人 DCBLD2 抗体对
01AB01352
DCBLD2 is a transmembrane protein that is highly expressed in various cancers, including colorectal cancer and lung adenocarcinoma, where it promotes tumor occurrence, development, and metastasis. DCBLD2 overexpression is associated with poor prognosis and drug resistance in these cancers. Mechanistically, DCBLD2 induces epithelial-mesenchymal transition (EMT) and angiogenesis, leading to increased migration and metastasis. Additionally, ultra-rare damaging variants in DCBLD2 are likely risk factors contributing to the complex disease process of relapsing polychondritis, a rare autoimmune disease. A homozygous nonsense mutation in DCBLD2 has also been identified as a candidate cause of restrictive cardiomyopathy, developmental delay, and spasticity, potentially through dysregulation of calcium and reactive oxygen species homeostasis.
| 规格 | 起售价 |
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技术参数
- 靶点基因名
- DCBLD2
- 基因别名
- CLCP1; ESDN
- 蛋白别名
- discoidin, CUB and LCCL domain containing 2; DCBLD2
- UniProt
- Q96PD2
- 物种
- Human
产品详情
- 靶点名称
- DCBLD2
- 蛋白名称
- discoidin, CUB and LCCL domain containing 2
- 蛋白别名
- Discoidin; CUB and LCCL domain-containing protein 2; CUB; LCCL and coagulation factor V/VIII-homology domains protein 1; Endothelial and smooth muscle cell-derived neuropilin-like protein
- 靶点基因名
- DCBLD2
- 基因别名
- CLCP1; ESDN
- UniProt
- Q96PD2
- 来源物种
- Homo sapiens (Human)
- 物种反应性
- Human
背景介绍
DCBLD2 is a transmembrane protein that is highly expressed in various cancers, including colorectal cancer and lung adenocarcinoma, where it promotes tumor occurrence, development, and metastasis. DCBLD2 overexpression is associated with poor prognosis and drug resistance in these cancers. Mechanistically, DCBLD2 induces epithelial-mesenchymal transition (EMT) and angiogenesis, leading to increased migration and metastasis. Additionally, ultra-rare damaging variants in DCBLD2 are likely risk factors contributing to the complex disease process of relapsing polychondritis, a rare autoimmune disease. A homozygous nonsense mutation in DCBLD2 has also been identified as a candidate cause of restrictive cardiomyopathy, developmental delay, and spasticity, potentially through dysregulation of calcium and reactive oxygen species homeostasis.