HLA-DQB1: A Drug Target / Disease Biomarker (G3119)

Target Name: HLA-DQB1

NCBI ID: G3119

HLA-DQB1

HLA-DQB1: A Drug Target / Disease Biomarker

HLA-DQB1 is a highly polymorphic human leukocyte antigen (HLA) class I molecule that is expressed in the majority of human tissues and cells. HLA-DQB1 is involved in the immune response and is a key factor in the development of autoimmune diseases, such as rheumatoid arthritis, lupus, and multiple sclerosis.

HLA-DQB1 is a member of the HLA-DQ family of molecules, which are characterized by the presence of a variable region that contains a core region of highly conserved amino acids and a variable region that contains a variety of amino acids. The HLA-DQ family of molecules is one of the most well-studied families of antigens and is known for their ability to trigger an immune response in humans.

HLA-DQB1 is a 190-kDa protein that is expressed in most tissues and cells in the human body. It is primarily located in the cytoplasm of human cells and is involved in the regulation of cellular processes such as apoptosis, cell signaling, and inflammation.

One of the key functions of HLA-DQB1 is its role in the immune response. HLA-DQB1 is a major receptor for the T cell receptor, which is responsible for regulating the activity of T cells, a critical part of the immune system. When a T cell encounters an HLA-DQB1 molecule on an antigen-presenting cell (APC), it becomes activated and begins to divide and differentiate into a T cell clonal expansion. This process is essential for the development and maintenance of an immune response against infections and viruses.

In addition to its role in the immune response, HLA-DQB1 is also involved in the regulation of cellular processes that are critical for tissue homeostasis. For example, HLA-DQB1 is involved in the regulation of cell death, as it can induce apoptosis in damaged or infected cells. It is also involved in the regulation of cell signaling, as it can interact with various signaling molecules to regulate cellular processes such as cell proliferation and migration.

HLA-DQB1 is also involved in the development of autoimmune diseases. Many autoimmune diseases, such as rheumatoid arthritis, lupus, and multiple sclerosis, are characterized by the production of antibodies that target the HLA-DQB1 molecule. This leads to the activation of T cells and the production of other immune cells, which can cause inflammation and damage in the affected tissues.

Despite its involvement in the immune response and the development of autoimmune diseases, HLA-DQB1 is not a potent therapeutic target for human diseases. This is because HLA-DQB1 is a complex protein that is expressed in a variety of tissues and cells in the human body, making it difficult to target specific variations in the protein with small molecules or antibodies.

However, researchers are actively working to identify new targets for HLA-DQB1. One approach is to use small molecules or antibodies that can interact with specific regions of HLA-DQB1 to regulate its activity. This approach is based on the idea that the immune system is capable of targeting specific proteins with small molecules or antibodies, just like a targeting agent in a movie.

Another approach is to use genetic engineering techniques to introduce new variants of HLA-DQB1 that can be more easily targeted by small molecules or antibodies. This approach is called click-through technology, and it allows researchers to rapidly generate new variants of HLA-DQB1 that can be tested for their potential as drug targets.

While there is still much to be learned about the biology and pharmacology of HLA-DQB1, it is clear that this molecule plays a critical role in the immune system and is involved in the development of many autoimmune diseases. Further research is needed to fully understand the full potential of HLA-DQB1 as a drug target and to develop effective treatments for

Protein Name: Major Histocompatibility Complex, Class II, DQ 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-DQB1 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-DQB1 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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