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pro vyhledávání: '"Timothy R Gamache"'
Autor:
Yoichi Araki, Ingie Hong, Timothy R Gamache, Shaowen Ju, Leonardo Collado-Torres, Joo Heon Shin, Richard L Huganir
Publikováno v:
eLife, Vol 9 (2020)
SynGAP is a synaptic Ras GTPase-activating protein (GAP) with four C-terminal splice variants: α1, α2, β, and γ. Although studies have implicated SYNGAP1 in several cognitive disorders, it is not clear which SynGAP isoforms contribute to disease.
Externí odkaz:
https://doaj.org/article/22e28034c08d4174946d8855570038c2
Autor:
Timothy R Gamache, Leonardo Collado-Torres, Yoichi Araki, Ingie Hong, Shaowen Ju, Richard L. Huganir, Joo Heon Shin
Publikováno v:
eLife, Vol 9 (2020)
eLife
eLife
SynGAP is a synaptic Ras GTPase-activating protein (GAP) with four C-terminal splice variants: α1, α2, β, and γ. Although studies have implicated SYNGAP1 in several cognitive disorders, it is not clear which SynGAP isoforms contribute to disease.
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::bc79625f1fe1c3a1f0b94d914dc007a0
https://doi.org/10.7554/elife.56273
https://doi.org/10.7554/elife.56273
Publikováno v:
J Neurosci
SynGAP is a potent regulator of biochemical signaling in neurons and plays critical roles in neuronal function. It was first identified in 1998, and has since been extensively characterized as a mediator of synaptic plasticity. Because of its involve
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::8b0f85a4ce743080386245eb92ff3ad6
https://europepmc.org/articles/PMC7046327/
https://europepmc.org/articles/PMC7046327/
Autor:
Timothy R Gamache, Leonardo Collado-Torres, Joo Heon Shin, Shaowen Ju, Richard L. Huganir, Ingie Hong, Yoichi Araki
SummarySynGAP is a synaptic Ras GTPase-activating protein (GAP) with four C-terminal splice variants: α1, α2, β, and γ. Although recent studies have implicatedSYNGAP1haploinsufficiency in ID/ASD pathogenesis, the degree to which each SynGAP isofo
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::83ff727799934137d918c191696d9a8b
Publikováno v:
Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease. 1852(9):1810-1823
A large body of evidence support major roles of mitochondrial dysfunction and insulin action in the Alzheimer's disease (AD) brain. However, interaction between cellular expression of β-amyloid (Aβ) and insulin resistance on mitochondrial metabolis
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::38d230c4ed580ede2b6c19dde7bf587f