scispace - formally typeset
H

Hideki Sanjo

Researcher at Shinshu University

Publications -  53
Citations -  25146

Hideki Sanjo is an academic researcher from Shinshu University. The author has contributed to research in topics: Signal transduction & MAP kinase kinase kinase. The author has an hindex of 30, co-authored 46 publications receiving 24075 citations. Previous affiliations of Hideki Sanjo include Hyogo College of Medicine & Osaka University.

Papers
More filters
Journal ArticleDOI

A Toll-like receptor recognizes bacterial DNA.

TL;DR: It is shown that cellular response to CpG DNA is mediated by a Toll-like receptor, TLR9, and vertebrate immune systems appear to have evolved a specific Toll- like receptor that distinguishes bacterial DNA from self-DNA.
Journal Article

Cutting edge: Toll-like receptor 4 (TLR4)-deficient mice are hyporesponsive to lipopolysaccharide: evidence for TLR4 as the Lps gene product.

TL;DR: It is demonstrated that TLR4 is the gene product that regulates LPS response, and a single point mutation of the amino acid that is highly conserved among the IL-1/Toll receptor family is found.
Journal ArticleDOI

Differential roles of TLR2 and TLR4 in recognition of gram-negative and gram-positive bacterial cell wall components.

TL;DR: It is demonstrated that TLR2 and TLR4 recognize different bacterial cell wall components in vivo andTLR2 plays a major role in Gram-positive bacterial recognition.
Journal ArticleDOI

Role of adaptor TRIF in the MyD88-independent toll-like receptor signaling pathway.

TL;DR: It is shown that TRIF is essential for TLR3- and TLR4-mediated signaling pathways facilitating mammalian antiviral host defense and complete loss of nuclear factor kappa B activation in response toTLR4 stimulation is demonstrated.
Journal ArticleDOI

Small anti-viral compounds activate immune cells via the TLR7 MyD88-dependent signaling pathway.

TL;DR: It is shown that the imidazoquinolines activate immune cells via the Toll-like receptor 7 (TLR7)-MyD88–dependent signaling pathway, and that neither MyD88- nor TLR7-deficient mice showed any inflammatory cytokine production by macrophages, proliferation of splenocytes or maturation of dendritic cells.