一般描述
可识别HCT116细胞中的全长APC（p300）和SW480细胞中的截短APC（p147）。抗体靶基因符号：APC 目标同义词：AI047805，Apc7，AU020952，AW124434，BTPS2，DP2，DP2.5，DP3，家族性腺瘤性息肉病，FAP，GS，Min，RATAPC Entrez基因名称：腺瘤性息肉病 Hu Entrez ID：324（有关抗体：OP80，ST1150，OP62，OP47L） Mu Entrez ID：11789 大鼠Entrez ID：24205
抗APC（Ab-1），小鼠单克隆，克隆FE9，可识别HCT116细胞中的全长APC（p300）和SW480细胞中的截短APC（p147）。它已被验证可用于蛋白质印迹法。
蛋白G纯化小鼠单克隆抗体是通过用指定的免疫原免疫小鼠并将脾细胞与SP40细胞融合而产生的。可识别~300 kDa APC蛋白以及多种截短形式。
免疫原
一种与APC N端35个氨基酸对应的合成肽
应用
免疫印迹（1 µg/ml，参见注释）
包装
请参考特定浓度批号的标签。
外形
溶于50 mM磷酸钠缓冲液（pH 7.5），含0.2％明胶。
分析说明
阳性对照
HCT116细胞用于p300，SW480细胞用于截短APC（p147）
HCT116细胞用于p300，SW480细胞用于截短APC（p147）
其他说明
Koetsier, P. A., et al. 1993.BioTechniques15, 258.
Smith, K. J., et al. 1993.Proc.Natl.Acad.Sci., USA90, 2846.
Su, L.-K., et al. 1993.Can.Res.53, 2728.
Boynton, R. F., et al. 1992.Proc.Natl.Acad.Sci. USA89, 3385.
D′Amico, D., et al. 1992.Cancer Res.52, 1996.
Fearon, E. R., and Jones, P. A., 1992.FASEB J.6, 2783.
Miyoshi, Y., et al. 1992.Proc.Natl.Acad.Sci. USA89, 4452.
Powell, S. M., et al. 1992.Nature359, 235.
Groden, J., et al. 1991.Cell66, 589.
Kinzler, K. W., et al. 1991.Science253, 661.
Nishisho, I., et al. 1991.Science253, 665.
Smith, K. J., et al. 1993.Proc.Natl.Acad.Sci., USA90, 2846.
Su, L.-K., et al. 1993.Can.Res.53, 2728.
Boynton, R. F., et al. 1992.Proc.Natl.Acad.Sci. USA89, 3385.
D′Amico, D., et al. 1992.Cancer Res.52, 1996.
Fearon, E. R., and Jones, P. A., 1992.FASEB J.6, 2783.
Miyoshi, Y., et al. 1992.Proc.Natl.Acad.Sci. USA89, 4452.
Powell, S. M., et al. 1992.Nature359, 235.
Groden, J., et al. 1991.Cell66, 589.
Kinzler, K. W., et al. 1991.Science253, 661.
Nishisho, I., et al. 1991.Science253, 665.
法律信息
CALBIOCHEM is a registered trademark of Merck KGaA, Darmstadt, Germany
免责声明
毒性：标准处理（A）
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储存分类代码
11 - Combustible Solids
WGK
WGK 1
闪点(°F)
Not applicable
闪点(°C)
Not applicable
Dipon Das et al.
DNA repair, 24, 15-25 (2014-12-03)
Colorectal cancer (CRC) patients with APC mutations do not benefit from 5-FU therapy. It was reported that APC physically interacts with POLβ and FEN1, thus blocking LP-BER via APC's DNA repair inhibitory (DRI) domain in vitro. The aim of this
Jason L Larabee et al.
The Journal of biological chemistry, 286(22), 19364-19372 (2011-04-14)
The production of cAMP from Bacillus anthracis edema toxin (ET) activates gene expression in macrophages through a complex array of signaling pathways, most of which remain poorly defined. In this study, the tumor suppressor protein adenomatous polyposis coli (APC) was
Tamar Evron et al.
Oncogenesis, 10(9), 63-63 (2021-09-24)
The Wnt signaling pathways play fundamental roles during both development and adult homeostasis. Aberrant activation of the canonical Wnt signal transduction pathway is involved in many diseases including cancer, and is especially implicated in the development and progression of colorectal
Claudia Gaspar et al.
PLoS genetics, 5(7), e1000547-e1000547 (2009-07-07)
Germline mutations in the adenomatous polyposis coli (APC) gene are responsible for familial adenomatous polyposis (FAP), an autosomal dominant hereditary predisposition to the development of multiple colorectal adenomas and of a broad spectrum of extra-intestinal tumors. Moreover, somatic APC mutations
Nathaniel S Rial et al.
International journal of cancer, 124(10), 2270-2280 (2009-01-29)
Elevated deoxycholic acid (DCA), mutations in the adenomatous polyposis coli (APC) gene and chronic inflammation are associated with increased risk of colorectal cancer. APC status was manipulated to determine whether DCA mediates inflammatory molecules in normal or initiated colonic mucosa.
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