aav-hgfap-gfp-shctrl (Addgene inc)
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Addgene inc
aav-hgfap-gfp-shctrl
Aav Hgfap Gfp Shctrl, supplied by Addgene inc, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/aav-hgfap-gfp-shctrl/aav+hgfap+gfp+shctrl/pm40409253-302-58-70
Average 90 stars, based on 1 article reviews
Aav Hgfap Gfp Shctrl, supplied by Addgene inc, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/aav-hgfap-gfp-shctrl/aav+hgfap+gfp+shctrl/pm40409253-302-58-70
Average 90 stars, based on 1 article reviews
aav-hgfap-gfp-shctrl - by Bioz Stars,
2026-09
90/100 stars
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other:Article Title: GADD45G operates as a pathological sensor orchestrating reactive gliosis and neurodegeneration. Article Snippet: Article GADD45G operates as a pathological sensor orchestrating reactive gliosis and neurodegeneration Highlights • Diverse pathological stimuli upregulate GADD45G in astrocytes • Astrocytic GADD45G drives neuropathology via autonomous and nonautonomous actions • GADD45G interacts with MAP3K4 to activate neuroimmune signaling in astrocytes • GADD45G inhibition mitigates pathology and behavior deficits in an AD mouse model Authors Tianjin Shen, Wenjiao Tai, Dongfang Jiang, Shuaipeng Ma, Xiaoling Zhong, Yuhua Zou, Chun-Li Zhang Correspondence chun-li.zhang@utsouthwestern.edu In brief Shen et al. identify GADD45G as an astrocytic sensor of diverse pathological stimuli and show that it drives reactive gliosis, neuroinflammation, and synapse loss through cell-autonomous and -nonautonomous mechanisms.. Conversely, GADD45G inhibition mitigates histological and behavioral pathology in an Alzheimer’s disease model, highlighting it as a potential therapeutic target.. Shen et al., 2025, Neuron 113, 2176–2195 July 9, 2025 © 2025 Elsevier Inc. All rights are reserved, including those for text and data mining, AI training, and similar technologies. https://doi.org/10.1016/j.neuron.2025.04.033 ll |