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Bortezomib reverses a post‐translational mechanism of tumorigenesis for patched1 haploinsufficiency in medulloblastoma
Authors:Eri Taniguchi PhD  Min Jung Cho MD  Benjamin R. Arenkiel PhD  Mark S. Hansen  Omar J. Rivera PhD  Amanda T. McCleish  Stephen J. Qualman MD  Denis C. Guttridge PhD  Matthew P. Scott PhD  Mario R. Capecchi PhD  Charles Keller MD
Affiliation:1. Departments of Cellular & Structural Biology and Pediatrics, Greehey Children's Cancer Research Institute, University of Texas Health Science Center, San Antonio, Texas;2. Howard Hughes Medical Institute and Department of Human Genetics, University of Utah, Salt Lake City, Utah;3. Department of Laboratory Medicine, Columbus Children's Hospital, Children's Research Institute, Columbus, Ohio;4. Human Cancer Genetics Program, The Ohio State University College of Medicine, Columbus, Ohio;5. Howard Hughes Medical Institute and Departments of Developmental Biology, Genetics, and Bioengineering, Stanford University School of Medicine, Stanford, California
Abstract:
Keywords:bortezomib  haploinsufficiency  hedgehog  medulloblastoma  patched1  proteasome
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