Volume : 100 µg
Purification : Immunogen affinity purified
Form : liquid
Purity : 95% as determined by SDS-PAGE
Host : Rabbit
Clonality : polyclonal Ab
Clone ID :
Isotype : IgG
Storage : PBS with 0.02% sodium azide and 50% glycerol pH 7.3,-20? for 12 months(Avoid repeated freeze / thaw cycles.)
Background : 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 molec µLes 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 molec µLes, 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 molec µLes and CD74 and act as APCs, which is an unusual trait of the GI tract. To produce a MHC class II molec µLe that presents an antigen, three MHC class II molec µLes(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 molec µLes until primary high affinity antigenic peptides are bound. The MHC II molec µLe bound to a peptide is then transported to the cell membrane surface. In B-cells, the interaction between HLA-DM and MHC class II molec µLes is reg µLated by HLA-DO. Primary dendritic cells(DCs) also to express HLA-DO. Lysosomal microenvironment has been implicated in the reg µLation of antigen loading into MHC II molec µLes, increased acidification produces increased proteolysis and efficient peptide loading.
Immunogen : major histocompatibility complex, class II, DR beta 5
Aliases :
Observed MW : 30 kDa
Uniprot ID : Q30154
Reactivity : Human, Mouse, Rat
Application : ELISA, WB, IHC
Recommended dilution : WB : 1 : 500-1 : 2000; IHC : 1 : 20-1 : 200
Gene ID : 3127
Research Area : Neuroscience, Immunology