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Key Specifications Table
| Species Reactivity | Key Applications | Host | Format | Antibody Type |
|---|---|---|---|---|
| H | ELISA, IP, WB, IHC | M | Purified | Monoclonal Antibody |
| Description | |
|---|---|
| Catalogue Number | MAB3785 |
| Replaces | AB1268 |
| Brand Family | Chemicon® |
| Trade Name |
|
| Description | Anti-APC Antibody, NT, clone Ali 12.28 |
| Alternate Names |
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| Background Information | The adenomatous polyposis coli tumor suppressor gene is mutated (often deletion of the C-terminal portion of APC) in the inherited disease, familial adenomatous polyposis (FAP), and over 80% of colorectal cancers. Ali 12-28 can be used for APC expression and detection of APC mutations. |
| Product Information | |
|---|---|
| Format | Purified |
| Control |
|
| Presentation | Purified immunoglobulin. Liquid in 0.02M phosphate buffer, 0.25M NaCl, pH 7.6, with 0.1% sodium azide. |
| Quality Level | MQ100 |
| Applications | |
|---|---|
| Application | Use Anti-APC Antibody, N-terminus, clone Ali 12.28 (Mouse Monoclonal Antibody) validated in ELISA, IP, WB, IHC to detect APC also known as Adenomatous Polyposis Coli Protein. |
| Key Applications |
|
| Application Notes | Western blot: 4 μg/mL Immunohistochemistry (Acetone Fixed, Frozen) ELISA Immunoprecipitation Optimal working dilutions must be determined by end user. |
| Biological Information | |
|---|---|
| Immunogen | N-terminal APC-MBP fusion protein (first 1.3 kb of APC which includes the first 433 aa and the first 9 exons of the gene). |
| Epitope | N-terminus |
| Clone | Ali 12.28 |
| Host | Mouse |
| Specificity | Recognizes human APC, molecular weight ~310 kDa, as well as C-terminal truncation mutants containing the epitope mapped between amino acids 135 to 422. |
| Isotype | IgG1 |
| Species Reactivity |
|
| Antibody Type | Monoclonal Antibody |
| Entrez Gene Number |
|
| Entrez Gene Summary | This gene encodes a tumor suppressor protein that includes among its many intracellular functions one of nuclear export. 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. |
| Gene Symbol |
|
| Non-Reactive Species |
|
| UniProt Number |
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| UniProt Summary | FUNCTION: SwissProt: P25054 # Tumor suppressor. Promotes rapid degradation of CTNNB1 and participates in Wnt signaling. APC activity is correlated with its phosphorylation state. SIZE: 2843 amino acids; 311646 Da SUBUNIT: Forms homooligomers. Interacts with DIAPH1 and DIAPH2 (By similarity). Interacts with PDZ domains of DLG1 and DLG3. Associates with catenins. Binds axin. Interacts with the N- terminus of ARHGEF4, and the C-terminus of MAPRE1, MAPRE2 and MAPRE3. Found in a complex consisting of ARHGEF4, APC and CTNNB1. TISSUE SPECIFICITY: Expressed in a variety of tissues. PTM: Phosphorylated by GSK3B. DISEASE: SwissProt: P25054 # 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. & APC mutations have led to some interesting observations. (1) the great majority of the mutations found to date would result in truncation of the APC product. (2) almost all the mutations have occurred within the first half of the coding sequence, and somatic mutations in colorectal tumors are further clustered in a particular region, called MCR (mutation cluster region). (3) most identified point mutations in the APC gene are transitions from cytosine to other nucleotides. (4) the location of germline mutations tends to correlate with the number of colorectal polyps in FAP patients. Inactivation of both alleles of the APC gene seems to be required as an early event to develop most adenomas and carcinomas in the colon and rectum as well as some of those in the stomach. & Defects in APC are a cause of hereditary desmoid disease (HDD) [MIM:135290]; also called familial infiltrative fibromatosis (FIF). It 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 Turcot syndrome [MIM:276300]. Turcot syndrome 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. SIMILARITY: SwissProt: P25054 ## Contains 7 ARM repeats. |
| Product Usage Statements | |
|---|---|
| Usage Statement |
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| Storage and Shipping Information | |
|---|---|
| Storage Conditions | Maintain at 2-8°C in undiluted aliquots for up to 12 months from date of receipt. |
| Packaging Information | |
|---|---|
| Material Size | 100 µg |