| the spectrum of oncogenic lesions activating NOTCH1 signaling in human T-ALL. | None |
| NOTCH1 nuclear interactome reveals key regulators of its transcriptional activity and oncogenic function. | None |
| Pharmacologic inhibition of vacuolar H+ ATPase reduces physiologic and oncogenic Notch signaling. | None |
| These results indicate that Notch1 signaling in human hematopoietic stem cells promotes CD8(+) single posistive T cell development, and that T cell leukemogenesis may require additional oncogenic factors other than Notch1 activation. | None |
| Garcinol downregulates Notch1 signaling via modulating miR-200c and suppresses oncogenic properties of PANC-1 cancer stem-like cells. | None |
| study identified a critical role for PRL2 phosphatase in the proliferation and survival of human T-ALL cells; demonstrated that PRL2 is important for the leukemogenic potential of oncogenic NOTCH1 in vivo | None |
| Our findings demonstrate Hsp90 blockade leads to ICN1 destabilization, providing an alternative strategy to antagonize oncogenic Notch1 signaling with Hsp90-selective inhibitors | None |
| This study indicates that NOTCH1 acts as an oncogene and that the NOTCH1 mutation (p.A465T) in the ligand-binding region causes the loss of tumorigenicity by downregulating the NOTCH1 pathway | None |
| Chloroquine (CQ) impairs the redox balance, induces ds DNA breaks and activates the DNA damage response. CQ also interferes with intracellular trafficking and processing of oncogenic NOTCH1 | None |
| Oncogenic forms of NOTCH1 lacking either the primary binding site for RBP-Jkappa or nuclear localization sequences retain the ability to associate with RBP-Jkappa and activate transcription. | None |