抗人 SRC 抗体对
01AB00692
The SRC proto-oncogene encodes a non-receptor tyrosine kinase (SRC) that regulates critical cellular processes, including proliferation, adhesion, and migration, via signaling pathways such as MAPK and PI3K-AKT. Structurally, SRC contains SH3 and SH2 domains that mediate protein-protein interactions and a kinase domain responsible for its enzymatic activity. Its function is tightly regulated by phosphorylation; inhibitory phosphorylation at Tyr530 suppresses activity, while dephosphorylation (e.g., via receptor tyrosine kinases) activates it. Dysregulation of SRC, through mutations (e.g., kinase domain mutations) or overexpression, drives oncogenesis by promoting tumor growth, invasion, and metastasis. SRC is implicated in colorectal, breast, and pancreatic cancers, as well as hematologic malignancies. Hyperactive SRC enhances survival signaling, angiogenesis, and chemotherapy resistance, underscoring its role as a therapeutic target. Clinical inhibitors like dasatinib block SRC activity, highlighting its translational relevance. SRC’s dual role in normal signaling and cancer pathogenesis makes it pivotal in oncology research and drug development.
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技术参数
- 靶点基因名
- SRC
- 基因别名
- SRC1
- 蛋白别名
- SRC proto-oncogene, non-receptor tyrosine kinase; SRC
- UniProt
- P12931
- 物种
- Human
产品详情
- 靶点名称
- SRC
- 蛋白名称
- SRC proto-oncogene, non-receptor tyrosine kinase
- 蛋白别名
- Proto-oncogene tyrosine-protein kinase Src; Proto-oncogene c-Src; pp60c-src; p60-Src
- 靶点基因名
- SRC
- 基因别名
- SRC1
- UniProt
- P12931
- 来源物种
- Homo sapiens (Human)
- 物种反应性
- Human
背景介绍
The SRC proto-oncogene encodes a non-receptor tyrosine kinase (SRC) that regulates critical cellular processes, including proliferation, adhesion, and migration, via signaling pathways such as MAPK and PI3K-AKT. Structurally, SRC contains SH3 and SH2 domains that mediate protein-protein interactions and a kinase domain responsible for its enzymatic activity. Its function is tightly regulated by phosphorylation; inhibitory phosphorylation at Tyr530 suppresses activity, while dephosphorylation (e.g., via receptor tyrosine kinases) activates it. Dysregulation of SRC, through mutations (e.g., kinase domain mutations) or overexpression, drives oncogenesis by promoting tumor growth, invasion, and metastasis. SRC is implicated in colorectal, breast, and pancreatic cancers, as well as hematologic malignancies. Hyperactive SRC enhances survival signaling, angiogenesis, and chemotherapy resistance, underscoring its role as a therapeutic target. Clinical inhibitors like dasatinib block SRC activity, highlighting its translational relevance. SRC’s dual role in normal signaling and cancer pathogenesis makes it pivotal in oncology research and drug development.