Splicing factor hnRNPH drives an oncogenic splicing switch in gliomas

• Clare V LeFave ^[1] ; Massimo Squatrito ^[2] ; Sandra Vorlova ^[1] ; Gina L Rocco ^[1] ; Cameron W Brennan ^[3] ; Eric C Holland ^[4] ; Ying-Xian Pan ^[5] ; Luca Cartegni ^[1]
  1. [1] Memorial Sloan Kettering Cancer Center

     Memorial Sloan Kettering Cancer Center

     Estados Unidos

     
  2. [2] Brain Tumor Center, MSKCC, New York, NY, USA; Department of Cancer Biology and Genetics, MSKCC, New York, NY, USA
  3. [3] Brain Tumor Center, MSKCC, New York, NY, USA; Department of Neurosurgery, MSKCC, New York, NY, USA
  4. [4] Brain Tumor Center, MSKCC, New York, NY, USA; Department of Cancer Biology and Genetics, MSKCC, New York, NY, USA; Department of Neurosurgery, MSKCC, New York, NY, USA
  5. [5] Department of Neurology, MSKCC, New York, NY, USA

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• Localización: EMBO journal: European Molecular Biology Organization, ISSN 0261-4189, Vol. 30, Nº. 19, 2011, págs. 4084-4097
• Idioma: inglés
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• Resumen

  • This study reveals two alternative splicing events that contribute to the development of glioma. HnRNPH is shown to control production of a pro-survival splice variant of the death-domain adaptor protein IG20-MADD and the motility-enhancing isoform of the RON receptor tyrosine kinase.