Marie E Benoit
Overview
Explore the profile of Marie E Benoit including associated specialties, affiliations and a list of published articles.
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Articles
6
Citations
362
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Recent Articles
1.
Clarke E, Benoit M, Tenner A
Bio Protoc
. 2016 Apr;
3(23).
PMID: 27081666
Investigations of the activation processes involved in human monocytes and monocyte-derived macrophages and dendritic cells often required large numbers of cells that have not been possibly altered or activated by...
2.
Benoit M, Clarke E, Tenner A
Bio Protoc
. 2016 Apr;
3(17).
PMID: 27064237
To characterize macrophage gene expression profiles during the uptake of autologous apoptotic cells, we developed a unique, more physiologic system using primary human monocyte derived macrophages purified via a nonactivating...
3.
Benoit M, Hernandez M, Dinh M, Benavente F, Vasquez O, Tenner A
J Biol Chem
. 2012 Nov;
288(1):654-65.
PMID: 23150673
Complement protein C1q is induced in the brain in response to a variety of neuronal injuries, including Alzheimer disease (AD), and blocks fibrillar amyloid-β (fAβ) neurotoxicity in vitro. Here, we...
4.
Benoit M, Clarke E, Morgado P, Fraser D, Tenner A
J Immunol
. 2012 Apr;
188(11):5682-93.
PMID: 22523386
Deficiency in C1q, the recognition component of the classical complement cascade and a pattern recognition receptor involved in apoptotic cell clearance, leads to lupus-like autoimmune diseases characterized by auto-antibodies to...
5.
Benoit M, Tenner A
J Neurosci
. 2011 Mar;
31(9):3459-69.
PMID: 21368058
Activation of the complement cascade, a powerful effector mechanism of the innate immune system, is associated with neuroinflammation but also with elimination of inappropriate synapses during development. Synthesis of C1q,...
6.
Fonseca M, Chu S, Berci A, Benoit M, Peters D, Kimura Y, et al.
J Neuroinflammation
. 2011 Jan;
8(1):4.
PMID: 21235806
Background: Complement proteins and activation products have been found associated with neuropathology in Alzheimer's disease (AD). Recently, a C5a receptor antagonist was shown to suppress neuropathology in two murine models...