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生物来源
mouse
质量水平
抗体形式
purified antibody
抗体产品类型
primary antibodies
克隆
IgG-A9, monoclonal
种属反应性
human, rat, hamster
技术
immunocytochemistry: suitable
immunoprecipitation (IP): suitable
western blot: suitable
同位素/亚型
IgG1κ
UniProt登记号
运输
ambient
靶向翻译后修饰
unmodified
基因信息
human ... HMGCR(3156)
一般描述
3-羟基-3-甲基戊二酰辅酶A还原酶（EC 1.1.1.34；UniProt P00347；也称HMG-CoA还原酶）由灰仓鼠（中国仓鼠）的HMGCR基因（基因ID 100756363）编码。HMG-CoA还原酶可催化HMG-CoA转化为甲羟戊酸，是甲羟戊酸-异戊二烯类化合物生物合成（MIB）途径的限制性酶，负责生成胆固醇和其他异戊二烯类化合物，以及蛋白质异戊二烯化所需的法尼基焦磷酸盐（FPP）。HMG-CoA还原酶受到低密度脂蛋白（LDL）通过LDL受体内化和降解产生的胆固醇以及氧化胆固醇类物质的抑制。HMG-CoA还原酶的竞争性抑制剂诱导肝脏中LDL受体的表达，进而增加血浆LDL的分解代谢，降低血浆胆固醇的浓度。HMG-CoA还原酶是一种多跨膜内质网蛋白，具有N端甾醇敏感结构域（SSD；a.a.61-218）和C端催化结构域（a.a.450-888），其活性在SSD与胆固醇结合时受到抑制。许多研究表明HMG-CoA还原酶和甲羟戊酸途径参与肿瘤发生。
特异性
克隆IgG-A9靶向HMC-CoA还原酶催化结构域内的表位（a.a. 450 887）。
免疫原
Membrane preapration from compactin-adapted CHO cells (Liscum, L., et al. (1983).J. Biol. Chem. 258(13) 8450-8455).
应用
可使用这种小鼠HMG-CoA还原酶单克隆抗体（克隆IgG-A9，货号MABS1233）检测HMG CoA还原酶，该抗体经验证可用于免疫细胞化学、免疫沉淀和蛋白质印迹。
研究类别
信号传导
信号传导
Western Blotting Analysis: A 1:100 dilution from a representative lot detected in 15 µg of membrane extract from CHO7 cells treated overnight with 0.01 mM compactin (Courtesy of Linda Donnelly, Department of Molecular Genetics, UT Southwestern Medical Center, Dallas, TX, USA).
Immunocytochemistry Analysis: A representative lot detected HMG CoA reductase-positive ER membrane structures by indirect immunofluorescence staining of paraformaldehyde-fixed, 0.1% Triton X-100-permeabilized CHO-K1 cells cultured with compactin, mevalonate, and MG-132, in the presence or absence of 25-hydroxycholesterol (25-HC) (Hartman, I.Z., et al. (2010). J. Biol. Chem. 285(25):19288-19298).
Immunoprecipitation Analysis: A representative lot immunodepleted HMC-CoA reductase activity from compactin-adapted CHO cell (UT-1) extract (Liscum, L., et al. (1983). J. Biol. Chem. 258(13) 8450-8455).
Western Blotting Analysis: A representative lot detected 25-hydroxycholesterol (25-HC) treatment-induced HMC-CoA reductase dislocation from ER membrane to the cytosol and lipid droplet in CHO-K1 cells cultured with lipoprotein-deficient serum in the presence of compactin, MG-132, with or without mevalonate. Cellular VCP knockdown prevented sterol-induced HMC-CoA reductase cytosolic, but not lipid droplet, translocation (Hartman, I.Z., et al. (2010). J. Biol. Chem. 285(25):19288-19298).
Western Blotting Analysis: A representative lot detected 25-hydroxycholesterol (25-HC) treatment-induced ubiquitination of HMC-CoA reductase in SV-589 human fibroblasts cultured with compactin and mevalonate in the presence of proteasome inhibitor MG-132. Cellular knockdown of gp78A, but not gp78B or Hrd1, reduced 25-HC-induced HMC-CoA reductase ubiquitination (Song, B.L., et al. (2005). Mol. Cell. 19(6):829-840).
Western Blotting Analysis: A representative lot detected 25-hydroxycholesterol (25-HC) treatment-induced degradation of HMC-CoA reductase in SV-589 human fibroblasts cultured with compactin and mevalonate. Cellular knockdown of gp78A, VCP, or Insig-1/-2 suppressed sterol-induced HMC-CoA reductase degradation (Song, B.L., et al. (2005). Mol. Cell. 19(6):829-840).
Western Blotting Analysis: A representative lot detected HMC-CoA reductase in both membrane and nuclear fractions from HEK-293S cells cultured with compactin and mevalonate. Additional treatment with 25-hydroxycholesterol (25-HC) resulted in HMC-CoA reductase degradation (Sever, N., et al. (2003). Mol. Cell. 11(1):25-33).
