Year: 2018
Type: dissertation
Abstract: Cell size within animal tissues is highly uniform. Previous data has shown that the p38 pathway plays a role in this regulation. The mTOR inhibitor Torin2 reversibly decreases cell size, and upregulates p38 activity. After removal of Torin2 (recovery phase), p38 activity continues to be upregulated. Chemical inhibition of the p38 pathway, but not ERK and JNK pathways, delays the ability of cells to recover their original size. The inability of cells with inhibited p38 to recover in size is not due to continued mTOR inhibition during recovery. Genetic knockdown of p38 itself does not, whereas knockdown of its upstream effector MKK3 but not MKK6 does. In addition, our lab has generated doxycycline inducible cell lines that can express inactive forms of MKK3 and MKK6. Overexpression of inactive MKK3 in conjunction with simultaneous knockdown of endogenous MKK3, but not MKK6, may prevent cell size recovery.
Source: TSpace (University of Toronto)
Author: Chun Yin Bosco Leung
Language: English
Subfield: Molecular Biology
Domain: Life Sciences
Open Access status: green
OpenAlex ID: W3093883954