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抗人 KAZALD1 抗体对
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抗人 KAZALD1 抗体对

01AB01184

Kazal type serine peptidase inhibitor domain 1 (KAZALD1) is a secreted protein encoded by the KAZALD1 gene, characterized by a multi-domain structure including an N-terminal insulin-like growth factor-binding domain, a central Kazal-type serine protease inhibitor and follistatin-like domain, and a C-terminal immunoglobulin-like domain. This configuration enables KAZALD1 to inhibit serine proteases, enzymes critical in processes such as digestion, coagulation, immune response, and cellular signaling. Functionally, KAZALD1 is involved in promoting osteoblast proliferation and matrix assembly during bone formation and regeneration, as suggested by studies on its mouse ortholog. Structurally, the Kazal domain contains conserved cysteine residues forming disulfide bonds that stabilize its inhibitory interaction with target proteases. Clinically, KAZALD1 is implicated in disease states including high-grade glioma, where its hypomethylation and overexpression correlate with increased tumor cell proliferation and poorer patient survival. It is also associated with multiple congenital anomalies due to deletions involving the gene locus.

Human
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技术参数

靶点基因名
KAZALD1
蛋白别名
Kazal type serine peptidase inhibitor domain 1; KAZALD1
UniProt
Q96I82
物种
Human

产品详情

靶点名称
KAZALD1
蛋白名称
Kazal type serine peptidase inhibitor domain 1
蛋白别名
Kazal-type serine protease inhibitor domain-containing protein 1
靶点基因名
KAZALD1
UniProt
Q96I82
来源物种
Homo sapiens (Human)
物种反应性
Human

背景介绍

Kazal type serine peptidase inhibitor domain 1 (KAZALD1) is a secreted protein encoded by the KAZALD1 gene, characterized by a multi-domain structure including an N-terminal insulin-like growth factor-binding domain, a central Kazal-type serine protease inhibitor and follistatin-like domain, and a C-terminal immunoglobulin-like domain. This configuration enables KAZALD1 to inhibit serine proteases, enzymes critical in processes such as digestion, coagulation, immune response, and cellular signaling. Functionally, KAZALD1 is involved in promoting osteoblast proliferation and matrix assembly during bone formation and regeneration, as suggested by studies on its mouse ortholog. Structurally, the Kazal domain contains conserved cysteine residues forming disulfide bonds that stabilize its inhibitory interaction with target proteases. Clinically, KAZALD1 is implicated in disease states including high-grade glioma, where its hypomethylation and overexpression correlate with increased tumor cell proliferation and poorer patient survival. It is also associated with multiple congenital anomalies due to deletions involving the gene locus.