Cadherin 5 Antikörper (FITC)

Produktnummer ABIN2191899

Produktdetails anti-Cadherin 5 Antikörper (FITC)

Target: Cadherin 5 (CDH5)

Reaktivität: Human

Wirt: Maus

Klonalität: Monoklonal

Konjugat: Dieser Cadherin 5 Antikörper ist konjugiert mit FITC

Applikation: Western Blotting (WB), Flow Cytometry (FACS), Immunofluorescence (IF), Functional Studies (Func), Immunoassay (IA)

Sterilität: 0.2 μm filtered

Klon: BV9

Anwendungsinformationen

Applikationshinweise: For immunohistochemistry, flow cytometry and Western blotting, dilutions to be used depend on detection system applied. It is recommended that users test the reagent and determine their own optimal dilutions. The typical starting working dilution is 1:50. For functional studies, in vitro dilutions have to be optimized in user's experimental setting. Positive HUVECs grown on coverslips control

Beschränkungen: Nur für Forschungszwecke einsetzbar

Handhabung

Buffer: PBS, containing 1 % bovine serum albumin and 0.02 % sodium azide.

Konservierungsmittel: Sodium azide

Vorsichtsmaßnahmen: This product contains Sodium azide: a POISONOUS AND HAZARDOUS SUBSTANCE which should be handled by trained staff only.

Lagerung: 4 °C

Informationen zur Lagerung: Product should be stored at 4 °C. Under recommended storage conditions, product is stable for at least one year. The exact expiry date is indicated on the label.

Referenzen für anti-Cadherin 5 Antikörper (FITC) (ABIN2191899)

Abraham, Yeo, Montero-Balaguer, Paterson, Dejana, Marshall, Mavria: "VE-Cadherin-mediated cell-cell interaction suppresses sprouting via signaling to MLC2 phosphorylation." in: Current biology : CB, Vol. 19, Issue 8, pp. 668-74, (2009) (PubMed).

Spagnuolo, Corada, Orsenigo, Zanetta, Deuschle, Sandy, Schneider, Drake, Breviario, Dejana: "Gas1 is induced by VE-cadherin and vascular endothelial growth factor and inhibits endothelial cell apoptosis." in: Blood, Vol. 103, Issue 8, pp. 3005-12, (2004) (PubMed).

Gill, Dias, Hattori, Rivera, Hicklin, Witte, Girardi, Yurt, Himel, Rafii: "Vascular trauma induces rapid but transient mobilization of VEGFR2(+)AC133(+) endothelial precursor cells." in: Circulation research, Vol. 88, Issue 2, pp. 167-74, (2001) (PubMed).

Navarro, Caveda, Breviario, Mândoteanu, Lampugnani, Dejana: "Catenin-dependent and -independent functions of vascular endothelial cadherin." in: The Journal of biological chemistry, Vol. 270, Issue 52, pp. 30965-72, (1996) (PubMed).

Martìn-Padura, De Castellarnau, Uccini, Pilozzi, Natali, Nicotra, Ughi, Azzolini, Dejana, Ruco: "Expression of VE (vascular endothelial)-cadherin and other endothelial-specific markers in haemangiomas." in: The Journal of pathology, Vol. 175, Issue 1, pp. 51-7, (1995) (PubMed).

Breviario, Caveda, Corada, Martin-Padura, Navarro, Golay, Introna, Gulino, Lampugnani, Dejana: "Functional properties of human vascular endothelial cadherin (7B4/cadherin-5), an endothelium-specific cadherin." in: Arteriosclerosis, thrombosis, and vascular biology, Vol. 15, Issue 8, pp. 1229-39, (1995) (PubMed).

Details zu Cadherin 5

Target: Cadherin 5 (CDH5)

Andere Bezeichnung: Vascular Endothelial Cadherin (CDH5 Produkte)

Synonyme: 7B4 antikoerper, AA408225 antikoerper, Cd144 antikoerper, VE-Cad antikoerper, VECD antikoerper, VEcad antikoerper, Vec antikoerper, wu:fc88a07 antikoerper, CD144 antikoerper, cadherin-5 antikoerper, cadherin 5 antikoerper, CDH5 antikoerper, Cdh5 antikoerper, cdh5 antikoerper

Hintergrund: The monoclonal antibody BV9 binds to the extracellular domain (EC3-EC4) of human VE-cadherin (vascular endothelial cadherin). Endothelial cells control the passage of plasma constituents and circulating cells from blood to the underlying tissues. VE-cadherin is of vital importance for the maintenance and control of endothelial cell contacts. Mechanisms that regulate VE-cadherin- mediated adhesion are important for the control of vascular permeability and leukocyte extravasation. VE-cadherin regulates various cellular processes such as cell proliferation and apoptosis and modulates vascular endothelial growth factor receptor functions. Therefore, VE-cadherin is also essential during embryonic angiogenesis. The specialized function of VE-cadherin is lost or impaired in several pathological conditions - including inflammation, sepsis, ischemia and diabetes - which leads to severe, and sometimes fatal, organ dysfunction. Furthermore, abnormal increase in vascular permeability is often observed in pathological conditions, such as tumor-induced angiogenesis, macular degeneration, allergy, and brain stroke. Endothelial permeability is regulated in part by the dynamic opening and closure of cell-cell adherent junctions. In vascular endothelium, adherent junctions are mainly composed of VE-cadherin, an adhesive receptor that is able to self-associate at endothelial cell-cell contacts. VE-cadherin links endothelial cells together by homophilic interactions mediated by its extracellular part and associates intracellularly with the actin cytoskeleton via catenins. VE-cadherin belongs to the cadherin super- family of cell-cell adhesion molecules, which are encoded by more than 200 genes in the human 2+ genome. Classical cadherins are Ca -dependent, homophilic, cell to cell adhesion molecules expressed in nearly all cells within solid tissues. Cadherins form a core adhesion complex that consists of a cadherin dimer, binding through its extracellular region to another dimer of cadherins expressed in adjacent cells, while its intracellular region is anchored to the plasma membrane and linked to the cytoskeleton. The VE-cadherin extracellular domain consists of five cadherin-type repeats, called EC (extracellular cadherin) domains that are bound together by calcium ions in a rod- like structure. Aliases 7B4 antigen, Cadherin-5, CD144

Pathways: Cell-Cell Junction Organization, Signaling Events mediated by VEGFR1 and VEGFR2