人 GSTP1 抗体对
01AB00256
Glutathione S-transferase pi 1 (GSTP1) is a cytosolic enzyme belonging to the pi class of the glutathione S-transferase (GST) superfamily. It plays a crucial role in detoxification by catalyzing the conjugation of glutathione to various electrophilic compounds, including metabolites generated by oxidative processes, environmental toxins, and anti-cancer drugs. GSTP1 is associated with susceptibility to cancer, anti-cancer drug resistance, and other diseases. It is expressed in many human tissues, particularly in the biliary tree, renal distal convoluted tubules, and lungs. GSTP1 also regulates kinase signaling pathways through protein-protein interactions and has been implicated in the regulation of cell signaling pathways, including the inhibition of c-Jun N-terminal kinase (JNK1) signaling. Its polymorphic forms can differentially mediate the activation of peroxiredoxin VI, affecting the response to reactive oxygen species/reactive nitrogen species.
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技术参数
- 靶点基因名
- GSTP1
- 基因别名
- FAEES3; GST3
- 蛋白别名
- glutathione S-transferase pi 1; GSTP1
- UniProt
- P09211
- 物种
- Human
产品详情
- 靶点名称
- GSTP1
- 蛋白名称
- glutathione S-transferase pi 1
- 蛋白别名
- Glutathione S-transferase P; GST class-pi; GSTP1-1
- 靶点基因名
- GSTP1
- 基因别名
- FAEES3; GST3
- UniProt
- P09211
- 来源物种
- Homo sapiens (Human)
- 物种反应性
- Human
背景介绍
Glutathione S-transferase pi 1 (GSTP1) is a cytosolic enzyme belonging to the pi class of the glutathione S-transferase (GST) superfamily. It plays a crucial role in detoxification by catalyzing the conjugation of glutathione to various electrophilic compounds, including metabolites generated by oxidative processes, environmental toxins, and anti-cancer drugs. GSTP1 is associated with susceptibility to cancer, anti-cancer drug resistance, and other diseases. It is expressed in many human tissues, particularly in the biliary tree, renal distal convoluted tubules, and lungs. GSTP1 also regulates kinase signaling pathways through protein-protein interactions and has been implicated in the regulation of cell signaling pathways, including the inhibition of c-Jun N-terminal kinase (JNK1) signaling. Its polymorphic forms can differentially mediate the activation of peroxiredoxin VI, affecting the response to reactive oxygen species/reactive nitrogen species.