Preparation And Storage
Product Notices
- Since applications vary, each investigator should titrate the reagent to obtain optimal results.
- An isotype control should be used at the same concentration as the antibody of interest.
- Caution: Sodium azide yields highly toxic hydrazoic acid under acidic conditions. Dilute azide compounds in running water before discarding to avoid accumulation of potentially explosive deposits in plumbing.
- Sodium azide is a reversible inhibitor of oxidative metabolism; therefore, antibody preparations containing this preservative agent must not be used in cell cultures nor injected into animals. Sodium azide may be removed by washing stained cells or plate-bound antibody or dialyzing soluble antibody in sodium azide-free buffer. Since endotoxin may also affect the results of functional studies, we recommend the NA/LE (No Azide/Low Endotoxin) antibody format, if available, for in vitro and in vivo use.
- Please refer to http://regdocs.bd.com to access safety data sheets (SDS).
- Species cross-reactivity detected in product development may not have been confirmed on every format and/or application.
- Please refer to www.bdbiosciences.com/us/s/resources for technical protocols.
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The DECMA-1 monoclonal antibody specifically recognizes the extracellular domain of mouse E-Cadherin (CD324). E-Cadherin is a 120-kDa transmembrane glycoprotein that is localized in the adherens junctions of epithelial cells. There it interacts with the cytoskeleton through the associated cytoplasmic catenin proteins. In addition to being a calcium-dependent adhesion molecule, E-Cadherin is also a critical regulator of epithelial junction formation. Its association with catenins is necessary for cell-to-cell adhesion. These E-Cadherin/catenin complexes associate with cortical actin bundles at both the zonula adherens and the lateral adhesion plaques. Tyrosine phosphorylation can disrupt these complexes, leading to changes in cell adhesion properties. E-Cadherin expression is often down-regulated in highly invasive, poorly differentiated carcinomas. Increased expression of E-Cadherin in these cells reduces their invasiveness. Thus, loss of expression or function of E-Cadherin appears to be an important step in tumorigenic progression. Pluripotent stem cells express E-Cadherin. Upon differentiation, an epithelial to mesenchymal transition results in the loss of E-cadherin expression and a gain in the expression of N-cadherin. The DECMA-1 mAb recognizes the membrane proximal part of the extracellular region of E-Cadherin and blocks E-Cadherin-mediated aggregation of cells. It has been reported to cross-react with E-Cadherin in humans, as well as several other species. However, the human cross-reactivity was weak when tested by flow cytometry on the MCF-7 breast cancer cell line in comparison to BD Biosciences' Anti-Human DECMA-1 mAb 67A4.
Development References (9)
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Batchuluun K, Azuma M, Yashiro T, Kikuchi M. Notch signaling-mediated cell-to-cell interaction is dependent on E-cadherin adhesion in adult rat anterior pituitary.. Cell Tissue Res. 2017; 368(1):125-133. (Clone-specific: Immunohistochemistry). View Reference
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Brouxhon SM, Kyrkanides S, Teng X, et al. Monoclonal antibody against the ectodomain of E-cadherin (DECMA-1) suppresses breast carcinogenesis: involvement of the HER/PI3K/Akt/mTOR and IAP pathways. Clin Cancer Res. 2013; 19(12):3234-46. (Clone-specific: Functional assay). View Reference
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Mohri Y. Prognostic significance of E-cadherin expression in human colorectal cancer tissue.. Surg Today. 1997; 27(7):606-12. (Clone-specific: Immunohistochemistry). View Reference
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Ozawa M, Hoschützky H, Herrenknecht K, Kemler R. A possible new adhesive site in the cell-adhesion molecule uvomorulin.. Mech Dev. 1990; 33(1):49-56. (Clone-specific: Immunofluorescence). View Reference
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Schuh R, Vestweber D, Riede I, et al. Molecular cloning of the mouse cell adhesion molecule uvomorulin: cDNA contains a B1-related sequence.. Proc Natl Acad Sci USA. 1986; 83(5):1364-8. (Clone-specific: Immunoaffinity chromatography). View Reference
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Sugiyama D, Joshi A, Kulkeaw K, et al. A Transcriptional Switch Point During Hematopoietic Stem and Progenitor Cell Ontogeny.. Stem Cells Dev. 2017; 26(5):314-327. (Biology). View Reference
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Takeichi M. The cadherins: cell-cell adhesion molecules controlling animal morphogenesis.. Development. 1988; 102(4):639-55. (Biology). View Reference
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Vestweber D, Kemler R. Identification of a putative cell adhesion domain of uvomorulin.. EMBO J. 1985; 4(13A):3393-8. (Immunogen: Blocking, Immunofluorescence, Immunoprecipitation). View Reference
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Vleminckx K, Vakaet L, Mareel M, Fiers W, van Roy F. Genetic manipulation of E-cadherin expression by epithelial tumor cells reveals an invasion suppressor role.. Cell. 1991; 66(1):107-19. (Biology). View Reference
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Comparisons, where applicable, are made against older BD Technology, manual methods or are general performance claims. Comparisons are not made against non-BD technologies, unless otherwise noted.
For Research Use Only. Not for use in diagnostic or therapeutic procedures.
