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Laurent Monney

Researcher at Brigham and Women's Hospital

Publications -  17
Citations -  3793

Laurent Monney is an academic researcher from Brigham and Women's Hospital. The author has contributed to research in topics: Apoptosis & Programmed cell death. The author has an hindex of 14, co-authored 17 publications receiving 3569 citations. Previous affiliations of Laurent Monney include University of Fribourg & Harvard University.

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Th1-specific cell surface protein Tim-3 regulates macrophage activation and severity of an autoimmune disease

TL;DR: In vivo administration of antibody to Tim-3 enhances the clinical and pathological severity of experimental autoimmune encephalomyelitis (EAE), a Th1-dependent autoimmune disease, and increases the number and activation level of macrophages.
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Bcl-2 prolongs cell survival after Bax-induced release of cytochrome c

TL;DR: It is shown that in cells transiently transfected with bax, Bax localizes to mitochondria and induces the release of cytochrome c, activation of caspase-3, membrane blebbing, nuclear fragmentation, and cell death, indicating that Bcl-2 can interfere with Bax killing downstream of and independently of cy tochrome c release.
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Apoptotic crosstalk between the endoplasmic reticulum and mitochondria controlled by Bcl-2.

TL;DR: A hitherto unrecognized, apoptotic crosstalk between the ER and mitochondria is uncovered that can be interrupted by ER-based Bcl-2, an agent interfering with N-linked glycosylations in the secretory system.
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Apoptosis without caspases: an inefficient molecular guillotine?

TL;DR: The current knowledge about caspase-independent apoptosis is reviewed, the strengths and weaknesses of the reasoning that led to its proposition are discussed and insights into its possible regulation and physiological significance are provided.
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Alphaviruses induce apoptosis in Bcl-2-overexpressing cells: evidence for a caspase-mediated, proteolytic inactivation of Bcl-2

TL;DR: It is shown that three cell types highly overexpressing functional Bcl‐2 displayed caspase‐3 activation and underwent apoptosis in response to infection with alphaviruses Semliki Forest and Sindbis as efficiently as vector control counterparts.