Akihiko Yokoyama

Summary

Affiliation: National Cancer Center
Country: Japan

Publications

  1. ncbi Menin critically links MLL proteins with LEDGF on cancer-associated target genes
    Akihiko Yokoyama
    Department of Pathology, Stanford University School of Medicine, Stanford, CA 94305, USA
    Cancer Cell 14:36-46. 2008
  2. ncbi A higher-order complex containing AF4 and ENL family proteins with P-TEFb facilitates oncogenic and physiologic MLL-dependent transcription
    Akihiko Yokoyama
    National Cancer Center Research Institute, Tokyo, Japan
    Cancer Cell 17:198-212. 2010
  3. ncbi Proteolytically cleaved MLL subunits are susceptible to distinct degradation pathways
    Akihiko Yokoyama
    Division of Hematological Malignancy, National Cancer Center Research Institute, Tokyo 104 0045, Japan
    J Cell Sci 124:2208-19. 2011
  4. ncbi Leukemia proto-oncoprotein MLL forms a SET1-like histone methyltransferase complex with menin to regulate Hox gene expression
    Akihiko Yokoyama
    Department of Pathology, Stanford University School of Medicine, Stanford, CA 94305, USA
    Mol Cell Biol 24:5639-49. 2004
  5. ncbi The menin tumor suppressor protein is an essential oncogenic cofactor for MLL-associated leukemogenesis
    Akihiko Yokoyama
    Department of Pathology, Stanford University School of Medicine, Stanford, California 94305, USA
    Cell 123:207-18. 2005
  6. ncbi Leukemia proto-oncoprotein MLL is proteolytically processed into 2 fragments with opposite transcriptional properties
    Akihiko Yokoyama
    Chromatin Function in Leukemogenesis Project and Cancer Genomics Division, National Cancer Center Research Institute, Tokyo, Japan
    Blood 100:3710-8. 2002

Detail Information

Publications6

  1. ncbi Menin critically links MLL proteins with LEDGF on cancer-associated target genes
    Akihiko Yokoyama
    Department of Pathology, Stanford University School of Medicine, Stanford, CA 94305, USA
    Cancer Cell 14:36-46. 2008
    ..Thus, LEDGF critically associates with MLL and menin at the nexus of transcriptional pathways that are recurrently targeted in diverse diseases...
  2. ncbi A higher-order complex containing AF4 and ENL family proteins with P-TEFb facilitates oncogenic and physiologic MLL-dependent transcription
    Akihiko Yokoyama
    National Cancer Center Research Institute, Tokyo, Japan
    Cancer Cell 17:198-212. 2010
    ..Thus, AEP recruitment is an integral part of both physiological and pathological MLL-dependent transcriptional pathways. Bypass of its normal recruitment mechanisms is the strategy most frequently used by MLL oncoproteins...
  3. ncbi Proteolytically cleaved MLL subunits are susceptible to distinct degradation pathways
    Akihiko Yokoyama
    Division of Hematological Malignancy, National Cancer Center Research Institute, Tokyo 104 0045, Japan
    J Cell Sci 124:2208-19. 2011
    ..Our data demonstrate that the dissociated MLL subunits are subjected to distinct degradation pathways and thus not likely to have separate functions unless the degradation mechanisms are inhibited...
  4. ncbi Leukemia proto-oncoprotein MLL forms a SET1-like histone methyltransferase complex with menin to regulate Hox gene expression
    Akihiko Yokoyama
    Department of Pathology, Stanford University School of Medicine, Stanford, CA 94305, USA
    Mol Cell Biol 24:5639-49. 2004
    ..These studies link the menin tumor suppressor protein with the MLL histone methyltransferase machinery, with implications for Hox gene expression in development and leukemia pathogenesis...
  5. ncbi The menin tumor suppressor protein is an essential oncogenic cofactor for MLL-associated leukemogenesis
    Akihiko Yokoyama
    Department of Pathology, Stanford University School of Medicine, Stanford, California 94305, USA
    Cell 123:207-18. 2005
    ....
  6. ncbi Leukemia proto-oncoprotein MLL is proteolytically processed into 2 fragments with opposite transcriptional properties
    Akihiko Yokoyama
    Chromatin Function in Leukemogenesis Project and Cancer Genomics Division, National Cancer Center Research Institute, Tokyo, Japan
    Blood 100:3710-8. 2002
    ..These observations suggest that posttranslational modifications of MLL may participate in regulating its activity as a transcription factor and that this aspect of its function is perturbed by leukemogenic fusions...