HLA-DRB1 (基因名), HLA class II histocompatibility antigen, DRB1-13 beta chain (蛋白名), 2B1D_HUMAN.
Human HLA-DRB1/ HLA class II histocompatibility antigen, DRB1-13 beta chain Recombinant Protein
MHC class II antigen DRB1*13, DR-13
>90% by SDS-PAGE
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50mM NaH2PO4, 500mM NaCl Buffer with 500mM Imidazole, 10%glycerol(PH8.0)
Store at -20°C. (Avoid repeated freezing and thawing.)
Heterodimer of an alpha and a beta subunit; also referred as MHC class II molecule. In the endoplasmic reticulum (ER) it forms a heterononamer; 3 MHC class II molecules bind to a CD74 homotrimer (also known as invariant chain or HLA class II histocompatibility antigen gamma chain). In the endosomal/lysosomal system; CD74 undergoes sequential degradation by various proteases; leaving a small fragment termed CLIP on each MHC class II molecule. MHC class II molecule interacts with HLA_DM, and HLA_DO in B-cells, in order to release CLIP and facilitate the binding of antigenic peptides.
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.
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 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.
MVCLRLPGGS | CMAVLTVTLM | VLSSPLALAG | DTRPRFLEYS | TSECHFFNGT |
ERVRFLDRYF | HNQEENVRFD | SDVGEFRAVT | ELGRPDAEYW | NSQKDILEDE |
RAAVDTYCRH | NYGVVESFTV | QRRVHPKVTV | YPSKTQPLQH | HNLLVCSVSG |
FYPGSIEVRW | FRNGQEEKTG | VVSTGLIHNG | DWTFQTLVML | ETVPRSGEVY |
TCQVEHPSVT | SPLTVEWRAR | SESAQSKMLS | GVGGFVLGLL | FLGAGLFIYF |
RNQKGHSGLQ | PRGFLS
"MICA polymorphisms and haplotypes with HLA-B and HLA-DRB1 in Koreans."
"Familial disease, the HLA-DRB1 shared epitope and anti-CCP antibodies influence time at appearance of substantial joint damage in rheumatoid arthritis."
"Association study of CCR5 delta 32 polymorphism among the HLA-DRB1 Caucasian population in Northern Paraná, Brazil."
"The association between the genetic polymorphism of HLA-DQA1, DQB1, and DRB1 and serum alanine aminotransferase levels in chronic hepatitis C in the Chinese population."
"Association of the HLA-DRB1 alleles with characteristic MRI features of Asian multiple sclerosis."
"Meta-analysis of HLA-DRB1 and HLA-DQB1 polymorphisms in Latin American patients with systemic lupus erythematosus."
"[Expression and analysis of HLA-A, B and DRB1 genes in patients with chronic myelogenous leukemia in Guangdong area]."
"Role of HLA-DRB1 and PTPN22 genes in susceptibility to juvenile idiopathic arthritis in Hungarian patients."
"Uncoupling the roles of HLA-DRB1 and HLA-DRB5 genes in multiple sclerosis."
"Association of the HLA-DRB1 gene with premature death, particularly from cardiovascular disease, in patients with rheumatoid arthritis and inflammatory polyarthritis."
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