MABD42
抗-Cyp7a1抗体，克隆15B9.1
clone 15B9.1, from mouse
别名:
Cholesterol 7-alpha-monooxygenase, CYPVII, Cholesterol 7-alpha-hydroxylase, Cytochrome P450 7A1
产品名称
抗-Cyp7a1抗体，克隆15B9.1, clone 15B9.1, from mouse
biological source
mouse
conjugate
unconjugated
antibody form
purified immunoglobulin
antibody product type
primary antibodies
clone
15B9.1, monoclonal
species reactivity
rat, mouse, human
technique(s)
immunohistochemistry: suitable
western blot: suitable
isotype
IgG2aκ
NCBI accession no.
UniProt accession no.
shipped in
wet ice
target post-translational modification
unmodified
Quality Level
Gene Information
human ... CYP7A1(1581)
Analysis Note
对照
人肝组织裂解物
人肝组织裂解物
通过蛋白质印迹法在人肝组织裂解物中进行评价。
蛋白质印迹分析：0.5 µg/mL该抗体在10 µg人肝组织裂解物中检测到Cyp7a1。
蛋白质印迹分析：0.5 µg/mL该抗体在10 µg人肝组织裂解物中检测到Cyp7a1。
Application
免疫组织化学分析：一个代表性批次以1:50-1,000稀释度在大鼠和人肝组织中检测到Cyp7a1。
研究子类别
凋亡 - 附加
凋亡 - 附加
研究类别
细胞凋亡 & 癌症
细胞凋亡 & 癌症
该Cyp7a1抗体经验证可用于WB&IHC检测Cyp7a1蛋白。
Disclaimer
除非我们的目录或产品随附的其他公司文件中另有说明，否则我们的产品预期仅用于研究用途，不得用于任何其他目的，包括但不限于未经授权的商业用途、体外诊断用途、离体或体内治疗用途或对人类或动物的任何类型的消费或应用。
General description
细胞色素P450 7A1（CYP7A1、CYPVII），也称为胆固醇7-α-单加氧酶或胆固醇7-α-羟化酶，属于细胞色素P450家族，对胆固醇稳态很重要。CYP7A1通过在胆固醇的7位引入亲水部分来催化胆固醇分解代谢和胆汁酸生物合成中的限速步骤。CYP7A1主要在肝脏中检测到，可催化以下反应: 胆固醇+NADPH+O2=7-α-羟基胆固醇+NADP++H2O。CYP7A1被葡萄糖和胆甾胺上调，而被鹅去氧胆酸下调。
观测分子量〜52 kDa
Immunogen
对应于人Cyp7a1的带有GST标记的重组蛋白。
Other Notes
浓度：关于批次特定浓度请参见检验报告。
Physical form
形式：纯化
纯化的小鼠单克隆IgG2aκ，溶于含0.1 M Tris-甘氨酸（pH 7.4）、150 mM NaCl和0.05％叠氮化钠的缓冲液中。
纯化蛋白G
Preparation Note
自接收之日起，在2-8°C下可稳定保存1年。
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存储类别
12 - Non Combustible Liquids
wgk
WGK 1
flash_point_f
Not applicable
flash_point_c
Not applicable
Atorvastatin Modulates Bile Acid Homeostasis in Mice with Diet-Induced Nonalcoholic Steatohepatitis.
Hana Lastuvkova et al.
International journal of molecular sciences, 22(12) (2021-07-03)
Bile acids (BA) play a significant role in the pathophysiology of nonalcoholic steatohepatitis (NASH). The present study evaluates the modulation of bile acid metabolomics by atorvastatin, a cholesterol-lowering agent commonly used to treat cardiovascular complications accompanying NASH. NASH was induced
Yongtao Xiao et al.
Cell death & disease, 8(10), e3110-e3110 (2017-10-13)
The p38α mitogen-activated protein kinase (MAPK) has been related to gluconeogenesis and lipid metabolism. However, the roles and related mechanisms of p38α MAPK in intestinal failure (IF)-associated liver steatosis remained poor understood. Here, our experimental evidence suggested that p38α MAPK
Hepatocyte peroxisome proliferator-activated receptor α regulates bile acid synthesis and transport.
Cen Xie et al.
Biochimica et biophysica acta. Molecular and cell biology of lipids, 1864(10), 1396-1411 (2019-06-14)
Peroxisome proliferator-activated receptor alpha (PPARα) controls lipid homeostasis through regulation of lipid transport and catabolism. PPARα activators are clinically used for hyperlipidemia treatment. The role of PPARα in bile acid (BA) homeostasis is beginning to emerge. Herein, Ppara-null and hepatocyte-specific
Arvin Iracheta-Vellve et al.
Hepatology communications, 2(11), 1379-1391 (2018-11-10)
Bile acids (BAs) activate various dedicated receptors, including the farnesoid X receptor (FXR) and the Takeda G protein-coupled receptor 5 (TGR5). The FXR agonist obeticholic acid (OCA) is licensed for the treatment of primary biliary cholangitis and has shown promising
Mao-Xu Ge et al.
Acta pharmacologica Sinica, 40(7), 895-907 (2018-12-24)
The manipulation of bile acid (BA) homeostasis by blocking the ileal apical Na+-dependent bile salt transporter (ASBT/SLC10A2) may have therapeutic effects in nonalcoholic fatty liver disease. We developed a novel ASBT inhibitor, an N-(3,4-o-dichlorophenyl)-2-(3-trifluoromethoxy) benzamide derivative referred to as IMB17-15
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