Boris Reva

Summary

Affiliation: Memorial Sloan-Kettering Cancer Center
Country: USA

Publications

  1. ncbi request reprint Threading with chemostructural restrictions method for predicting fold and functionally significant residues: application to dipeptidylpeptidase IV (DPP-IV)
    Boris Reva
    Novartis Institute for Biomedical Research, Summit, New Jersey, USA
    Proteins 47:180-93. 2002
  2. pmc Matrix Metalloproteinase-9 (MMP-9) polymorphisms in patients with cutaneous malignant melanoma
    Javier Cotignola
    Memorial Sloan Kettering Cancer Center, New York, NY, USA
    BMC Med Genet 8:10. 2007
  3. pmc Determinants of protein function revealed by combinatorial entropy optimization
    Boris Reva
    Computational Biology Center, Memorial Sloan Kettering Cancer Center, 1275 York Avenue, New York, NY 10065, USA
    Genome Biol 8:R232. 2007
  4. pmc Necdin, a p53 target gene, regulates the quiescence and response to genotoxic stress of hematopoietic stem/progenitor cells
    Takashi Asai
    Molecular Pharmacology and Chemistry Program, Sloan Kettering Institute, Memorial Sloan Kettering Cancer Center, New York, NY, USA
    Blood 120:1601-12. 2012
  5. doi request reprint The cBio cancer genomics portal: an open platform for exploring multidimensional cancer genomics data
    Ethan Cerami
    Computational Biology Center, Memorial Sloan Kettering Cancer Center, New York, New York 10021, USA
    Cancer Discov 2:401-4. 2012
  6. pmc Predicting the functional impact of protein mutations: application to cancer genomics
    Boris Reva
    Computational Biology Center, Memorial Sloan Kettering Cancer Center, NY 10065, USA
    Nucleic Acids Res 39:e118. 2011

Collaborators

Detail Information

Publications6

  1. ncbi request reprint Threading with chemostructural restrictions method for predicting fold and functionally significant residues: application to dipeptidylpeptidase IV (DPP-IV)
    Boris Reva
    Novartis Institute for Biomedical Research, Summit, New Jersey, USA
    Proteins 47:180-93. 2002
    ..Cell 1998;94:161-170) and use this structure for modeling the interaction of DPP-IV with inhibitor...
  2. pmc Matrix Metalloproteinase-9 (MMP-9) polymorphisms in patients with cutaneous malignant melanoma
    Javier Cotignola
    Memorial Sloan Kettering Cancer Center, New York, NY, USA
    BMC Med Genet 8:10. 2007
    ..Some polymorphisms are known to influence gene expression, protein activity, stability, and interactions, and they were shown to be associated with certain tumor phenotypes and cancer risk...
  3. pmc Determinants of protein function revealed by combinatorial entropy optimization
    Boris Reva
    Computational Biology Center, Memorial Sloan Kettering Cancer Center, 1275 York Avenue, New York, NY 10065, USA
    Genome Biol 8:R232. 2007
    ..Such predicted functional determinants are useful for interpreting the functional consequences of mutations in natural evolution and disease...
  4. pmc Necdin, a p53 target gene, regulates the quiescence and response to genotoxic stress of hematopoietic stem/progenitor cells
    Takashi Asai
    Molecular Pharmacology and Chemistry Program, Sloan Kettering Institute, Memorial Sloan Kettering Cancer Center, New York, NY, USA
    Blood 120:1601-12. 2012
    ..We conclude that necdin functions as a molecular switch in adult hematopoiesis, acting in a p53-like manner to promote HSC quiescence in the steady state, but suppressing p53-dependent apoptosis in response to genotoxic stress...
  5. doi request reprint The cBio cancer genomics portal: an open platform for exploring multidimensional cancer genomics data
    Ethan Cerami
    Computational Biology Center, Memorial Sloan Kettering Cancer Center, New York, New York 10021, USA
    Cancer Discov 2:401-4. 2012
    ....
  6. pmc Predicting the functional impact of protein mutations: application to cancer genomics
    Boris Reva
    Computational Biology Center, Memorial Sloan Kettering Cancer Center, NY 10065, USA
    Nucleic Acids Res 39:e118. 2011
    ..In addition, we estimate that at least 5% of cancer-relevant mutations involve switch of function, rather than simply loss or gain of function...