
人 CLEC11A 抗体对
01AB00184
C-type lectin domain containing 11A (CLEC11A), also known as osteolectin, is a secreted sulfated glycoprotein belonging to the C-type lectin superfamily. It functions as a growth factor for primitive hematopoietic progenitor cells and plays a crucial role in osteogenesis by promoting the differentiation of mesenchymal progenitors into mature osteoblasts. The protein contains an N-terminal RGD motif, a leucine zipper region, and a C-terminal lectin-like domain. CLEC11A is highly expressed in bone marrow stromal cells, chondrocytes, and osteoblast-like cells. It is essential for maintaining adult bone mass, strength, and fracture healing. CLEC11A-deficient mice exhibit accelerated bone loss during aging and delayed fracture healing. In terms of disease associations, CLEC11A methylation has been correlated with acute myeloid leukemia (AML) subtypes and cytogenetic risk factors. Additionally, it has been implicated in gastric cancer progression, with high expression levels associated with poor prognosis.
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技术参数
- 靶点基因名
- CLEC11A
- 基因别名
- CLECSF3; LSLCL; SCGF
- 蛋白别名
- C-type lectin domain containing 11A; CLEC11A
- UniProt
- Q9Y240
- 物种
- Human
产品详情
- 靶点名称
- CLEC11A
- 蛋白名称
- C-type lectin domain containing 11A
- 蛋白别名
- C-type lectin domain family 11 member A; C-type lectin superfamily member 3; Lymphocyte secreted C-type lectin; Osteolectin; Stem cell growth factor; p47
- 靶点基因名
- CLEC11A
- 基因别名
- CLECSF3; LSLCL; SCGF
- UniProt
- Q9Y240
- 来源物种
- Homo sapiens (Human)
- 物种反应性
- Human
背景介绍
C-type lectin domain containing 11A (CLEC11A), also known as osteolectin, is a secreted sulfated glycoprotein belonging to the C-type lectin superfamily. It functions as a growth factor for primitive hematopoietic progenitor cells and plays a crucial role in osteogenesis by promoting the differentiation of mesenchymal progenitors into mature osteoblasts. The protein contains an N-terminal RGD motif, a leucine zipper region, and a C-terminal lectin-like domain. CLEC11A is highly expressed in bone marrow stromal cells, chondrocytes, and osteoblast-like cells. It is essential for maintaining adult bone mass, strength, and fracture healing. CLEC11A-deficient mice exhibit accelerated bone loss during aging and delayed fracture healing. In terms of disease associations, CLEC11A methylation has been correlated with acute myeloid leukemia (AML) subtypes and cytogenetic risk factors. Additionally, it has been implicated in gastric cancer progression, with high expression levels associated with poor prognosis.