January 30, 2004Journal of Biological ChemistryOpen Access

Akt Activation in Platelets Depends on Gi Signaling Pathways

View Full Paper

Ask AI

Bookmark

Population

Mouse platelets

Comparison

Stimulation with agonists and treatment with… vs Wild-type platelets or absence of inhibitors

Design

Preclinical

Authors

SKSoochong KimChungbuk National University JJJianguo JinHangzhou First People's Hospital SKSatya P. KunapuliGeneral Cardiology

Discussion

Member takes

Implication

Gi-dependent Akt activation in platelets extends signaling models; hypothesis-generating and requires human validation before any clinical implications.

Structured PICO

Population

Mouse platelets (wild-type, Galphaq-deficient, P2Y1 receptor-deficient, and from mice treated with clopidogrel)

Intervention

Stimulation with agonists (thrombin, PAR1-activating peptide SFLLRN, PAR4-activating peptide AYPGKF, ADP) and treatment with inhibitors (AR-C69931MX, GF 109203X, clopidogrel)

Comparator

Wild-type platelets or absence of inhibitors

Outcome

Akt phosphorylation (Thr308 and Ser473) and activationsurrogate

This study demonstrates that Gi signaling, driven by secreted ADP, is essential for Akt activation in platelets, providing mechanistic insights into platelet activation and the effects of P2Y12 inhibitors like clopidogrel.

Cite This Study

Kim et al. (2004) studied this question.

synapsesocial.com/papers/6a833a96817bd1e6059c9873 https://doi.org/10.1074/jbc.m306162200

View Full Paper

Ask AI

Bookmark

Implication

Gi-dependent Akt activation in platelets extends signaling models; hypothesis-generating and requires human validation before any clinical implications.

Akt Activation in Platelets Depends on Gi Signaling Pathways

Discussion

Member takes

Implication

Structured PICO

Cite This Study

Akt Activation in Platelets Depends on Gi Signaling Pathways

Discussion

Member takes

Implication

Structured PICO

Cite This Study

Also Consider

Also Consider