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Anti-APC/Adenomatous Polyposis Coli腺瘤样息肉抗体

点击次数:223发布时间:2012/12/26 4:27:42

Anti-APC/Adenomatous Polyposis Coli腺瘤样息肉抗体

更新日期:2024/9/5 14:43:27

所 在 地:其它

产品型号:BY-3680R

简单介绍:本公司经销APC/Adenomatous Polyposis Coli,腺瘤样息肉抗体,克隆类型为polyclonal,宿主来源是Rabbit,APC/Adenomatous Polyposis Coli腺瘤样息肉抗体可应用于WB、elisa、IP、IF、IHC等实验,欢迎垂询订购!

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本公司经销APC/Adenomatous Polyposis Coli,腺瘤样息肉抗体,克隆类型为polyclonal,宿主来源是Rabbit,APC/Adenomatous Polyposis Coli腺瘤样息肉抗体可应用于WB、elisa、IP、IF、IHC等实验,欢迎垂询订购!

货号:BY-3680R
英文名称:Anti-APC/Adenomatous Polyposis Coli
中文名称:腺瘤样息肉抗体
其他名称:Adenomatous Polyposis Coli; APC; CC1; DP2; DP2.5; DP3; FAP; FPC; GS; Protein APC.
抗体来源:Rabbit
克隆类型:polyclonal
蛋白分子量:predicted molecular weight: 313kDa
纯化方法:affinity purified by Protein A
交叉反应:hu, mo, rat, Rb, hrs, pig, cow
产品介绍:This gene encodes a tumor suppressor protein that acts as an antagonist of the Wnt signaling pathway. It is also involved in other processes including cell migration and adhesion, transcriptional activation, and apoptosis. Defects in this gene cause familial adenomatous polyposis (FAP), an autosomal dominant pre-malignant disease that usually progresses to malignancy. Disease-associated mutations tend to be clustered in a small region designated the mutation cluster region (MCR) and result in a truncated protein product. [provided by RefSeq].Function : Tumor suppressor. Promotes rapid degradation of CTNNB1 and participates in Wnt signaling as a negative regulator. APC activity is correlated with its phosphorylation state. Activates the GEF activity of SPATA13 and ARHGEF4. Plays a role in hepatocyte growth factor (HGF)-induced cell migration. Required for MMP9 up-regulation via the JNK signaling pathway in colorectal tumor cells. Acts as a mediator of ERBB2-dependent stabilization of microtubules at the cell cortex. It is required for the localization of MACF1 to the cell membrane and this localization of MACF1 is critical for its function in microtubule stabilization.Subunit : Forms homooligomers and heterooligomers with APC2. Interacts with DIAPH1 and DIAPH2. Interacts withPDZ domains of DLG1 and DLG3. Associates with catenins. Binds axin. Interacts with ARHGEF4 (via N-terminus). Interacts with MAPRE1 (viaC-terminus); probably required for APC targeting to the growingmicrotubule plus ends. Interacts with MAPRE2 and MAPRE3 (viaC-terminus). Found in a complex consisting of ARHGEF4, APC andCTNNB1. Interacts with SCRIB; may mediate APC targeting to adherensjunctions of epithelial cells. Interacts with SPATA13 (viaN-terminus and SH3 domain). Interacts with ASAP1 (via SH3 domain). Found in a complex composed of MACF1, APC, AXIN1, CTNNB1 and GSK3B. Interacts at the cell membrane with FAM123A and FAM123B (via ARM repeats).Subcellular Location : Cell junction, adherens junction. Cytoplasm, cytoskeleton. Cell projection, lamellipodium. Cell projection, ruffle membrane. Cytoplasm. Cell membrane. Note=Associated with the microtubule network at the growing distal tip of microtubules. Accumulates in the lamellipodium and ruffle membrane in response to hepatocyte growth factor (HGF) treatment. The MEMO1-RHOA-DIAPH1 signaling pathway controls localization of the phosophorylated form to the cell membrane.Tissue Specificity : Expressed in a variety of tissues.Post-translational modifications : Phosphorylated by GSK3B.Ubiquitinated, leading to its degradation by the proteasome. Ubiquitination is facilitated by Axin. Deubiquitinated by ZRANB1/TRABID.DISEASE : Defects in APC are a cause of familial adenomatous polyposis (FAP) [MIM:175100]; which includes also Gardner syndrome (GS). FAP and GS contribute to tumor development in patients with uninherited forms of colorectal cancer. FAP is characterized by adenomatous polyps of the colon and rectum, but also of upper gastrointestinal tract (ampullary, duodenal and gastric adenomas). This is a viciously premalignant disease with one or more polyps progressing through dysplasia to malignancy in untreated gene carriers with a median age at diagnosis of 40 years. [DISEASE] Defects in APC are a cause of hereditary desmoid disease (HDD) [MIM:135290]; also known as familial infiltrative fibromatosis (FIF). HDD is an autosomal dominant trait with 100% penetrance and possible variable expression among affected relatives. HDD patients show multifocal fibromatosis of the paraspinal muscles, breast, occiput, arms, lower ribs, abdominal wall, and mesentery. Desmoid tumors appears also as a complication of familial adenomatous polyposis.Similarity : Belongs to the adenomatous polyposis coli (APC) family.Contains 7 ARM repeats.

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