ADAM10 overexpression dysregulates Notch signaling in favor of myeloid derived suppressor cell (MDSC) accumulation that deferentially modulates the host response depending on immune stimuli and interaction with mast cells.
Although the physiological consequences of Notch signaling in hematopoiesis have been extensively studied, the differential effects of individual notch cleavage products remain to be elucidated. Given that a disintegrin and metalloproteinase 10 (ADAM10) is a critical regulator of Notch and that its...
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| Format: | Others |
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VCU Scholars Compass
2013
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| Online Access: | http://scholarscompass.vcu.edu/etd/3196 http://scholarscompass.vcu.edu/cgi/viewcontent.cgi?article=4195&context=etd |