Kinnosuke Yahiro

TL;DR: 3T provides an approach to interrogate the thousands of predicted uORFs in mammalian genomes, characterize the importance of uORF biology for regulation, and generate fundamental insights into u ORF mutation-based diseases.

TL;DR: It is reported that mice deficient in protein tyrosine phosphatase receptor type Z (Ptprz) do not show mucosal damage by VacA, although VacA is incorporated into the gastric epithelial cells to the same extent as in wild-type mice, and pleiotrophin (PTN), an endogenous ligand of Ptprz, induced gastritis specifically in PtprZ+/+ mice when administered orally.

TL;DR: Immunoprecipitation with anti-human RPTPβ antibody of solubilized membrane preparations previously incubated with VacA or heat-inactivated VacA demonstrated thatRPTPβ bound native, but not denatured, VacA, and acidic and alkaline treatments were associated with activation of VacA and increased binding to the cell surface RPTP β.

TL;DR: It is suggested that early activation of mast cells by VacA may be the host early response to clear the bacteria and also may contribute to the pathogenesis of H. pylori-induced gastritis.

TL;DR: Results support the conclusion that VacA activates the PI3K/Akt signaling pathway, resulting in phosphorylation and inhibition of GSK3β, and subsequent translocation of β-catenin to the nucleus, consistent with effects of VacA on β- catenin-regulated transcriptional activity.