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MABF957

Sigma-Aldrich

Anti-CLEC-2 Antibody, clone AYP1

clone AYP1, from mouse

Synonyme(s) :

C-type lectin domain family 1 member B, C-type lectin-like receptor 2, CLEC-2

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About This Item

Code UNSPSC :
12352203
eCl@ss :
32160702
Nomenclature NACRES :
NA.43

Source biologique

mouse

Niveau de qualité

Forme d'anticorps

purified immunoglobulin

Type de produit anticorps

primary antibodies

Clone

AYP1, monoclonal

Espèces réactives

human

Technique(s)

flow cytometry: suitable

Isotype

IgG1κ

Numéro d'accès NCBI

Numéro d'accès UniProt

Conditions d'expédition

ambient

Modification post-traductionnelle de la cible

unmodified

Informations sur le gène

human ... CLEC1B(51266)

Description générale

C-type lectin domain family 1 member B (UniProt Q9P126; also known as C-type lectin-like receptor 2, CLEC-2) is encoded by the CLEC1B (also known as CLEC2, UNQ721/PRO1384) gene (Gene ID 51266) in human. CLEC-2 is a type II single-transmembrane (a.a. 34-54) protein with a large extracellular (a.a. 55-229) region that contains a C-type lectin domain (a.a. 109-217) and a short N-terminal cytoplasmic tail (a.a. 1-33) with a single hem-immunoreceptor tyrosine-based activation motif (hemITAM; a.a. 7-10). CLEC-2 expression is restricted to platelets, where it mediates platelets activation via its hemITAM motif, leading to proteolytic cleavage of two other platelet ITAM receptors, glycoprotein (GP)VI and Fc RIIa, but not of CLEC-2 itself. CLEC-2 functions as the receptor for the type I transmembrane GP podoplanin that is widely expressed outside of the vasculature, including lymphatic endothelial cells, type 1 lung alveolar cells, lymph node stromal cells, the choroid plexus epithelium, inflammatory macrophages, as well as a subset of activated T-helper (Th)17 cells. Patients with rheumatoid arthritis show increased plasma levels of CLEC-2-positive microparticles. These microparticles are derived from activated platelets and are negative for GPVI, while microparticles in healthy donors are predominantly derived from megakaryocytes and are positive for both CLEC-2 and GPVI. Platelet-specific deletion of CLEC-2 or one of its downstream signaling proteins, Syk, SLP-76, or PLC 2, leads to a number of developmental problems in mice, including blood-lymphatic mixing in midgestation.

Spécificité

Clone AYP1 targets an extracellular epitope present in both spliced isoforms of human CLEC-2/CLEC1B reported by UniProt (Q9P126).

Immunogène

His-tagged recombinant human CLEC-2 extracellular fragment.

Application

Analyse par cytométrie en flux : A representative lot detected doxycycline-dependent expression induction of exogenously transfected CLEC-2/CLEC1B using T-REx 293 cells (Gitz, E., et al. (2014).



µ

A representative lot immunoprecipitated CLEC-2/CLEC1B from human platelet lysates. Rhodocytin stimulation prior to cell lysis and IP induced CLEC-2/CLEC1B tyrosine phosphorylation (Gitz, E., et al. (2014). Blood. 124(14):2262-2270).
This mouse monoclonal Anti-CLEC-2 Antibody, clone AYP1, Cat. No. MABF957 is validated for use in Flow Cytometry, Function Assay, and Immunoprecipitation for the detection of CLEC-2.

Qualité

Evaluated by Flow Cytometry in human platelets.

Analyse par cytométrie en flux : µ

Description de la cible

26.60 kDa (isoform 1) and 23.10 kDa (isoform 2). ~32/40 kDa doublet reported due to differential glycosylation (Gitz, E., et al. (2014). Blood. 124(14):2262-2270).

Forme physique

Format : Produit purifié

Autres remarques

Concentration : Voir la fiche technique du lot concerné.

Informations légales

ALEXA FLUOR is a trademark of Life Technologies

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Code de la classe de stockage

12 - Non Combustible Liquids

Classe de danger pour l'eau (WGK)

WGK 2

Point d'éclair (°F)

Not applicable

Point d'éclair (°C)

Not applicable


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Consulter la Bibliothèque de documents

Manisha Yadav et al.
Microbiology spectrum, 11(3), e0412222-e0412222 (2023-05-01)
To initiate an antileishmanial adaptive immune response, dendritic cells (DCs) must carry Leishmania antigens from peripheral tissues to local draining lymph nodes. However, the migratory capacity of DCs is largely compromised during Leishmania donovani infection. The molecular mechanism underlying this

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