Western Blotting Analysis: A representative lot detected an upregulated HMC-CoA reductase expression in compactin-adapted CHO cells (UT-1), as well as a loss of HMC-CoA reductase expression in UT-1 cells cultured in the presence of LDL (Liscum, L., et al. (1983). J. Biol. Chem. 258(13) 8450-8455).
Western Blotting Analysis: A representative lot detected a greater HMC-CoA reductase upregulation in liver microsome preparation from rats on diet supplemented with cholestyramine and mevinolin than with cholestyramine alone, while supplementation with cholesterol in addition to cholestyramine and mevinolin downregulated liver HMC-CoA reductase (Liscum, L., et al. (1983). J. Biol. Chem. 258(13) 8450-8455).
Immunocytochemistry Analysis: A representative lot detected HMG CoA reductase-positive ER membrane structures by indirect immunofluorescence staining of paraformaldehyde-fixed, 0.1% Triton X-100-permeabilized CHO-K1 cells cultured with compactin, mevalonate, and MG-132, in the presence or absence of 25-hydroxycholesterol (25-HC) (Hartman, I.Z., et al. (2010). J. Biol. Chem. 285(25):19288-19298).
Immunoprecipitation Analysis: A representative lot immunodepleted HMC-CoA reductase activity from compactin-adapted CHO cell (UT-1) extract (Liscum, L., et al. (1983). J. Biol. Chem. 258(13) 8450-8455).
Western Blotting Analysis: A representative lot detected 25-hydroxycholesterol (25-HC) treatment-induced HMC-CoA reductase dislocation from ER membrane to the cytosol and lipid droplet in CHO-K1 cells cultured with lipoprotein-deficient serum in the presence of compactin, MG-132, with or without mevalonate. Cellular VCP knockdown prevented sterol-induced HMC-CoA reductase cytosolic, but not lipid droplet, translocation (Hartman, I.Z., et al. (2010). J. Biol. Chem. 285(25):19288-19298).
Western Blotting Analysis: A representative lot detected 25-hydroxycholesterol (25-HC) treatment-induced ubiquitination of HMC-CoA reductase in SV-589 human fibroblasts cultured with compactin and mevalonate in the presence of proteasome inhibitor MG-132. Cellular knockdown of gp78A, but not gp78B or Hrd1, reduced 25-HC-induced HMC-CoA reductase ubiquitination (Song, B.L., et al. (2005). Mol. Cell. 19(6):829-840).
Western Blotting Analysis: A representative lot detected 25-hydroxycholesterol (25-HC) treatment-induced degradation of HMC-CoA reductase in SV-589 human fibroblasts cultured with compactin and mevalonate. Cellular knockdown of gp78A, VCP, or Insig-1/-2 suppressed sterol-induced HMC-CoA reductase degradation (Song, B.L., et al. (2005). Mol. Cell. 19(6):829-840).
Western Blotting Analysis: A representative lot detected HMC-CoA reductase in both membrane and nuclear fractions from HEK-293S cells cultured with compactin and mevalonate. Additional treatment with 25-hydroxycholesterol (25-HC) resulted in HMC-CoA reductase degradation (Sever, N., et al. (2003). Mol. Cell. 11(1):25-33).
Western Blotting Analysis: A representative lot detected an upregulated HMC-CoA reductase expression in compactin-adapted CHO cells (UT-1), as well as a loss of HMC-CoA reductase expression in UT-1 cells cultured in the presence of LDL (Liscum, L., et al. (1983). J. Biol. Chem. 258(13) 8450-8455).
Western Blotting Analysis: A representative lot detected a greater HMC-CoA reductase upregulation in liver microsome preparation from rats on diet supplemented with cholestyramine and mevinolin than with cholestyramine alone, while supplementation with cholesterol in addition to cholestyramine and mevinolin downregulated liver HMC-CoA reductase (Liscum, L., et al. (1983). J. Biol. Chem. 258(13) 8450-8455).
质量
通过亚型检测进行鉴别确认。
亚型分析：通过亚型检测确认该单克隆抗体为小鼠IgG1。
亚型分析：通过亚型检测确认该单克隆抗体为小鼠IgG1。
目标描述
观测值〜92 kDa。计算分子量：97.08 kDa（仓鼠），97.48/92.02/99.75 kDa（人同工型1/2/3（HMGCR-1b）），96.69 kDa（大鼠）。在一些裂解液中可能会观察到未表征的条带。
外形
在含 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的纯化的小鼠 IgG1。
形式：纯化
纯化蛋白G。
储存及稳定性
自收到之日起，在2-8°C条件下可稳定保存1年。
其他说明
浓度：请参考特定批次的数据表。
免责声明
除非我们的产品目录或产品附带的其他公司文档另有说明，否则我们的产品仅供研究使用，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任何类型的消费或应用于人类或动物。
WGK
WGK 1
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