人 AKAP10 抗体对
01AB01908
A-kinase anchoring protein 10 (AKAP10) is a dual-specific anchoring protein that binds both type I and type II regulatory subunits of protein kinase A (PKA). It functions as a molecular scaffold that targets the PKA holoenzyme to specific subcellular compartments, primarily the mitochondria, to regulate cAMP-dependent pathways and mitochondrial apoptosis. AKAP10 also contains RGS-like regions, suggesting a role in coupling G protein signaling to PKA-mediated responses. Clinically, specific polymorphisms in the PKA-binding domain of AKAP10 are well-established risk factors for cardiac dysfunction. These variants are linked to altered heart rate, increased susceptibility to cardiac conduction disease, arrhythmias, and sudden cardiac death, highlighting the protein's critical role in maintaining cardiac electrophysiological stability.
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技术参数
- 靶点基因名
- AKAP10
- 蛋白别名
- A-kinase anchoring protein 10; AKAP10
- UniProt
- O43572
- 物种
- Human
产品详情
- 靶点名称
- AKAP10
- 蛋白名称
- A-kinase anchoring protein 10
- 蛋白别名
- A-kinase anchor protein 10; mitochondrial; AKAP-10; Dual specificity A kinase-anchoring protein 2; D-AKAP-2; Protein kinase A-anchoring protein 10; PRKA10
- 靶点基因名
- AKAP10
- UniProt
- O43572
- 来源物种
- Homo sapiens (Human)
- 物种反应性
- Human
背景介绍
A-kinase anchoring protein 10 (AKAP10) is a dual-specific anchoring protein that binds both type I and type II regulatory subunits of protein kinase A (PKA). It functions as a molecular scaffold that targets the PKA holoenzyme to specific subcellular compartments, primarily the mitochondria, to regulate cAMP-dependent pathways and mitochondrial apoptosis. AKAP10 also contains RGS-like regions, suggesting a role in coupling G protein signaling to PKA-mediated responses. Clinically, specific polymorphisms in the PKA-binding domain of AKAP10 are well-established risk factors for cardiac dysfunction. These variants are linked to altered heart rate, increased susceptibility to cardiac conduction disease, arrhythmias, and sudden cardiac death, highlighting the protein's critical role in maintaining cardiac electrophysiological stability.