ArticleThrombosis journal2025
Endoplasmic reticulum protein 29 negatively regulates platelet functions and thrombosis in mice.
Article in Thrombosis journal, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
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Who cites it
3 citing papers in PubMed.
- Endoplasmic Reticulum Redoxome: Protein Folding and Beyond.Biochemistry · 2026Review
- Thiol Isomerases: Enzymatic Mechanisms, Models of Oxidation, and Antagonism by Galloylated Polyphenols.Antioxidants (Basel, Switzerland) · 2025Review
- Extracellular PDI in thrombosis and vascular injury.Thrombosis journal · 2025Review
Corrections and comments
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Authors and funding
7 authors.
Funding
Abstract
backgroundSeveral members of protein disulfide isomerase (PDI) family with the CXYC active motif such as PDI, ERp57, ERp72, ERp46, ERp5 and TMX1 have important roles in platelet functions and thrombosis. These members contribute to the network of redox regulation of platelet activities. However, whether other PDI family members without the CXYC motif such as ERp29, have a role in these processes remains unknown.
aimsTo determine the role of ERp29 in platelet functions and thrombosis.
methodsThe phenotypes of platelet-specific ERp29-deficient (Pf4-Cre/ERp29
resultsCompared with WT mice, Pf4-Cre/ERp29 CONCLUSION(S): ERp29 is the first disulfide isomerase without the CXYC motif that negatively regulates platelet function. This study provides new insight into the redox network controlling thrombosis.
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