Akihiko Yokoyama

Summary

Affiliation: National Cancer Center
Country: Japan

Publications

  1. pmc 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. pmc 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. pmc 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. pmc 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 request reprint 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 request reprint 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
  7. pmc MLL fusion proteins link transcriptional coactivators to previously active CpG-rich promoters
    Hiroshi Okuda
    Laboratory for Malignancy Control Research, Medical Innovation Center, Kyoto University Graduate School of Medicine, Kyoto 606 8501, Japan, Division of Hematological Malignancy, National Cancer Center Research Institute, Tokyo 104 0045, Japan, Department of Molecular Oncology and Leukemia Program Project, Research Institute for Radiation Biology and Medicine, Hiroshima University, Hiroshima 734 8553, Japan and Department of Molecular Biology and Medicine, Laboratory for System Biology and Medicine LSBM, Research Center for Advanced Science and Technology RCAST, The University of Tokyo, Tokyo 153 8904, Japan
    Nucleic Acids Res 42:4241-56. 2014

Collaborators

Detail Information

Publications7

  1. pmc 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. pmc 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. pmc 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. pmc 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 request reprint 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 request reprint 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...
  7. pmc MLL fusion proteins link transcriptional coactivators to previously active CpG-rich promoters
    Hiroshi Okuda
    Laboratory for Malignancy Control Research, Medical Innovation Center, Kyoto University Graduate School of Medicine, Kyoto 606 8501, Japan, Division of Hematological Malignancy, National Cancer Center Research Institute, Tokyo 104 0045, Japan, Department of Molecular Oncology and Leukemia Program Project, Research Institute for Radiation Biology and Medicine, Hiroshima University, Hiroshima 734 8553, Japan and Department of Molecular Biology and Medicine, Laboratory for System Biology and Medicine LSBM, Research Center for Advanced Science and Technology RCAST, The University of Tokyo, Tokyo 153 8904, Japan
    Nucleic Acids Res 42:4241-56. 2014
    ..Our results indicate that such chromatin context-dependent gene activation is the fundamental mechanism by which MLL fusion proteins maintain the expression of the cellular memory/hematopoietic stem cell program genes. ..