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ABL1 — FUS

Text-mined interactions from Literome

Perrotti et al., Mol Cell Biol 2000 : BCR-ABL prevents c-jun mediated and proteasome dependent FUS ( TLS ) proteolysis through a protein kinase CbetaII dependent pathway ... The DNA binding activity of FUS ( also known as TLS ), a nuclear pro-oncogene involved in multiple translocations, is regulated by BCR-ABL in a protein kinase CbetaII ( PKCbetaII ) -dependent manner ... FUS proteolysis is induced by c-Jun, is suppressed by BCR-ABL or Jun kinase 1, and does not depend on c-Jun transactivation potential, ubiquitination, or its interaction with Jun kinase 1
Perrotti et al., Clin Cancer Res 2007 (Leukemia, Myelogenous, Chronic, BCR-ABL Positive...) : Here, we summarize the effects of increased BCR/ABL oncogenic activity on the expression and function of RNA binding proteins ( e.g., FUS , hnRNP A1, hnRNP E2, hnRNP K, and La/SSB ) with posttranscriptional and translational regulatory activities and their importance for the phenotype of BCR/ABL transformed hematopoietic progenitors