..
  4. P3K, RETROVIRAL ONCOGENE AND HOMOLOG OF PI 3-KINASE
    Peter Vogt; Fiscal Year: 2009
    ..A complete understanding of these mutant proteins, their wild-type counterparts and their oncogenic actions is necessary to take advantage of this unique opportunity for developing novel, targeted cancer therapies. ..
  5. P3K, RETROVIRAL ONCOGENE AND HOMOLOG OF PI 3-KINASE
    Peter K Vogt; Fiscal Year: 2010
    ..A complete understanding of these mutant proteins, their wild-type counterparts and their oncogenic actions is necessary to take advantage of this unique opportunity for developing novel, targeted cancer therapies. ..
  6. Activation of silenced tumor suppressor genes by non-coding RNA
    Peter K Vogt; Fiscal Year: 2010
    ..The results of this research will contribute to a mechanistic understanding of epigenetic changes in cancer and provide basic information for the development of new approaches to cancer diagnosis and treatment. ..
  7. P3K, RETROVIRAL ONCOGENE AND HOMOLOG OF PI 3-KINASE
    Peter K Vogt; Fiscal Year: 2011
    ..A complete understanding of these mutant proteins, their wild-type counterparts and their oncogenic actions is necessary to take advantage of this unique opportunity for developing novel, targeted cancer therapies. ..
  8. P3K, RETROVIRAL ONCOGENE AND HOMOLOG OF PI 3-KINASE
    Peter Vogt; Fiscal Year: 2002
    ..It will be analyzed in vivo and in vitro. These experiments will seek to elucidate the mechanisms of p3k-induced angiogenesis, deciding between autocrine and paracrine stimulation and identifying angiogenic factors. ..
  9. THE ONCOGENICITY OF WINGED HELIX PROTEINS
    Peter Vogt; Fiscal Year: 2003
    ..The nature of activating mutations, the interactions with the preinitiation complex, and the identity and function of target genes will reveal novel molecular targets for therapeutic intervention. ..
  10. Potent inhibitors of Anthrax Lethal Factor
    Peter Vogt; Fiscal Year: 2003
    ..Libraries will be targeted using the structural information available for LF, supplemented by information from point mutations of the substrate. Information from our previous synthesis of metalloprotease inhibitors will also be used. ..
  11. The Antisense Transcriptome and the Epigenetics of Cancer.
    Peter K Vogt; Fiscal Year: 2010
    ..The present application will examine antisense-dependent transcriptional regulation on a genome wide scale. ..