Helicobacter pylori: preying on SIVA for survival in the stomach.
Journal
The Journal of clinical investigation
ISSN: 1558-8238
Titre abrégé: J Clin Invest
Pays: United States
ID NLM: 7802877
Informations de publication
Date de publication:
01 05 2020
01 05 2020
Historique:
pubmed:
7
4
2020
medline:
22
1
2021
entrez:
7
4
2020
Statut:
ppublish
Résumé
Infection with the Gram-negative bacterium Helicobacter pylori remains the most important modifiable risk factor for the development of gastric cancer, a leading cause of cancer-related deaths worldwide. How the interactions between H. pylori and its host shape the gastric environment during chronic infection warrants further investigation. In this issue of the JCI, Palrasu et al. used human cell lines and mouse models to provide mechanistic insight into H. pylori's ability to delay apoptosis in gastric epithelial cells by actively driving the degradation of a proapoptotic factor, SIVA1. Their findings suggest that promoting the survival of gastric epithelial cells has implications not only for H. pylori pathogenesis but for host tumorigenesis.
Identifiants
pubmed: 32250343
pii: 135508
doi: 10.1172/JCI135508
pmc: PMC7190974
doi:
pii:
Substances chimiques
Bacterial Proteins
0
Types de publication
Journal Article
Research Support, N.I.H., Extramural
Research Support, Non-U.S. Gov't
Comment
Langues
eng
Sous-ensembles de citation
IM
Pagination
2183-2185Subventions
Organisme : NIDDK NIH HHS
ID : K08 DK122116
Pays : United States
Organisme : NIDDK NIH HHS
ID : P30 DK052574
Pays : United States
Organisme : NIDDK NIH HHS
ID : R01 DK094989
Pays : United States
Organisme : NIDDK NIH HHS
ID : R01 DK105129
Pays : United States
Commentaires et corrections
Type : CommentOn
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