Blood:XPR1 regulates the accumulation of plate plate plate polyphosphates to inhibit thrombosis.

Polyphosphate is a linearly connected coagulation-promoting inormeric polymer of positive phosphate residues.
studies have confirmed the importance of plateboard polyphosphates in clotting, but in mammals, the details of the mechanism of polyphosphate stabilization are largely unclear.
in this study, Mailer et al. demonstrated that heterophilic and polyintrophic retrovirus recipient 1 (XPR1) regulates polyphosphate in plate plateplates and is associated with thrombosis in the body.
XPR1 is the main phosphate transporter researchers on plateboard through bioinfossign analysis of histological data to clarify that XPR1 is the main phosphate transporter in plateboard.
XPR1 expression levels were negatively related to polyphosphate content in cells and the expression of proteins was negatively related to the content and release of polyphosphates in cells.
drug intervention with XPR1 activity can increase the storage of polyphosphates, leading to plate plate plate-driven clotting enhancement, and amplifying thrombosis under blood flow through polyphosphate/coagulation factor XII.
Xpr1 defects lead to an increase in pulmonary arterial thrombosis in mice conditional knock-out of plateplates in mice Xpr1 can lead to polyphosphate build-up, accelerate arterial thrombosis, and increase the active plateboard-driven pulmonary embolism without increasing bleeding.
addition, these data show that plate plate plate XPR1 is the overall regulatory factor of plateboard polyphosphate metabolism, emphasizing the basic role of phosphate stability in thrombosis.
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