Target Name: HLA-DPB1
NCBI ID: G3115
Review Report on HLA-DPB1 Target / Biomarker Content of Review Report on HLA-DPB1 Target / Biomarker
HLA-DPB1
Other Name(s): Major histocompatibility complex, class II, DP beta 1 | DPB1 | HLA-DPB | HLA class II histocompatibility antigen, DP(W4) beta chain | HLA class II histocompatibility antigen, DP beta 1 chain | major histocompatibility complex, class II, DP beta 1 | HLA-DP1B | HLA-DP histocompatibility type, beta-1 subunit | MHC class II HLA-DP-beta-1 | HLA-DP | MHC class II antigen DPB1 | MHC HLA DPB1 | DPB1_HUMAN

HLA-DPB1: A Drug Target / Disease Biomarker

HLA-DPB1 is a human leukocyte antigen (HLA) that is expressed in most tissues of the body, including the skin, hair, nails, and nervous system. It is a member of the major histocompatibility complex (MHC) class I molecules, which are responsible for presenting antigens from the environment to the immune system.

HLA-DPB1 is a 160 amino acid protein that consists of two heavy chains and two light chains that are held together by disulfide bonds. The heavy chains contain the major histocompatibility complex (MHC) regions that are responsible for presenting antigens to T-cells, while the light chains contain the variable and constant regions that are involved in the presentation of antigens.

One of the unique features of HLA-DPB1 is its expression in the nervous system. While HLA-DPB1 is not as well-known as some other MHC molecules, it is expressed in the central nervous system (CNS) and is thought to play a role in the immune response to neurological disorders.

One of the potential reasons why HLA-DPB1 is being targeted as a drug candidate is its role in the development and progression of multiple sclerosis (MS). MS is a chronic and debilitating autoimmune disorder that affects the central nervous system and is characterized by the destruction of nerve cells.

Studies have shown that HLA-DPB1 is expressed in the brains of people with MS and that it is involved in the immune response to the disease. Additionally, research has suggested that HLA-DPB1 may be a potential target for therapies that could suppress the immune system and slow the progression of MS.

Another potential reason why HLA-DPB1 is being targeted as a drug candidate is its role in cancer. Studies have shown that HLA-DPB1 is often expressed in the cells of people with cancer, and that it may be involved in the immune response to cancer cells.

Additionally, HLA-DPB1 has also been shown to play a role in the development of autoimmune diseases such as rheumatoid arthritis and psoriasis.

In conclusion, HLA-DPB1 is a protein that is expressed in most tissues of the body and is involved in the immune response. Its expression in the nervous system and its potential role in MS, cancer, and autoimmune diseases make it an attractive candidate for further research as a drug target.

Protein Name: Major Histocompatibility Complex, Class II, DP Beta 1

Functions: 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

The "HLA-DPB1 Target / Biomarker Review Report" is a customizable review of hundreds up to thousends of related scientific research literature by AI technology, covering specific information about HLA-DPB1 comprehensively, including but not limited to:
•   general information;
•   protein structure and compound binding;
•   protein biological mechanisms;
•   its importance;
•   the target screening and validation;
•   expression level;
•   disease relevance;
•   drug resistance;
•   related combination drugs;
•   pharmacochemistry experiments;
•   related patent analysis;
•   advantages and risks of development, etc.
The report is helpful for project application, drug molecule design, research progress updates, publication of research papers, patent applications, etc. If you are interested to get a full version of this report, please feel free to contact us at BD@silexon.ai

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