APC protein (Tagged-His Tag) (ab91663)
This protein was expressed as an N-terminal His-tag fusion protein using Escherichia coli, and purified using Immobilized Metal Ion Affinity Chromatography. In some cases, smaller protein fragments may be present in addition to the intended expression product as a result of premature termination during translation in E. coli and subsequent co-purification via the His-tag. In some cases purified proteins run at a molecular weight different to the theoretically calculated molecular weight. This may be as a result of unequally distributed charges in the amino acid sequence. Alternatively, dimerisation of the expression product can occur under oxygen limitation during expression/cultivation.
Constituents: 0.5% Trehalose, 6M Urea, 100mM Sodium hydrogen phosphate, 10mM Sodium chloride, pH 4.5
Our Abpromise guarantee covers the use of ab91663 in the following tested applications.
The application notes include recommended starting dilutions; optimal dilutions/concentrations should be determined by the end user.
SDS-PAGE: Use at an assay dependent dilution.
Not yet tested in other applications.
Optimal dilutions/concentrations should be determined by the end user.
- Adenomatous Polyposis ColiAdenomatous polyposis coli proteinAPC
- APC_HUMANCC1Deleted in polyposis 2.5DP2DP2.5DP3FAPFPCGSProtein APC
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.
Defects in APC are a cause of medulloblastoma (MDB) [MIM:155255]. MDB is a malignant, invasive embryonal tumor of the cerebellum with a preferential manifestation in children. Although the majority of medulloblastomas occur sporadically, some manifest within familial cancer syndromes such as Turcot syndrome and basal cell nevus syndrome (Gorlin syndrome).
Defects in APC are a cause of mismatch repair cancer syndrome (MMRCS) [MIM:276300]; also known as Turcot syndrome or brain tumor-polyposis syndrome 1 (BTPS1). MMRCS is an autosomal dominant disorder characterized by malignant tumors of the brain associated with multiple colorectal adenomas. Skin features include sebaceous cysts, hyperpigmented and cafe au lait spots.
Defects in APC are a cause of gastric cancer (GASC) [MIM:613659]; also called gastric cancer intestinal or stomach cancer. Gastric cancer is a malignant disease which starts in the stomach, can spread to the esophagus or the small intestine, and can extend through the stomach wall to nearby lymph nodes and organs. It also can metastasize to other parts of the body. The term gastric cancer or gastric carcinoma refers to adenocarcinoma of the stomach that accounts for most of all gastric malignant tumors. Two main histologic types are recognized, diffuse type and intestinal type carcinomas. Diffuse tumors are poorly differentiated infiltrating lesions, resulting in thickening of the stomach. In contrast, intestinal tumors are usually exophytic, often ulcerating, and associated with intestinal metaplasia of the stomach, most often observed in sporadic disease.
Defects in APC are a cause of hepatocellular carcinoma (HCC) [MIM:114550]. This defect includes also the disease entity termed hepatoblastoma.
Contains 7 ARM repeats.
modificationsPhosphorylated by GSK3B.
Ubiquitinated, leading to its degradation by the proteasome. Ubiquitination is facilitated by Axin. Deubiquitinated by ZRANB1/TRABID.
APC protein (Tagged-His Tag) images
The image shows an electrophoretic assay performed using an Agilent 5100 ALP. In some images coloured control bands can be seen at 15 kDa (green) and/or 240 kDa (purple). The protein-specific band is blue.
References for APC protein (Tagged-His Tag) (ab91663)
ab91663 has not yet been referenced specifically in any publications.