T
Timothy Y. Huang
Researcher at Discovery Institute
Publications - 46
Citations - 2738
Timothy Y. Huang is an academic researcher from Discovery Institute. The author has contributed to research in topics: Cofilin & Neurodegeneration. The author has an hindex of 19, co-authored 38 publications receiving 1839 citations. Previous affiliations of Timothy Y. Huang include Scripps Research Institute & Sanford-Burnham Institute for Medical Research.
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Journal ArticleDOI
TREM2 Is a Receptor for β-Amyloid that Mediates Microglial Function
Yingjun Zhao,Xi-Lin Wu,Xiaoguang Li,Lu Lin Jiang,Xun Gui,Yan Liu,Yu Sun,Bing Zhu,Juan C. Piña-Crespo,Muxian Zhang,Ningyan Zhang,Xiaochun Chen,Guojun Bu,Zhiqiang An,Timothy Y. Huang,Huaxi Xu,Huaxi Xu +16 more
TL;DR: TREM2 is demonstrated as a microglial Aβ receptor transducing physiological and AD-related pathological effects associated with Aβ, and TREM2 interaction with its signaling adaptor DAP12 is enhanced by A β, regulating downstream phosphorylation of SYK and GSK3β.
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Molecular and cellular mechanisms underlying the pathogenesis of Alzheimer's disease.
TL;DR: This work discusses glial dysfunction in AD with emphasis on neuronal and glial receptors that mediate Aβ-induced toxicity, and discusses other critical factors that may affect AD pathogenesis, including genetics, aging, variables related to environment, lifestyle habits, and APOE.
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Cofilin phosphatases and regulation of actin dynamics.
TL;DR: Cofilin is a ubiquitous actin-binding factor required for the reorganization of actin filaments in eukaryotes and the dephosphorylation of cofilin enables its actin severing and depolymerizing activity and drives directional cell motility.
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Dysregulation of Ubiquitin-Proteasome System in Neurodegenerative Diseases
TL;DR: Recent findings describing various aspects of UPS dysregulation in neurodegenerative disorders such as Alzheimer's disease, Parkinson’s disease, and Huntington's disease are reviewed.
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Reactive oxygen species regulate a slingshot-cofilin activation pathway.
TL;DR: It is suggested that the formation of ROS by NADPH oxidases engages a SSH-1L-cofilin pathway to regulate cytoskeletal organization and cell migration.