| Genetic and epigenetic silencing of microRNA-203 enhances ABL1 and BCR-ABL1 oncogene expression. | None |
| Differences in oncogenic potency but not target cell specificity distinguish the two forms of the BCR/ABL oncogene. | None |
| Intrinsic differences between the catalytic properties of the oncogenic NUP214-ABL1 and BCR-ABL1 fusion protein kinases. | None |
| The 5 non-coding region of the BCR/ABL oncogene augments its ability to stimulate the growth of immature lymphoid cells. | None |
| PTPROt inactivates the oncogenic fusion protein BCR/ABL and suppresses transformation of K562 cells. | None |
| Cloning, expression, purification and functional characterization of the oligomerization domain of Bcr-Abl oncoprotein fused to the cytoplasmic transduction peptide. | None |
| Suppression of vascular endothelial growth factor (VEGF) expression by targeting the Bcr-Abl oncogene and protein tyrosine kinase activity in Bcr-Abl-positive leukaemia cells. | None |
| Reciprocal t(9;22) ABL/BCR fusion proteins: leukemogenic potential and effects on B cell commitment. | None |
| reciprocal ABL/BCR fusion proteins as second oncogenes encoded by the t(9;22) in addition to BCR/ABL | None |
| Ascorbate/menadione-induced oxidative stress kills cancer cells that express normal or mutated forms of the oncogenic protein Bcr-Abl. An in vitro and in vivo mechanistic study. | None |
| The proximal signaling network of the BCR-ABL1 oncogene shows a modular organization. | None |
| Rho kinase regulates the survival and transformation of cells bearing oncogenic forms of KIT, FLT3, and BCR-ABL. | None |
| Oncogenic stress induced by acute hyper-activation of Bcr-Abl leads to cell death upon induction of excessive aerobic glycolysis. | None |
| Changing the subcellular location of the oncoprotein Bcr-Abl using rationally designed capture motifs. | None |
| Cyclin-dependent kinase 7/9 inhibitor SNS-032 abrogates FIP1-like-1 platelet-derived growth factor receptor alpha and bcr-abl oncogene addiction in malignant hematologic cells. | None |
| TAT-CC fusion protein depresses the oncogenicity of BCR-ABL through interrupting its oligomerization. | None |
| Transcriptional suppression of BACH2 by the Bcr-Abl oncoprotein is mediated by PAX5. | None |
| The tyrosine phosphatase TC48 interacts with and inactivates the oncogenic fusion protein BCR-Abl but not cellular Abl. | None |
| Tyrosine kinase activity and transformation potency of bcr-abl oncogene products. | None |
| BCR-ABL residues interacting with ponatinib are critical to preserve the tumorigenic potential of the oncoprotein. | None |