Atsuko Hayashida
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View article: Sulfated motifs in heparan sulfate inhibit <i>Streptococcus pneumoniae</i> adhesion onto fibronectin and attenuate corneal infection
Sulfated motifs in heparan sulfate inhibit <i>Streptococcus pneumoniae</i> adhesion onto fibronectin and attenuate corneal infection Open
A large number of bacterial pathogens bind to host extracellular matrix (ECM) components. For example, many Gram‐negative and Gram‐positive pathogens express binding proteins for fibronectin (FN) on their cell surface. Mutagenesis studies …
View article: Syndecan-1 Promotes Streptococcus pneumoniae Corneal Infection by Facilitating the Assembly of Adhesive Fibronectin Fibrils
Syndecan-1 Promotes Streptococcus pneumoniae Corneal Infection by Facilitating the Assembly of Adhesive Fibronectin Fibrils Open
Bacterial pathogens have evolved several ingenious mechanisms to subvert host cell biology for their pathogenesis. Bacterial attachment to the host ECM establishes a niche to grow and is considered one of the critical steps of infection. T…
View article: 2- O -Sulfated Domains in Syndecan-1 Heparan Sulfate Inhibit Neutrophil Cathelicidin and Promote Staphylococcus aureus Corneal Infection
2- O -Sulfated Domains in Syndecan-1 Heparan Sulfate Inhibit Neutrophil Cathelicidin and Promote Staphylococcus aureus Corneal Infection Open
Ablation of syndecan-1 in mice is a gain of function mutation that enables mice to significantly resist infection by several bacterial pathogens. Syndecan-1 shedding is induced by bacterial virulence factors, and inhibition of shedding att…
View article: Host syndecan-1 promotes listeriosis by inhibiting intravascular neutrophil extracellular traps
Host syndecan-1 promotes listeriosis by inhibiting intravascular neutrophil extracellular traps Open
Heparan sulfate proteoglycans (HSPGs) are at the forefront of host-microbe interactions. Molecular and cell-based studies suggest that HSPG-pathogen interactions promote pathogenesis by facilitating microbial attachment and invasion of hos…
View article: <i>EXTL3</i> mutations cause skeletal dysplasia, immune deficiency, and developmental delay
<i>EXTL3</i> mutations cause skeletal dysplasia, immune deficiency, and developmental delay Open
We studied three patients with severe skeletal dysplasia, T cell immunodeficiency, and developmental delay. Whole-exome sequencing revealed homozygous missense mutations affecting exostosin-like 3 (EXTL3), a glycosyltransferase involved in…