WB

Synthesized peptide derived from human HLA-DQA2. AA range:120-190

This antibody detects endogenous levels of HLA-DQA2 at Human

Liquid in PBS containing 50% glycerol, 0.5% BSA and 0.02% sodium azide.

WB 1:500-2000

The antibody was affinity-purified from rabbit antiserum by affinity-chromatography using epitope-specific immunogen.

1 mg/ml

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.

HLA-DQA2 HLA-DXA

HLA class II histocompatibility antigen, DQ alpha 2 chain (DX alpha chain) (HLA class II histocompatibility antigen, DQ (6) alpha chain) (HLA-DQA1) (MHC class II DQA2)

=_xlfn.TEXTJOIN(";",TRUE,W3183,X3183,Y3183,Z3183)

3118

P01906

Cell membrane ; Single-pass type I membrane protein . Endoplasmic reticulum membrane ; Single-pass type I membrane protein . Golgi apparatus , trans-Golgi network membrane ; Single-pass type I membrane protein . Endosome membrane ; Single-pass type I membrane protein . Lysosome membrane ; Single-pass type I membrane protein . The MHC class II complex transits through a number of intracellular compartments in the endocytic pathway until it reaches the cell membrane for antigen presentation.

Restricted to skin Langerhans cells , although some expression at low levels may occur at the surface of B lymphoblastoid cells.

-15°C to -25°C/1 year(Do not lower than -25°C)