C-terminal deletion of NOTCH1 intracellular domain (N1 ICD ) increases its stability but does not amplify and recapitulate N1 ICD -dependent signalling

摘要: Since the generation of a mouse strain conditionally expressing active intracellular domain Notch1 (N1ICD), many laboratories have exploited this model (RosaN1-ICD) to assess impact constitutive signalling activation in normal and pathological processes. It should be underscored that Cre-recombination leads expression C-terminally truncated form N1ICD (N1ICDdC) RosaN1-ICD mutant mice. Given no studies were undertaken delineate whether deletion region leaves intact function, stable cell lines with single targeted integration inducible N1ICDdC generated. We found C-terminal stabilized protein but did not promote activity Notch responsive promoters. Furthermore, despite higher levels, failed phenocopy promotion anchorage-independent growth. Our results thus suggest plays role shaping response. Therefore, it taken into consideration is when interpreting phenotypes