|Application ||IF, FC|
|Other Accession||3122, 520048|
|Isotype||Mouse / IgG3, kappa|
|Other Names||HLA class II histocompatibility antigen, DR alpha chain, MHC class II antigen DRA, HLA-DRA, HLA-DRA1|
|Storage||Store at 2 to 8°C.Antibody is stable for 24 months.|
|Precautions||HLA-DRA (MHC II) Antibody - Without BSA and Azide is for research use only and not for use in diagnostic or therapeutic procedures.|
|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.|
|Cellular Location||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. Late endosome membrane; Single-pass type I membrane protein. Note=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|
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MAb IPO-10 defines the antigen, which appears on B cell progenitors following HLA-DR and preceding CD10, CD19, CD22, CD37 and cym. It is expressed on resting B cells and than reappears and persists in cytoplasm and on cell surface until cytoplasmic Ig appears. It is a useful antibody for diagnostics of neoplasms of B cell origins. It reacts with human B cell lines Daudi, Raji, Namalva, EB-3, RPMI-8226 (50% of cells). The MAb does not label T cell lines, blood granulocytes, thymocytes or bone marrow stromal fibroblasts. No significant changes are detected after PHA or ConA stimulation while LPS and PWM stimulated cultures after 18-48h show decreased number of antigen-positive cells but in final terms of cultivation antigen is expressed again. This MAb labels B cell leukemias and some lymphomas. Hairy cell leukemia strongly reacts and 70% of B cell CLL and some B-NHL were also positive. IPO-10 reacts with AMML cells and in a majority of Hodgkinā€™s disease cases a significant percentage of affected lymph node cells were detected. ĀĀĀ
Pinchouk V.G. et al., Monoclonal antibodies IPO-3 and IPO-10 against human B cell differentiation antigens. Anticancer Research 8, 1377-1380, 1988. | Gluzman D.F. et al., Monoclonal antibodies IPO-3, IPO-4 and IPO-10 against lymphocyte differentiation antigens. Tissue Antigens 33, 151, 1989. | Sidorenko S.P. et al., Monoclonal antibodies of IPO series against B cell differentiation antigens in leukemia and lymphoma immunophenotyping. Neoplasma 39, 3-9, 1992
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