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In JoVE (1)
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Articles by Tambudzai Shamu in JoVE
चूहे में Cajal नेटवर्क (आईसीसी) के बीचवाला कक्ष के दृश्य
Yu Chen1,2, Tambudzai Shamu2, Hui Chen3, Peter Besmer3, Charles L. Sawyers2,4, Ping Chi1,5
1Department of Medicine, Memorial Sloan Kettering Cancer Center, 2Human Oncology and Pathogenesis Program, Memorial Sloan Kettering Cancer Center, 3Developmental Biology Program, Memorial Sloan Kettering Cancer Center, 4Howard Hughes, Medical Institute, 5Laboratory of Chromatin Biology and Epigenetics, The Rockefeller University
Cajal (आईसीसी) के बीचवाला कोशिकाओं जठरांत्र संबंधी मार्ग (जीआई) के पेसमेकर की कोशिकाओं रहे हैं. वे चिकनी मांसपेशियों की कोशिकाओं और बाद ganglionic neuronal सैनिक सिकुड़ना विनियमित फाइबर के बीच जटिल नेटवर्क के रूप में. यहाँ, हम immunofluorescence पार के अनुभागीय तरीकों और पूरे माउंट murine आईसीसी नेटवर्क के दृश्य प्रस्तुत करते हैं.
Other articles by Tambudzai Shamu on PubMed
Nature. Oct, 2010 | Pubmed ID: 20927104
Gastrointestinal stromal tumour (GIST) is the most common human sarcoma and is primarily defined by activating mutations in the KIT or PDGFRA receptor tyrosine kinases. KIT is highly expressed in interstitial cells of Cajal (ICCs)-the presumed cell of origin for GIST-as well as in haematopoietic stem cells, melanocytes, mast cells and germ cells. Yet, families harbouring germline activating KIT mutations and mice with knock-in Kit mutations almost exclusively develop ICC hyperplasia and GIST, suggesting that the cellular context is important for KIT to mediate oncogenesis. Here we show that the ETS family member ETV1 is highly expressed in the subtypes of ICCs sensitive to oncogenic KIT mediated transformation, and is required for their development. In addition, ETV1 is universally highly expressed in GISTs and is required for growth of imatinib-sensitive and resistant GIST cell lines. Transcriptome profiling and global analyses of ETV1-binding sites suggest that ETV1 is a master regulator of an ICC-GIST-specific transcription network mainly through enhancer binding. The ETV1 transcriptional program is further regulated by activated KIT, which prolongs ETV1 protein stability and cooperates with ETV1 to promote tumorigenesis. We propose that GIST arises from ICCs with high levels of endogenous ETV1 expression that, when coupled with an activating KIT mutation, drives an oncogenic ETS transcriptional program. This differs from other ETS-dependent tumours such as prostate cancer, melanoma and Ewing sarcoma where genomic translocation or amplification drives aberrant ETS expression. It also represents a novel mechanism of oncogenic transcription factor activation.