抗人 PRKAR1B 抗体对
01AB01560
Protein kinase cAMP-dependent type I regulatory subunit beta (PRKAR1B) is a regulatory subunit of the protein kinase A (PKA) holoenzyme, which is crucial in the cAMP signaling pathway. PRKAR1B encodes the RI-beta subunit that binds cAMP and regulates PKA activity by controlling the release of catalytic subunits upon cAMP binding. This protein is predominantly expressed in the brain, with highest levels in the cerebral cortex and hypothalamus, and is localized mainly in the cytoplasm of neuronal cells. PKA, composed of two regulatory and two catalytic subunits, phosphorylates various target proteins, thereby modulating metabolism, ion transport, gene transcription, apoptosis, and insulin signaling pathways. PRKAR1B interacts with A-kinase-anchoring proteins (AKAPs) to localize PKA within cellular compartments. Mutations in PRKAR1B cause an autosomal dominant neurodevelopmental disorder characterized by autism spectrum disorder, apraxia, and insensitivity to pain, with mutations arising de novo in affected individuals. These pathogenic variants disrupt normal PKA function, leading to impaired neuronal signaling and developmental abnormalities.
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技术参数
- 靶点基因名
- PRKAR1B
- 蛋白别名
- protein kinase cAMP-dependent type I regulatory subunit beta; PRKAR1B
- UniProt
- P31321
- 物种
- Human
产品详情
- 靶点名称
- PRKAR1B
- 蛋白名称
- protein kinase cAMP-dependent type I regulatory subunit beta
- 蛋白别名
- cAMP-dependent protein kinase type I-beta regulatory subunit
- 靶点基因名
- PRKAR1B
- UniProt
- P31321
- 来源物种
- Homo sapiens (Human)
- 物种反应性
- Human
背景介绍
Protein kinase cAMP-dependent type I regulatory subunit beta (PRKAR1B) is a regulatory subunit of the protein kinase A (PKA) holoenzyme, which is crucial in the cAMP signaling pathway. PRKAR1B encodes the RI-beta subunit that binds cAMP and regulates PKA activity by controlling the release of catalytic subunits upon cAMP binding. This protein is predominantly expressed in the brain, with highest levels in the cerebral cortex and hypothalamus, and is localized mainly in the cytoplasm of neuronal cells. PKA, composed of two regulatory and two catalytic subunits, phosphorylates various target proteins, thereby modulating metabolism, ion transport, gene transcription, apoptosis, and insulin signaling pathways. PRKAR1B interacts with A-kinase-anchoring proteins (AKAPs) to localize PKA within cellular compartments. Mutations in PRKAR1B cause an autosomal dominant neurodevelopmental disorder characterized by autism spectrum disorder, apraxia, and insensitivity to pain, with mutations arising de novo in affected individuals. These pathogenic variants disrupt normal PKA function, leading to impaired neuronal signaling and developmental abnormalities.