人 HS6ST2 抗体对
01AB02835
Heparan sulfate 6-O-sulfotransferase 2 (HS6ST2) is a Golgi-resident type II membrane enzyme that catalyzes the transfer of sulfate to the 6-O position of N-sulfoglucosamine residues in heparan sulfate (HS). This modification is critical for modulating the structure of HS and its subsequent interactions with growth factors, receptors, and morphogens. HS6ST2 exhibits tissue-specific expression, with various isoforms contributing to complex HS sulfation patterns, particularly in the brain and reproductive tissues. Through its role in heparan sulfate glycosaminoglycan metabolism, it influences cell growth, differentiation, and fibroblast growth factor signaling. Clinically, mutations in HS6ST2 have been linked to intellectual disability and Paganini-Miozzo syndrome. Loss of the enzyme in animal models results in neurological and metabolic deficits, highlighting its essential role in brain development and physiological homeostasis.
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技术参数
- 靶点基因名
- HS6ST2
- 蛋白别名
- heparan sulfate 6-O-sulfotransferase 2; HS6ST2
- UniProt
- Q96MM7
- 物种
- Human
产品详情
- 靶点名称
- HS6ST2
- 蛋白名称
- heparan sulfate 6-O-sulfotransferase 2
- 蛋白别名
- Heparan-sulfate 6-O-sulfotransferase 2; HS6ST-2
- 靶点基因名
- HS6ST2
- UniProt
- Q96MM7
- 来源物种
- Homo sapiens (Human)
- 物种反应性
- Human
背景介绍
Heparan sulfate 6-O-sulfotransferase 2 (HS6ST2) is a Golgi-resident type II membrane enzyme that catalyzes the transfer of sulfate to the 6-O position of N-sulfoglucosamine residues in heparan sulfate (HS). This modification is critical for modulating the structure of HS and its subsequent interactions with growth factors, receptors, and morphogens. HS6ST2 exhibits tissue-specific expression, with various isoforms contributing to complex HS sulfation patterns, particularly in the brain and reproductive tissues. Through its role in heparan sulfate glycosaminoglycan metabolism, it influences cell growth, differentiation, and fibroblast growth factor signaling. Clinically, mutations in HS6ST2 have been linked to intellectual disability and Paganini-Miozzo syndrome. Loss of the enzyme in animal models results in neurological and metabolic deficits, highlighting its essential role in brain development and physiological homeostasis.