eScholarship
metadata only
Loss of AKAP150 promotes pathological remodelling and heart failure propensity by disrupting calcium cycling and contractile reserve
AIMS: Impaired Ca2 + cycling and myocyte contractility are a hallmark of heart failure triggered by pathological stress such as hemodynamic overload. The A-Kinase anchoring protein AKAP150 has been shown to coordinate key aspects of adrenergic regulation of Ca2+ cycling and excitation-contraction in
Conceptio Open Archive
Analyze & explore related research in Conceptio
Connect this record directly into your research workflow or AI agent. Explore citations across open repositories, query full text, and export structured proof bundles.
This document is indexed with metadata only: full text is not available in the archive for this record. Open the official source ↗
Related documents
- PAK-family kinases promote cell fusion irreversibility by preventing cell wall repair#279907
- AKAP5 and Caveolin-1 organize opposing nanodomains that regulate smooth muscle contraction and blood pressure#779345
- Early Left Ventricular unLoading by Impella vs Intra-aortic Balloon Pump#1044399
- Closing the Loop: Experimental Validation of AI Predicted Ternary Complexes to Enable Rational Design of CDK8-Targeted Degraders#169593
- IP3R-driven increases in mitochondrial Ca2+ promote neuronal death in NPC disease#1249951
Record · ID 1358186
Retrieved via Conceptio: every document is proof-bundled with source, license, and retrieval metadata.
Retrieved via Conceptio: every document is proof-bundled with source, license, and retrieval metadata.
Bring this data into your agent: Connect via MCP or API · 20 free credits to start · no card required
Read the Docs → · View CLI source on GitHub · Conceptio Open Knowledge Archive
Read the Docs → · View CLI source on GitHub · Conceptio Open Knowledge Archive