My lab has recently found Notch ICD stability is regulated in a cell cycle dependent manner. We have shown this in HEK293 cells. This work is currently under revision. We want to move this into the embryo and into a translational context. In the embryo we wish to see how this links Notch function in cell differentiation with cell proliferation in the variety of tissue contexts where Notch plays a role.
Hormone therapy (endocrine therapy) is used to block (ER+) breast cancers which are stimulated by the hormone oestrogen, by causing cell cycle arrest. We would like to know if this treatment of breast cancer cell lines, causing cell cycle arrest, changes levels of NICD and if this would then prolong the half life of NICD and provide a possible mechanism of resistance to these drugs which would have significant translational implications