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As mouse platelets lacking PKCδ show increased aggregation in response to collagen, we investigated responses in platelets lacking PKCε.
In contrast, mouse platelets lacking PKCδ show enhanced aggregation and spreading when stimulated by collagen, suggesting a feedback inhibitory role [20].
In the present study we assessed static adhesion, cell spreading, granule secretion, integrin αIIbβ3 activation and platelet aggregation in washed mouse platelets lacking PKCθ.
There is a marked inhibition in aggregation and dense granule secretion to low concentrations of GPVI agonists in mouse platelets lacking PKCε in contrast to a minor inhibition in response to G protein-coupled receptor agonists.
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In mice, platelets lacking CFH are unable to effectively clear immune complexes which results in their accumulation in glomeruli.
Platelet aggregation, granule secretion, and integrin αIIbβ3 activation in response to the glycoprotein VI (GPVI) agonist collagen-related peptide (CRP) were significantly reduced in platelets lacking IR.
Like murine platelets lacking FAK, we found that PF-573,228 was effective at blocking human platelet spreading on fibrinogen-coated surfaces but did not affect the initial adhesion.
This is of particular significance considering that platelets lack a nucleus.
Mice in which platelets lack FAK have been shown to exhibit extended bleeding times and their platelets have been shown to display decreased spreading on fibrinogen-coated surfaces.
Although the lack of an identified role for Rif in mouse platelets does not preclude a role for the protein in human platelets, the question of which Rho GTPase(s) regulate platelet filopodia formation remains open.
To directly address if enhanced platelet activation caused the reduction in circulating platelets in mice lacking HRG, we employed the drug Plavix (clopidogrel), which inhibits platelet activation via the ADP receptor P2Y.
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