English (United Kingdom)

https://curated-unify.zendy.io/wp-json/zendy-region/v1/featured_content/oa?rat=en

https://curated-unify.zendy.io/wp-json/zendy-region/v1/highlighted_journal/

Global: Zendy Plus annual

Presents the access of premium content as premium feature

Premium Content

Presents the keyphrase highlighting as premium feature

Keyphrase Highlighting

Presents the summarisation as premium feature

Summarisation

Insights

Presents the pdf analysis as premium feature

PDF Analysis

Presents the zaia usage as premium feature

ZAIA

Global: Zendy Tools annual

Global: Zendy Free Plan

Global: Zendy Tools monthly

Global: Zendy Plus monthly

With a nod to Paul Simon, there may be more ways to activate platelets than there were ways to leave your lover in his song from the 70’s—or at least it seems that way. Gas6 is a vitamin K–dependent, protein-S–related protein found in the α-granules of resting platelets. Once platelet activation has occurred, Gas-6 appears in the fluid phase and on the platelet surface, where it presumably becomes bound after secretion. In this issue of Arteriosclerosis, Thrombosis, and Vascular Biology , Chen et al show that platelets express at least one of the known receptors for Gas-6, the receptor tyrosine kinase, Mer.1 According to their observations, deletion of the gene encoding Mer in mice does not produce an overt bleeding phenotype or even prolong the bleeding time, but it does inhibit platelet aggregation, diminish the thrombotic response to vascular injury, and provide some protection against disseminated thrombosis.1 These effects are less profound, but qualitatively similar to those reported several years ago by Angelillo-Scherrer et al in their studies on mice that lack Gas6,2 and essentially similar to those they have subsequently reported in abstract form using mice that lack either Mer or two related receptors, Axl and Rse (also known as Sky).3See page 1118 Gas6 is a 75-kDa protein with several distinct structural domains, starting with an N-terminal domain that includes γ-carboxylated glutamic acid (Gla) residues, a central domain with epidermal growth factor (EGF) repeats and two C-terminal G domains responsible for receptor binding and activation.4,5 Gla residues are glutamic acid residues that have undergone vitamin K–dependent γ-carboxylation, allowing them to support Ca++-dependent binding to phosphatidylserine. Like the Mer knockout, the Gas6 knockout causes decreased secretion and impairs platelet aggregation, particularly at low agonist concentrations. It also provides some degree of protection …

Fifty (or More) Ways to Leave Your Platelets (in a Thrombus)