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Rabbit Anti-E cadherin/FITC Conjugated antibody
background:
Cadherins comprise a family of Ca2+-dependent adhesion molecules that function to mediate cell-cell binding critical to the maintenance of tissue structure and morphogenesis. Members of this family of adhesion proteins include rat cadherin K (and its human homolog, cadherin-6), R-cadherin, B-cadherin, E/P cadherin and cadherin-5. The classical cadherins, E-, N- and P-cadherin, consist of large extracellular domains characterized by a series of five homologous NH2 terminal repeats. The most distal of these cadherins is thought to be responsible for binding specificity, transmembrane domains and carboxy terminal intracellular domains. The relatively short intracellular domains interact with a variety of cytoplasmic proteins, such as ∫-catenin, to regulate cadherin function.
Function:
Cadherins are calcium-dependent cell adhesion proteins. They preferentially interact with themselves in a homophilic manner in connecting cells; cadherins may thus contribute to the sorting of heterogeneous cell types. CDH1 is involved in mechanisms regulating cell-cell adhesions, mobility and proliferation of epithelial cells. Has a potent invasive suppressor role. It is a ligand for integrin alpha-E/beta-7.
E-Cad/CTF2 promotes non-amyloidogenic degradation of Abeta precursors. Has a strong inhibitory effect on APP C99 and C83 production.
Subunit:
Homodimer.
Subcellular Location:
Cell junction. Cell membrane; Single-pass type I membrane protein.
Tissue Specificity:
Non-neural epithelial tissues.
Post-translational modifications:
During apoptosis or with calcium influx, cleaved by a membrane-bound metalloproteinase (ADAM10), PS1/gamma-secretase and caspase-3 to produce fragments of about 38 kDa (E-CAD/CTF1), 33 kDa (E-CAD/CTF2) and 29 kDa (E-CAD/CTF3), respectively. Processing by the metalloproteinase, induced by calcium influx, causes disruption of cell-cell adhesion and the subsequent release of beta-catenin into the cytoplasm. The residual membrane-tethered cleavage product is rapidly degraded via an intracellular proteolytic pathway. Cleavage by caspase-3 releases the cytoplasmic tail resulting in disintegration of the actin microfilament system. The gamma-secretase-mediated cleavage promotes disaaaembly of adherens junctions.
DISEASE:
Defects in CDH1 are the cause of hereditary diffuse gastric cancer (HDGC) . An autosomal dominant cancer predisposition syndrome with increased susceptibility to diffuse gastric cancer. Diffuse gastric cancer is a malignant disease characterized by poorly differentiated infiltrating lesions resulting in thickening of the stomach. Malignant tumors start 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. Note=Heterozygous germline mutations CDH1 are responsible for familial cases of diffuse gastric cancer. Somatic mutations in the has also been found in patients with sporadic diffuse gastric cancer and lobular breast cancer.
Similarity:
Contains 5 cadherin domains.
Database links:
Entrez Gene: 999 Human
Entrez Gene: 12550 Mouse
Entrez Gene: 83502 Rat
Entrez Gene: 282637 Cow
Entrez Gene: 442858 Dog
Omim: 192090 Human
SwissProt: Q6R8F2 Cow
SwissProt: P12830 Human
SwissProt: P01963 Mouse
SwissProt: Q9R0T4 Rat
Unigene: 461086 Human
Unigene: 35605 Mouse
Unigene: 1303 Rat
Important Note:
This product as supplied is intended for research use only, not for use in human, therapeutic or diagnostic applications.
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