Key result
PLC gamma 2-null platelets showed a markedly reduced residual aggregation response to collagen fibres compared to wild-type (6% vs 74%), with minimal granule secretion and no shape change.
Why the study?
Does PLCgamma2 knockout alter platelet activation and aggregation in response to collagen in mice?
Population
PLC gamma 2 -/- mice and wild-type mice
Comparison
Genetic knockout of PLC gamma 2 and exposure to… vs Wild-type mice
Design
Preclinical
Authors
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Reveals PLCγ2-independent collagen responses in mice; leaves open translation to human platelet function and antithrombotic strategies.
Does PLCgamma2 knockout alter platelet activation and aggregation in response to collagen in mice?
Absolute Event Rate: 6% vs 74%
The study identifies a PLCgamma2-independent collagen activation pathway in platelets requiring cooperation between GPVI and integrin alpha2beta1.
Mangin et al. (2003) studied Platelet activation. PLC gamma 2 deficiency vs. Wild-type mice was evaluated on Platelet aggregation response to collagen fibres. PLC gamma 2-null platelets showed a markedly reduced residual aggregation response to collagen fibres compared to wild-type (6% vs 74%), with minimal granule secretion and no shape change.
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