ArticleThrombosis research2018
Characterization of hemostasis in mice lacking the novel thrombosis susceptibility gene Slc44a2.
Article in Thrombosis research, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 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.
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Who cites it
7 citing papers in PubMed, 20 citations in OpenAlex.
- Venous thromboembolic disease genetics: from variants to function.Journal of thrombosis and haemostasis : JTH · 2024Review
- Lack of the human choline transporter-like protein SLC44A2 causes hearing impairment and a rare red blood phenotype.EMBO molecular medicine · 2023Article
- Platelet-Neutrophil Crosstalk in Thrombosis.International journal of molecular sciences · 2023Review
- SLC44A2 deficient mice have a reduced response in stenosis but not in hypercoagulability driven venous thrombosis.Journal of thrombosis and haemostasis : JTH · 2020Article
- Activated αeLife · 2020Article
- Rare Variants of Putative Candidate Genes Associated With Sporadic Meniere's Disease in East Asian Population.Frontiers in neurology · 2019Article
- Choline transporter-like proteins 1 and 2 are newly identified plasma membrane and mitochondrial ethanolamine transporters.The Journal of biological chemistryArticle
Corrections and comments
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Authors and funding
12 authors at 3 institutions in 2 countries.
Funding
Abstract
introductionRecent genome wide association studies (GWAS) identified a novel susceptibility locus for thrombosis, harbouring the SLC44A2 gene which encodes the Solute Carrier Family 44 Member 2 protein (SLC44A2). Thus far, SLC44A2 has not been studied in the context of thrombosis, and may be a unique contributor to thrombotic disease. Here we utilize mice lacking SLC44A2 (Slc44a2
methodsSlc44a2
resultsSlc44a2
conclusionsAlthough mice lacking SLC44A2 are normal for several hemostasis parameters, we do observe a reduction of plasma VWF levels and an altered response upon vascular damage, which suggests that SLC44A2 contributes to hemostasis upon injury. These findings are in line with the reported GWAS data and support further research on SLC44A2 in thrombosis.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.