Made-to-order (12-14 weeks)
Note: All of our proteins are default shipped with normal blue ice packs, if you request to ship with dry ice, please communicate with us in advance and extra fees will be charged.
Value-added Deliverables
① 200ug * antigen (positive control); ② 1ml * Pre-immune serum (negative control);
Quality Guarantee
① Antibody purity can be guaranteed above 90% by SDS-PAGE detection; ② ELISA titer can be guaranteed 1: 64,000; ③ WB validation with antigen can be guaranteed positive;
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.
Gene References into Functions
Variation at HLA-DRB5 being associated both with Parkinson's disease and Alzheimer's disease, ariation at HLA-DRB5 being associated both with Parkinson's disease and Alzheimer's disease.PMID:27713094
This study identified genetic overlap between Alzheimer disease and immune-mediated diseases, implicating the HLA locus and IPMK in the pathobiology of Alzheimer disease.PMID:27088644
HLA-DRB5 affects type 1 diabetes risk and islet autoantibodies.PMID:26740600
Brain DNA methylation in HLA-DRB5 was associated with pathological Alzheimer disease.PMID:25365775
findings indicated that copy number variants of HLA-DRB5 was associated with the risk of systemic lupus erythematosus, and copy number deletion appeared to be protective for SLE.PMID:24366815
DRB5*01:01 is associated with Thai systemic lupus erythematosus; the association is stronger than that of DRB1*15:01; genetic contribution of DRB5*01:01 is due partially to linkage disequilibrium between DRB1*16:02 and DRB5*01:01 in northern Thai populationPMID:22862923
HLA-DRB5 was highly expressed in peripheral blood mononuclear cells from patients with systemic sclerosis-related interstitial lung disease. The HLA-DRB5*01:05 allele is a risk factor for interstitial lung disease in patients with systemic sclerosis.PMID:22723597
Transgenic mice expressing HLA-DRB5*01:01 genes are crossed with histocompatibility class (MHC) II knockout mice to replace mouse MHC class II genes with human MHC class II genes in a humanized model of autoimmunity.PMID:22888134
Eighteen out of 19 individuals showed HLA-DRB5, and none of the HLA-DRB5*null individuals, carried the HLADRB1* 15 allele. The findings support a contribution for HLA-DRB5 in keloid pathogenesis.PMID:22033527
HLA-DRB5 was found to have bimodal expression in human skeletal muscle tissue.PMID:21299892
In our study, we found that the HLA-DR9 allele and HPV16E6 infection had a function of synergy in the process of malignant transformation of esophageal epithelial cells, and jointly promoting the occurrence and development of esophageal cancer.PMID:20193235
the identification of a new HLA-DRB5 allele found in two members of a British Caucasoid family.PMID:14617041
hMBP82-100-specific type B T cells escaped tolerance in HLA-DRB5*0101 Tg micePMID:18713991
the gene frequency of HLADR5 was significantly decreased in the total group of patients with autoimmune liver diseasePMID:19811438
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Subcellular 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.