人 CDK5RAP3 抗体对
01AB02642
CDK5 regulatory subunit associated protein 3 (CDK5RAP3) is a multifunctional cytoplasmic protein that regulates signaling and stress-response pathways. As a core component of the UREL complex, it acts as a substrate adaptor for the UFL1 E3 ligase, directing the mono-ufmylation of ribosomal protein RPL26 to manage ribosome recycling and ER homeostasis. CDK5RAP3 also modulates transcription by negatively regulating NF-kappaB activity and controls cell-cycle checkpoints through interactions with CDKN2A/ARF and MDM2. It influences proliferation, apoptosis, and autophagy via mTOR signaling. In clinical oncology, CDK5RAP3 often functions as a tumor suppressor; its reduced expression in gastric cancer is associated with epithelial-mesenchymal transition, increased metastasis, and chemoresistance, while its overexpression can reverse these malignant phenotypes.
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技术参数
- 靶点基因名
- CDK5RAP3
- 基因别名
- IC53; LZAP
- 蛋白别名
- CDK5 regulatory subunit associated protein 3; CDK5RAP3
- UniProt
- Q96JB5
- 物种
- Human
产品详情
- 靶点名称
- CDK5RAP3
- 蛋白名称
- CDK5 regulatory subunit associated protein 3
- 蛋白别名
- CDK5 regulatory subunit-associated protein 3; CDK5 activator-binding protein C53; LXXLL/leucine-zipper-containing ARF-binding protein; Protein HSF-27
- 靶点基因名
- CDK5RAP3
- 基因别名
- IC53; LZAP
- UniProt
- Q96JB5
- 来源物种
- Homo sapiens (Human)
- 物种反应性
- Human
背景介绍
CDK5 regulatory subunit associated protein 3 (CDK5RAP3) is a multifunctional cytoplasmic protein that regulates signaling and stress-response pathways. As a core component of the UREL complex, it acts as a substrate adaptor for the UFL1 E3 ligase, directing the mono-ufmylation of ribosomal protein RPL26 to manage ribosome recycling and ER homeostasis. CDK5RAP3 also modulates transcription by negatively regulating NF-kappaB activity and controls cell-cycle checkpoints through interactions with CDKN2A/ARF and MDM2. It influences proliferation, apoptosis, and autophagy via mTOR signaling. In clinical oncology, CDK5RAP3 often functions as a tumor suppressor; its reduced expression in gastric cancer is associated with epithelial-mesenchymal transition, increased metastasis, and chemoresistance, while its overexpression can reverse these malignant phenotypes.