2000
DOI: 10.1038/sj.onc.1203396
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The ETV6-NTRK3 gene fusion encodes a chimeric protein tyrosine kinase that transforms NIH3T3 cells

Abstract: The congenital ®brosarcoma t(12;15)(p13;q25) rearrangement splices the ETV6 (TEL) gene on chromosome 12p13 in frame with the NTRK3 (TRKC) neurotrophin-3 receptor gene on chromosome 15q25. Resultant ETV6-NTRK3 fusion transcripts encode the helix ± loop ± helix (HLH) dimerization domain of ETV6 fused to the protein tyrosine kinase (PTK) domain of NTRK3. We show here that ETV6-NTRK3 homodimerizes and is capable of forming heterodimers with wild-type ETV6. Moreover, ETV6-NTRK3 has PTK activity and is autophosphory… Show more

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Cited by 156 publications
(135 citation statements)
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“…Tandem mass spectrometry analysis was used to compare proteins bound to HA-EN under both conditions. In untreated cells, we observed EN in high abundance as well as the previously described EN interactor, PLCg (Wai et al, 2000) (data not shown). Strikingly, the most abundant EN interactor in untreated cells was another IRS family member, IRS4.…”
Section: En Interacts With Irs4 In Hek293 Cells and This Is Reversed supporting
confidence: 58%
See 1 more Smart Citation
“…Tandem mass spectrometry analysis was used to compare proteins bound to HA-EN under both conditions. In untreated cells, we observed EN in high abundance as well as the previously described EN interactor, PLCg (Wai et al, 2000) (data not shown). Strikingly, the most abundant EN interactor in untreated cells was another IRS family member, IRS4.…”
Section: En Interacts With Irs4 In Hek293 Cells and This Is Reversed supporting
confidence: 58%
“…Wild-type NTRK3 utilizes the juxtamembrane residue Y516 to bind adapters such as Shc, SH2B or the PI3K p85 subunit to activate downstream signaling pathways (Huang and Reichardt, 2003). However, direct binding of EN to known NTRK3 adapters has not been demonstrable (Wai et al, 2000;Lannon and Sorensen, 2005), likely because Tyr-516 is absent from EN due to the position of the t(12;15) fusion point (Wai et al, 2000). Instead, EN directly binds the major insulin-like growth factor 1 receptor (IGF1R) substrate, insulin receptor substrate 1 (IRS1) through an NPXY motif in the EN C-terminus and the PTB domain of IRS1 (Lannon et al, 2004).…”
Section: Introductionmentioning
confidence: 99%
“…ABL is known to be involved as a fusion partner in other oncogenes, such as Gag/ABL and BCR/ABL. ABL oncoproteins (BCR/ABL and ETV6/ABL), and other ETV6/TK fusion proteins (ETV6/PDGFRB, ETV6/ JAK2 and ETV6/NTRK3) transform growth-factordependent hematopoietic cell lines to factor-independence or transform ®broblast cell lines to anchorage independence (Carroll et al, 1996;Golub et al, 1996;Lugo and Witte, 1989;Schwaller et al, 1998;Wai et al, 2000).…”
Section: Introductionmentioning
confidence: 99%
“…Subsequently, several translocations involving ETV6 and various partners have been documented in di erent hematological malignancies as well as in congenital ®brosarcoma, most of these leading to the formation of chimeric fusion products (reviewed in Rubnitz et al, 1999). Many of the resulting fusion proteins have been shown to transform cells in vitro (Carroll et al, 1996;Lacronique et al, 1997;Hannemann et al, 1998;Buijs et al, 2000;Liu et al, 2000;Wai et al, 2000) or to induce hematological malignancies in mice (Tomasson et al, 1999;Schwaller et al, 1998;Carron et al, 2000) Also, allelic loss at the ETV6 locus on the short arm of chromosome 12 has been observed in various cancers (reviewed in Aissani et al, 1999) suggesting that the human ETV6 gene lies within a region frequently altered in cancer cells.…”
mentioning
confidence: 99%