======= HLA-DQB2 =======
== Gene Information ==
* **Official Symbol**: HLA-DQB2
* **Official Name**: major histocompatibility complex, class II, DQ beta 2
* **Aliases and Previous Symbols**: N/A
* **Entrez ID**: [[https://www.ncbi.nlm.nih.gov/gene/?term=3120|3120]]
* **UniProt**: [[https://www.uniprot.org/uniprot/P05538|P05538]]
* **Interactions**: [[https://thebiogrid.org/search.php?search=HLA-DQB2&organism=9606|BioGRID]]
* **PubMed articles**: [[https://www.ncbi.nlm.nih.gov/pubmed/?term=gene%20HLA-DQB2|Open PubMed]]
* **OMIM**: [[https://omim.org/entry/615161|Open OMIM]]
== Function Summary ==
* **Entrez Summary**: N/A
* **UniProt Summary**: 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. {ECO:0000269|PubMed:22407913}.
|C2-set 2|
|MHC II beta|
|C1-set|
|MHC class II receptor activity|
|MHC class II protein complex|
|integral component of lumenal side of endoplasmic reticulum membrane|
|clathrin-coated endocytic vesicle membrane|
|transport vesicle membrane|
|ER to Golgi transport vesicle membrane|
|endocytic vesicle membrane|
|interferon-gamma-mediated signaling pathway|
|trans-Golgi network membrane|
|antigen processing and presentation of exogenous peptide antigen via MHC class II|
|antigen processing and presentation of peptide antigen via MHC class II|
|antigen processing and presentation of peptide or polysaccharide antigen via MHC class II|
|cellular response to interferon-gamma|
|T cell receptor signaling pathway|
|antigen processing and presentation of exogenous peptide antigen|
|response to interferon-gamma|
|antigen processing and presentation of exogenous antigen|
|antigen processing and presentation of peptide antigen|
|endosome membrane|
|antigen processing and presentation|
|antigen receptor-mediated signaling pathway|
|lysosomal membrane|
|immune response-activating cell surface receptor signaling pathway|
|immune response-regulating cell surface receptor signaling pathway|
|immune response-activating signal transduction|
|immune response-regulating signaling pathway|
|adaptive immune response|
|Golgi membrane|
|activation of immune response|
|cytokine-mediated signaling pathway|
|innate immune response|
|positive regulation of immune response|
|defense response to other organism|
|cellular response to cytokine stimulus|
|response to cytokine|
|positive regulation of immune system process|
|regulation of immune response|
|response to other organism|
|response to external biotic stimulus|
|response to biotic stimulus|
|defense response|
|regulation of immune system process|
|immune response|
\\
=== CRISPR Data ===
^Screen^Score^
|[[:results:exp359|FK-506 30μM R07 exp359]]|1.89|
No correlation found to any other genes in chemogenomics.
Global Fraction of Cell Lines Where Essential: 1/739
^Tissue^Fraction Of Cell Lines Where Essential^
|1290807.0|0/1|
|909776.0|0/1|
|bile duct|0/28|
|blood|0/28|
|bone|0/26|
|breast|0/33|
|central nervous system|0/56|
|cervix|0/4|
|colorectal|0/17|
|esophagus|0/13|
|fibroblast|0/1|
|gastric|0/16|
|kidney|0/21|
|liver|0/20|
|lung|0/75|
|lymphocyte|0/16|
|ovary|0/26|
|pancreas|0/24|
|peripheral nervous system|1/16|
|plasma cell|0/15|
|prostate|0/1|
|skin|0/24|
|soft tissue|0/9|
|thyroid|0/2|
|upper aerodigestive|0/22|
|urinary tract|0/29|
|uterus|0/5|
== Essentiality in NALM6 ==
* **Essentiality Rank**: 6161
* **Expression level (log2 read counts)**: 1.08
{{:chemogenomics:nalm6 dist.png?nolink |}}