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Andrea J. Tenner
Researcher at University of California, Irvine
Publications - 167
Citations - 14706
Andrea J. Tenner is an academic researcher from University of California, Irvine. The author has contributed to research in topics: Complement system & Classical complement pathway. The author has an hindex of 64, co-authored 152 publications receiving 13110 citations. Previous affiliations of Andrea J. Tenner include American Red Cross & Oak Ridge National Laboratory.
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Journal ArticleDOI
Cell surface expression of C1qRP/CD93 is stabilized by O-glycosylation.
Minha Park,Andrea J. Tenner +1 more
TL;DR: It is demonstrated that O‐glycosylation is important in the stable cell surface expression of C1qRP/CD93, a cell surface receptor predominantly expressed on monocytes, neutrophils, endothelial cells, and early stem cell precursors.
Journal ArticleDOI
Localization of the Site on the Complement Component C1q Required for the Stimulation of Neutrophil Superoxide Production
TL;DR: A specific conformation conferred by the collagen triple helix constitutes the functional receptor interaction site of the C1q-CLR and should direct the design of future specific therapeutic reagents to selectively modulate this response.
Journal ArticleDOI
Translational animal models for Alzheimer's disease: An Alzheimer's Association Business Consortium Think Tank.
Michael P. Vitek,Joseph A. Araujo,Michael Fossel,Barry D. Greenberg,Gareth R. Howell,Stacey J. Sukoff Rizzo,Nicholas T. Seyfried,Andrea J. Tenner,Paul R. Territo,Manfred Windisch,Lisa J. Bain,April Ross,Maria C. Carrillo,Bruce T. Lamb,Rebecca M. Edelmayer +14 more
TL;DR: The Alzheimer's Association Business Consortium Think Tank meeting as discussed by the authors focused on the unmet need to improve the discovery and successful development of Alzheimer's therapies by exploring the current state of AD animal models, identifying knowledge gaps and recommending actions for development of next-generation models with better predictability.
Journal ArticleDOI
Novel Aβ peptide immunogens modulate plaque pathology and inflammation in a murine model of Alzheimer's disease
Jun Zhou,Maria I. Fonseca,Rakez Kayed,Irma Arias Hernández,Scott D. Webster,O. Yazan,David H. Cribbs,David H. Cribbs,Charles G. Glabe,Andrea J. Tenner +9 more
TL;DR: It is suggested that a more specific immunogen such as oligomeric Aβ can be designed that achieves the goal of depleting amyloid while reducing potential detrimental inflammatory reactions.
Book ChapterDOI
The double-edged flower : Roles of complement protein C1q in neurodegenerative diseases
TL;DR: The observed diminished glial activation and reduced loss of neuronal integrity in a murine model overexpressing mutant human APP but lacking the ability to activate the classical complement cascade provide the first direct evidence for a detrimental role of C1q.