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Updated: Jun 11, 2025

A Kinetic Fluorescence-based Ca2+ Mobilization Assay to Identify G Protein-coupled Receptor Agonists, Antagonists, and Allosteric Modulators
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ACKR3的激动性诱导与化学因子受体CXCR4的异构化,并减弱血小板功能

Valerie Dicenta-Baunach1, Zoi Laspa1, David Schaale1

  • 1Department of Cardiology and Angiology, University Hospital Tübingen, Eberhard Karls University Tübingen, Tübingen, Germany.

European journal of clinical investigation
|October 7, 2024
PubMed
概括

血小板受体ACKR3和CXCR4形成异构体,其中ACKR3的激动性抑制了血小板激活. 这表明ACKR3激动剂可能在心血管疾病中具有治疗潜力.

关键词:
C-X-C 动机化学因联接体 12在C-X-C基因基因基因受体4型.非典型的化学受体3异构化的异构化血小板 血小板 血小板是什么?

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