| The reciprocal role of Egr-1 and Sp family proteins in regulation of the PTP1B promoter in response to the p210 Bcr-Abl oncoprotein-tyrosine kinase. | None |
| Mechanisms of transformation by the BCR/ABL oncogene. | None |
| TFIIH functions are altered by the P210BCR-ABL oncoprotein produced on the Philadelphia chromosome. | None |
| Structure of the Bcr-Abl oncoprotein oligomerization domain. | None |
| Association of Bcr-Abl with the proto-oncogene Vav is implicated in activation of the Rac-1 pathway. | None |
| Inhibition of the Bcr-Abl oncoprotein by Bcr requires phosphoserine 354. | None |
| Intracellular antibody capture technology: application to selection of intracellular antibodies recognising the BCR-ABL oncogenic protein. | None |
| Oncogenic interaction between BCR-ABL and NUP98-HOXA9 demonstrated by the use of an in vitro purging culture system. | None |
| Cell context-specific effects of the BCR-ABL oncogene monitored in hematopoietic progenitors. | None |
| Bcr and Abl interaction: oncogenic activation of c-Abl by sequestering Bcr. | None |
| Phosphotyrosine mapping in Bcr/Abl oncoprotein using phosphotyrosine-specific immonium ion scanning. | None |
| Molecular mechanisms of transformation by the BCR-ABL oncogene. | None |
| Oncogenic v-Abl tyrosine kinase can inhibit or stimulate growth, depending on the cell context. | None |
| Mechanisms of transformation by the BCR-ABL oncogene: new perspectives in the post-imatinib era. | None |
| Translational regulation by the p210 BCR/ABL oncoprotein. | None |
| BCR/ABL oncogenic kinase promotes unfaithful repair of the reactive oxygen species-dependent DNA double-strand breaks. | None |
| the ability to regulate the cellular abundance of mitogen-activated protein kinase 7 contributes to the oncogenic potential of Abl kinases | None |
| Abl oncogene bypasses normal regulation of Jak/STAT activation. | None |
| Osteopontin is upregulated by BCR-ABL. | None |
| Overall these results show that OPN is deregulated by BCR-ABL oncogene and suggest that OPN could be involved in CML stem cell biology. | None |