JavaScript is currently not supported/disabled by this browser. Please enable JavaScript for full functionality.

Call Us 1 - 866 - 986 - 9598
[email protected]

Sign Up

Login
- My Order
- Return Requests
- Track my Order

Home / Proteins & Peptide

Recombinant Human HLA class II histocompatibility antigen, DRB1 beta chain(HLA-DRB1),partial

SKU : BHP10504695

Contact us to order

Tel

+1 866.986.9598

Email

[email protected]

Get a Quote

Request More Infos

CUSABIO TECHONOLOGY LLC

view supplier details

Order Now

Credit card payments now incur a 3% fee.

Contact us to order

Tel

+1 866.986.9598

Email

[email protected]

Get a Quote

Ask Merchant

Request More Infos

Sample Request

Mfr.No.	CSB-EP361230HU
Description	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. (Microbial infection) Acts as a receptor for Epstein-Barr virus on lymphocytes.
Alternative Names	MHC class II antigen DRB1*1
Tag	N-terminal 10xHis-SUMO-tagged and C-terminal Myc-tagged
Regulatory	RUO
Relevance	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. (Microbial infection) Acts as a receptor for Epstein-Barr virus on lymphocytes.
Source	E.coli
Notes	Repeated freezing and thawing is not recommended. Store working aliquots at 4°C for up to one week.
Expression Region	30-227aa
Mol Weight	42.9kDa
Nature	Recombinant
Protein Description	Partial

Involvement In Disease	Sarcoidosis 1 (SS1)
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
Uniprot	P04229, P04229
Database Links	HGNC:4948 OMIM:142857 UniGene:Hs.534322
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.; FUNCTION
Pathway	Antigen processing and presentation; Hematopoietic cell lineage; Th1 and Th2 cell differentiation; Th17 cell differentiation
Protein Families	MHC class II family
Research Area	Immunology
Weight	42.9 kDa

Stotage Note	Repeated freezing and thawing is not recommended. Store working aliquots at 4℃ for up to one week.
Buffer	Tris-based buffer，50% glycerol
Purity	Greater than 90% as determined by SDS-PAGE.
Storage	The shelf life is related to many factors, storage state, buffer ingredients, storage temperature and the stability of the protein itself. Generally, the shelf life of liquid form is 6 months at -20°C/-80°C. The shelf life of lyophilized form is 12 months at -20°C/-80°C.
Storage Buffer	Tris-based buffer,50% glycerol

Immunogen Species	Homo Sapiens (Human)

Have you used this product?

Rate it now..!!

Login to Review

SKU	Supplier No.	Size	Your price	Quantity
BHP10504695	CSB-EP361230HU	1mg	$1812		Add to Cart
BHP10504695	CSB-EP361230HU	100ug	$419		Add to Cart
BHP10504695	CSB-EP361230HU	20ug	$224		Add to Cart

ebiohippo.com provides biomedical researchers with a one-stop informatic shopping experience by transforming biotechnology products’ data into a ready-to-analyze state. We collect and unify suppliers’ data on a single platform to reduce the time of searching, uncertainty, and cost of scientific experiments.

© 2024 Biohippo. All rights reserved.