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人 INPP4B 抗体对
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人 INPP4B 抗体对

01AB03191

Inositol polyphosphate 4-phosphatase type II (INPP4B) is a dual specificity phosphatase that plays a significant role in phosphatidylinositol signaling pathways by dephosphorylating phosphatidylinositol 3,4-bisphosphate (PI(3,4)P2) to produce phosphatidylinositol 3-phosphate (PI(3)P). This enzymatic activity is crucial for regulating the PI3K/AKT signaling pathway, which is involved in cell growth, survival, and metabolism. INPP4B is recognized as a tumor suppressor, with its expression often reduced in various cancers, including breast, ovarian, and prostate cancers. Loss of INPP4B function can lead to enhanced activation of the PI3K/AKT pathway, promoting tumorigenesis and cancer progression. Additionally, studies have shown that INPP4B is downregulated in glioma tissues, where it inhibits cell proliferation and immune escape by modulating the PI3K/AKT pathway and reducing PD-L1 expression.

Human
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技术参数

靶点基因名
INPP4B
蛋白别名
inositol polyphosphate-4-phosphatase type II B; INPP4B
UniProt
O15327
物种
Human

产品详情

靶点名称
INPP4B
蛋白名称
inositol polyphosphate-4-phosphatase type II B
蛋白别名
Inositol polyphosphate 4-phosphatase type II; Type II inositol 3; 4-bisphosphate 4-phosphatase
靶点基因名
INPP4B
UniProt
O15327
来源物种
Homo sapiens (Human)
物种反应性
Human

背景介绍

Inositol polyphosphate 4-phosphatase type II (INPP4B) is a dual specificity phosphatase that plays a significant role in phosphatidylinositol signaling pathways by dephosphorylating phosphatidylinositol 3,4-bisphosphate (PI(3,4)P2) to produce phosphatidylinositol 3-phosphate (PI(3)P). This enzymatic activity is crucial for regulating the PI3K/AKT signaling pathway, which is involved in cell growth, survival, and metabolism. INPP4B is recognized as a tumor suppressor, with its expression often reduced in various cancers, including breast, ovarian, and prostate cancers. Loss of INPP4B function can lead to enhanced activation of the PI3K/AKT pathway, promoting tumorigenesis and cancer progression. Additionally, studies have shown that INPP4B is downregulated in glioma tissues, where it inhibits cell proliferation and immune escape by modulating the PI3K/AKT pathway and reducing PD-L1 expression.