Protein kinase C eta is activated in reactive astrocytes of an Alzheimer's disease mouse model: Evidence for its immunoregulatory function in primary astrocytes-Reference-Cited by-同舟云学术

Protein kinase C eta is activated in reactive astrocytes of an Alzheimer's disease mouse model: Evidence for its immunoregulatory function in primary astrocytes

Published:2020-10-17 Issue:3 Volume:69 Page:697-714
ISSN:0894-1491
Container-title:Glia
language:en
Short-container-title:Glia

Author:

Muraleedharan Amitha¹²^ORCID,Rotem‐Dai Noa¹,Strominger Itai¹²,Anto Nikhil Ponnoor¹,Isakov Noah¹,Monsonego Alon¹²,Livneh Etta¹

Affiliation:

1. The Shraga Segal Department of Microbiology, Immunology, and Genetics, Faculty of Health Sciences Ben‐Gurion University of the Negev Beer‐Sheva Israel

2. The National Institute of Biotechnology in the Negev, Zlotowski Neuroscience Center, and Regenerative Medicine and Stem Cell Research Center Ben‐Gurion University of the Negev Beer‐Sheva Israel

Funder

Israel Science Foundation

Publisher

Wiley

Subject

Cellular and Molecular Neuroscience,Neurology

Link

https://onlinelibrary.wiley.com/doi/pdf/10.1002/glia.23921

Reference100 articles.

1. Gain-of-function mutations in protein kinase Cα (PKCα) may promote synaptic defects in Alzheimer’s disease

2. PKC signaling deficits: a mechanistic hypothesis for the origins of Alzheimer's disease

3. Amram S. Iram T. Lazdon E. Vassar R. Porath I. B. &Frenkel D.(2019).Astrocyte senescence in an Alzheimer's disease mouse model is mediated by TGF‐β1 and results in neurotoxicity. Cold Spring Harbor Laboratory bioRxiv.