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Takayuki Itoh

Researcher at University of California, Davis

Publications -  44
Citations -  1798

Takayuki Itoh is an academic researcher from University of California, Davis. The author has contributed to research in topics: Progenitor cell & Oligodendrocyte. The author has an hindex of 20, co-authored 44 publications receiving 1689 citations. Previous affiliations of Takayuki Itoh include University of Pennsylvania & Shriners Hospitals for Children.

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Microglia Express CCR5, CXCR4, and CCR3, but of These, CCR5 Is the Principal Coreceptor for Human Immunodeficiency Virus Type 1 Dementia Isolates

TL;DR: It is found that virus pseudotyped with the DS-br and RC-br envelopes can infect cells transfected with CD4 in conjunction with the G-protein-coupled receptors APJ, CCR8, and GPR15, which have been previously implicated in HIV entry.
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AMPA glutamate receptor-mediated calcium signaling is transiently enhanced during development of oligodendrocytes.

TL;DR: Stage‐specific up‐regulation of edited GluR2‐free, and hence Ca2+‐permeable, AMPA‐GluR explains the selective susceptibility to excitotoxicity of cells at these stages of oligodendroglial differentiation, and is likely to be important to these cells in the trans‐synaptic Ca2 +‐signaling from glutamatergic neurons, which occurs in hippocampus in vivo.
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Caspase-3 expression by cerebellar granule neurons is regulated by calcium and cyclic AMP

TL;DR: It is concluded that, in immature CGNs, both caspase‐3 transcription and the subsequent processing of caspite‐3 are induced by a fall in [Ca2+]i, and elevating cyclic AMP content delays casp enzyme activity by a mechanism that does not require an increase in [ Ca2+]-i.
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Impaired regenerative response of primary sensory neurons in ZPK/DLK gene-trap mice.

TL;DR: Results indicate that ZPK/DLK is involved in regenerative responses of mammalian DRG neurons to axonal injury through activation of c-JUN.
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Oligodendroglial differentiation induces mitochondrial genes and inhibition of mitochondrial function represses oligodendroglial differentiation.

TL;DR: Mitochondrial DNA content per cell and acetyl CoA-related transcripts increased significantly, and the large buildup of cholesterol necessary for myelination appears to require mitochondrial production of acetyl-CoA, suggesting mechanisms for demyelination observed in mitochondrial disease.