Université de Sherbrooke

About: Université de Sherbrooke is a education organization based out in Sherbrooke, Quebec, Canada. It is known for research contribution in the topics: Population & Receptor. The organization has 14922 authors who have published 28783 publications receiving 792511 citations. The organization is also known as: Universite de Sherbrooke & Sherbrooke University.

Preparation of Azobenzene-Containing Amphiphilic Diblock Copolymers for Light-Responsive Micellar Aggregates

Abstract: Diblock copolymers composed of a side-chain liquid crystalline azobenzene-containing polymethacrylate and poly(tert-butyl acrylate) (PAzoMA-b-PtBA) were prepared using atom-transfer radical polymerization (ATRP). After subsequent selective hydrolysis of PtBA yielding poly(acrylic acid) (PAA), amphiphilic diblock copolymers of PAzoMA-b-PAA were obtained. Aggregation of either PAzoMA or PAA block occurs in solvents selective for one of the blocks. Adding water into dioxane solution of PAzoMA-b-PAA forms micellar aggregates due to the hydrophobic PAzoMA block. Under alternating UV and visible light illumination, reversible changes in micellar aggregates, for both core-shell micelles and vesicles, took place as a result of the reversible trans-cis photoisomerization of azobenzene mesogens in PAzoMA.

MEK/ERK signaling pathway regulates the expression of Bcl‐2, Bcl‐XL, and Mcl‐1 and promotes survival of human pancreatic cancer cells

Abstract: Background and aims: Growth factors are well known for their participation in the regulation of cell proliferation and survival. However, the intracellular signaling pathways by which growth factors promote survival are still poorly understood. In the present study, using the MIA PaCa-2 cell line, a well-established model of pancreatic cancer cells, we analyzed the roles of ERK1/2 activities in the regulation of cell survival and investigated some of the mechanisms involved. Methods: The ability of the MEK inhibitor PD98059 to modulate survival of the MIA PaCa-2 cells was evaluated, and the responses were correlated with expression of Bcl-2 homologs and caspases 1, 3, 6, 8, and 9 activities. Results. Herein, we showed that inhibition of ERK1/2 activities caused (1) a G1 arrest; (2) a down-regulation of the expression levels of the anti-apoptotic homologs Bcl-2, Mcl-1, and Bcl-XL without affecting the pro-apoptotic levels of Bax and Bak; (3) a promotion of caspases 3, 6, 8, and 9 activities; (4) a stimulation of PARP cleavage; and (5) a programmed cell death by apoptosis. Conclusion: Our data suggest that activation of the ERK pathway functions to protect pancreatic tumor cells from apoptosis as well as to regulate their progression in the cell cycle. J. Cell. Biochem. 79:355–369, 2000. © 2000 Wiley-Liss, Inc.