人 SMAD5 抗体对
01AB04153
Mothers against decapentaplegic homolog 5 (SMAD5) is a member of the SMAD protein family, which are intracellular signaling molecules that mediate the effects of transforming growth factor-beta (TGF-β) and bone morphogenetic protein (BMP) pathways. SMAD5 is primarily involved in regulating gene expression during embryonic development and tissue homeostasis. It acts as a transcription factor, translocating to the nucleus upon activation by BMPs, where it influences various developmental processes. Dysregulation of SMAD5 has been linked to several diseases, particularly skeletal disorders and cancers; mutations in the SMAD5 gene can lead to conditions such as pulmonary arterial hypertension and have been associated with certain types of leukemia. Additionally, aberrant SMAD5 signaling can contribute to tumorigenesis by promoting cell proliferation and survival.
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技术参数
- 靶点基因名
- SMAD5
- 基因别名
- MADH5
- 蛋白别名
- SMAD family member 5; SMAD5
- UniProt
- Q99717
- 物种
- Human
产品详情
- 靶点名称
- SMAD5
- 蛋白名称
- SMAD family member 5
- 蛋白别名
- Mothers against decapentaplegic homolog 5; MAD homolog 5; Mothers against DPP homolog 5; JV5-1; SMAD family member 5; SMAD 5; Smad5; hSmad5
- 靶点基因名
- SMAD5
- 基因别名
- MADH5
- UniProt
- Q99717
- 来源物种
- Homo sapiens (Human)
- 物种反应性
- Human
背景介绍
Mothers against decapentaplegic homolog 5 (SMAD5) is a member of the SMAD protein family, which are intracellular signaling molecules that mediate the effects of transforming growth factor-beta (TGF-β) and bone morphogenetic protein (BMP) pathways. SMAD5 is primarily involved in regulating gene expression during embryonic development and tissue homeostasis. It acts as a transcription factor, translocating to the nucleus upon activation by BMPs, where it influences various developmental processes. Dysregulation of SMAD5 has been linked to several diseases, particularly skeletal disorders and cancers; mutations in the SMAD5 gene can lead to conditions such as pulmonary arterial hypertension and have been associated with certain types of leukemia. Additionally, aberrant SMAD5 signaling can contribute to tumorigenesis by promoting cell proliferation and survival.