ArticleThe Journal of clinical investigation2013
Thrombocytopathy and type 2B von Willebrand disease.
Article in The Journal of clinical investigation, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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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
1 citing paper in PubMed, 4 citations in OpenAlex.
- Of von Willebrand factor and platelets.Cellular and molecular life sciences : CMLS · 2015Review
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1 author at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The knowledge gained from "experiments of nature" has always been paramount in identifying key players in pathophysiologic pathways. This is well characterized by naturally occurring bleeding and thrombotic disorders. In most cases, it is the absence of a particular protein that leads to recognition of its importance for normal physiology. On the other hand, gain-of-function mutations highlight not only the presence of the protein, but also how it regulates a particular physiologic response. In this issue of the JCI, Casari and colleagues define a previously unrecognized consequence of variant type 2B von Willebrand factor (vWF) binding to blood platelets. More than 30 years after an initial description of type 2B variant vWF, the consequence of this spontaneous variant vWF binding to platelets is viewed as a dysregulation of platelet signaling pathways contributing to the type 2B bleeding phenotype.
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