Anti-HLA-DRB5

Anti-HLA-DRB5
Artikelnummer Größe Datenblatt Manual SDB Lieferzeit Menge Preis
CSB-PA657235ZA01HU.100 100 µg - -

10 - 14 Werktage*

1.529,00 €
CSB-PA657235ZA01HU.2 2 mg - -

10 - 14 Werktage*

2.328,00 €
 
Make to order. Production time: 70-80 business days. Deliverables: 1. 200 µg antigen (used as... mehr
Produktinformationen "Anti-HLA-DRB5"
Make to order. Production time: 70-80 business days. Deliverables: 1. 200 µg antigen (used as positive control), 2. 1 ml pre-immune serum (used as negative control) , 3. Rabbit polyclonal antibody, antigen affinity purified. Quality Guarantee: 1. Antibody purity > 90% confirmed by SDS-PAGE, 2. Antibody titer > 1: 64,000 confirmed by ELISA, 3. WB positive with the immunogen protein (not applicable for synthetic peptide). Applications: ELISA, WB (positive for the recombinant immunogen protein/peptide). Buffer: Preservative: 0.03% Proclin 300, Constituents: 50% Glycerol, 0.01M PBS, pH 7.4. Protein function: Binds peptides derived from antigens that access the endocytic route of antigen presenting cells (APC) and presents them on the cell surface for recognition by the CD4 T-cells. The peptide binding cleft accommodates peptides of 10-30 residues. The peptides presented by MHC class II molecules are generated mostly by degradation of proteins that access the endocytic route, where they are processed by lysosomal proteases and other hydrolases. Exogenous antigens that have been endocytosed by the APC are thus readily available for presentation via MHC II molecules, and for this reason this antigen presentation pathway is usually referred to as exogenous. As membrane proteins on their way to degradation in lysosomes as part of their normal turn-over are also contained in the endosomal/lysosomal compartments, exogenous antigens must compete with those derived from endogenous components. Autophagy is also a source of endogenous peptides, autophagosomes constitutively fuse with MHC class II loading compartments. In addition to APCs, other cells of the gastrointestinal tract, such as epithelial cells, express MHC class II molecules and CD74 and act as APCs, which is an unusual trait of the GI tract. To produce a MHC class II molecule that presents an antigen, three MHC class II molecules (heterodimers of an alpha and a beta chain) associate with a CD74 trimer in the ER to form a heterononamer. Soon after the entry of this complex into the endosomal/lysosomal system where antigen processing occurs, CD74 undergoes a sequential degradation by various proteases, including CTSS and CTSL, leaving a small fragment termed CLIP (class-II-associated invariant chain peptide). The removal of CLIP is facilitated by HLA-DM via direct binding to the alpha-beta-CLIP complex so that CLIP is released. HLA-DM stabilizes MHC class II molecules until primary high affinity antigenic peptides are bound. The MHC II molecule bound to a peptide is then transported to the cell membrane surface. In B-cells, the interaction between HLA-DM and MHC class II molecules is regulated by HLA-DO. Primary dendritic cells (DCs) also to express HLA-DO. Lysosomal microenvironment has been implicated in the regulation of antigen loading into MHC II molecules, increased acidification produces increased proteolysis and efficient peptide loading. [The UniProt Consortium]
Schlagworte: Anti-Dw2, Anti-DR beta-5, Anti-DR2-beta-2, Anti-MHC class II antigen DRB5, Anti-HLA class II histocompatibility antigen, DR beta 5 chain, HLA-DRB5 Antibody
Hersteller: Cusabio
Hersteller-Nr: PA657235ZA01HU

Eigenschaften

Anwendung: ELISA, WB
Antikörper-Typ: Polyclonal
Konjugat: No
Wirt: Rabbit
Spezies-Reaktivität: Homo sapiens (Human)
Immunogen: Recombinant Homo sapiens HLA-DRB5 protein. Sequence: enquire (Customer can provide a specific protein sequence for the antibody production and the price may vary depending on immunogen options)
Format: Antigen Affinity Purified

Handhabung & Sicherheit

Lagerung: -20°C
Versand: +4°C (International: +4°C)
Achtung
Nur für Forschungszwecke und Laboruntersuchungen: Nicht für die Anwendung im oder am Menschen!
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