Overview

  • Product nameAnti-APC (phospho S2054) antibodySee all APC primary antibodies ...
  • Description
    Rabbit polyclonal to APC (phospho S2054)
  • SpecificityDetects endogenous levels of APC only when phosphorylated at serine 2054.
  • Tested applicationsELISA, IHC-Pmore details
  • Species reactivity
    Reacts with: Human
    Predicted to work with: Mouse, Rat
  • Immunogen

    Synthetic phosphopeptide derived from human APC around the phosphorylation site of serine 2054 (K-P-SP-R-L).

  • Positive control
    • Brain tissue

Properties

Applications

Our Abpromise guarantee covers the use of ab59421 in the following tested applications.

The application notes include recommended starting dilutions; optimal dilutions/concentrations should be determined by the end user.

Application Abreviews Notes
ELISA 1/40000.
IHC-P 1/50 - 1/100.

Target

  • FunctionTumor 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.
  • Tissue specificityExpressed in a variety of tissues.
  • Involvement in diseaseDefects 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.
    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.
  • Sequence similaritiesBelongs to the adenomatous polyposis coli (APC) family.
    Contains 7 ARM repeats.
  • DomainThe microtubule tip localization signal (MtLS) motif; mediates interaction with MAPRE1 and targeting to the growing microtubule plus ends.
  • Post-translational
    modifications
    Phosphorylated by GSK3B.
    Ubiquitinated, leading to its degradation by the proteasome. Ubiquitination is facilitated by Axin. Deubiquitinated by ZRANB1/TRABID.
  • Cellular localizationCell junction > adherens junction. Cytoplasm > cytoskeleton. Cell projection > lamellipodium. Cell projection > ruffle membrane. Cytoplasm. Cell membrane. 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.
  • Information by UniProt
  • Database links
  • Alternative names
    • Adenomatous Polyposis Coli antibody
    • Adenomatous polyposis coli protein antibody
    • APC antibody
    • APC_HUMAN antibody
    • CC1 antibody
    • Deleted in polyposis 2.5 antibody
    • DP2 antibody
    • DP2.5 antibody
    • DP3 antibody
    • FAP antibody
    • FPC antibody
    • GS antibody
    • Protein APC antibody
    see all

Anti-APC (phospho S2054) antibody images

  • ab59421, at a 1/50 dilution, staining paraffin embedded human brain tissue sections by Immunohistochemistry in the absence (left image) or presence (right image) of the phosphopeptide.

References for Anti-APC (phospho S2054) antibody (ab59421)

This product has been referenced in:
  • Dong B  et al. Mammalian diaphanous-related formin 1 regulates GSK3ß-dependent microtubule dynamics required for T cell migratory polarization. PLoS One 8:e80500 (2013). Mouse . Read more (PubMed: 24260404) »

See 1 Publication for this product

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Please note: All products are "FOR RESEARCH USE ONLY AND ARE NOT INTENDED FOR DIAGNOSTIC OR THERAPEUTIC USE"