3qb7: Difference between revisions
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==Interleukin-4 mutant RGA bound to cytokine receptor common gamma== | ==Interleukin-4 mutant RGA bound to cytokine receptor common gamma== | ||
<StructureSection load='3qb7' size='340' side='right' caption='[[3qb7]], [[Resolution|resolution]] 3.25Å' scene=''> | <StructureSection load='3qb7' size='340' side='right'caption='[[3qb7]], [[Resolution|resolution]] 3.25Å' scene=''> | ||
== Structural highlights == | == Structural highlights == | ||
<table><tr><td colspan='2'>[[3qb7]] is a 4 chain structure with sequence from [ | <table><tr><td colspan='2'>[[3qb7]] is a 4 chain structure with sequence from [https://en.wikipedia.org/wiki/Homo_sapiens Homo sapiens]. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=3QB7 OCA]. For a <b>guided tour on the structure components</b> use [https://proteopedia.org/fgij/fg.htm?mol=3QB7 FirstGlance]. <br> | ||
</td></tr><tr id=' | </td></tr><tr id='method'><td class="sblockLbl"><b>[[Empirical_models|Method:]]</b></td><td class="sblockDat" id="methodDat">X-ray diffraction, [[Resolution|Resolution]] 3.245Å</td></tr> | ||
<tr id=' | <tr id='ligand'><td class="sblockLbl"><b>[[Ligand|Ligands:]]</b></td><td class="sblockDat" id="ligandDat"><scene name='pdbligand=NAG:N-ACETYL-D-GLUCOSAMINE'>NAG</scene>, <scene name='pdbligand=SO4:SULFATE+ION'>SO4</scene></td></tr> | ||
<tr id='resources'><td class="sblockLbl"><b>Resources:</b></td><td class="sblockDat"><span class='plainlinks'>[ | <tr id='resources'><td class="sblockLbl"><b>Resources:</b></td><td class="sblockDat"><span class='plainlinks'>[https://proteopedia.org/fgij/fg.htm?mol=3qb7 FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=3qb7 OCA], [https://pdbe.org/3qb7 PDBe], [https://www.rcsb.org/pdb/explore.do?structureId=3qb7 RCSB], [https://www.ebi.ac.uk/pdbsum/3qb7 PDBsum], [https://prosat.h-its.org/prosat/prosatexe?pdbcode=3qb7 ProSAT]</span></td></tr> | ||
</table> | </table> | ||
== Disease == | == Disease == | ||
[ | [https://www.uniprot.org/uniprot/IL4_HUMAN IL4_HUMAN] Genetic variations in IL4 may be a cause of susceptibility to ischemic stroke (ISCHSTR) [MIM:[https://omim.org/entry/601367 601367]; also known as cerebrovascular accident or cerebral infarction. A stroke is an acute neurologic event leading to death of neural tissue of the brain and resulting in loss of motor, sensory and/or cognitive function. Ischemic strokes, resulting from vascular occlusion, is considered to be a highly complex disease consisting of a group of heterogeneous disorders with multiple genetic and environmental risk factors.<ref>PMID:14681304</ref> | ||
== Function == | == Function == | ||
[ | [https://www.uniprot.org/uniprot/IL4_HUMAN IL4_HUMAN] Participates in at least several B-cell activation processes as well as of other cell types. It is a costimulator of DNA-synthesis. It induces the expression of class II MHC molecules on resting B-cells. It enhances both secretion and cell surface expression of IgE and IgG1. It also regulates the expression of the low affinity Fc receptor for IgE (CD23) on both lymphocytes and monocytes. | ||
<div style="background-color:#fffaf0;"> | <div style="background-color:#fffaf0;"> | ||
== Publication Abstract from PubMed == | == Publication Abstract from PubMed == | ||
| Line 23: | Line 23: | ||
==See Also== | ==See Also== | ||
*[[Interleukin|Interleukin]] | *[[Interleukin 3D structures|Interleukin 3D structures]] | ||
*[[Interleukin receptor|Interleukin receptor]] | *[[Interleukin receptor 3D structures|Interleukin receptor 3D structures]] | ||
== References == | == References == | ||
<references/> | <references/> | ||
__TOC__ | __TOC__ | ||
</StructureSection> | </StructureSection> | ||
[[Category: | [[Category: Homo sapiens]] | ||
[[Category: Bates | [[Category: Large Structures]] | ||
[[Category: Creusot | [[Category: Bates DL]] | ||
[[Category: Fathman | [[Category: Creusot RJ]] | ||
[[Category: Garcia | [[Category: Fathman CG]] | ||
[[Category: Junttila | [[Category: Garcia KC]] | ||
[[Category: Lupardus | [[Category: Junttila IS]] | ||
[[Category: Moraga | [[Category: Lupardus P]] | ||
[[Category: Paul | [[Category: Moraga I]] | ||
[[Category: Paul WE]] | |||
Latest revision as of 03:34, 28 December 2023
Interleukin-4 mutant RGA bound to cytokine receptor common gammaInterleukin-4 mutant RGA bound to cytokine receptor common gamma
Structural highlights
DiseaseIL4_HUMAN Genetic variations in IL4 may be a cause of susceptibility to ischemic stroke (ISCHSTR) [MIM:601367; also known as cerebrovascular accident or cerebral infarction. A stroke is an acute neurologic event leading to death of neural tissue of the brain and resulting in loss of motor, sensory and/or cognitive function. Ischemic strokes, resulting from vascular occlusion, is considered to be a highly complex disease consisting of a group of heterogeneous disorders with multiple genetic and environmental risk factors.[1] FunctionIL4_HUMAN Participates in at least several B-cell activation processes as well as of other cell types. It is a costimulator of DNA-synthesis. It induces the expression of class II MHC molecules on resting B-cells. It enhances both secretion and cell surface expression of IgE and IgG1. It also regulates the expression of the low affinity Fc receptor for IgE (CD23) on both lymphocytes and monocytes. Publication Abstract from PubMedCytokines dimerize their receptors, with the binding of the 'second chain' triggering signaling. In the interleukin (IL)-4 and IL-13 system, different cell types express varying numbers of alternative second receptor chains (gammac or IL-13Ralpha1), forming functionally distinct type I or type II complexes. We manipulated the affinity and specificity of second chain recruitment by human IL-4. A type I receptor-selective IL-4 'superkine' with 3,700-fold higher affinity for gammac was three- to ten-fold more potent than wild-type IL-4. Conversely, a variant with high affinity for IL-13Ralpha1 more potently activated cells expressing the type II receptor and induced differentiation of dendritic cells from monocytes, implicating the type II receptor in this process. Superkines showed signaling advantages on cells with lower second chain numbers. Comparative transcriptional analysis reveals that the superkines induce largely redundant gene expression profiles. Variable second chain numbers can be exploited to redirect cytokines toward distinct cell subsets and elicit new actions, potentially improving the selectivity of cytokine therapy. Redirecting cell-type specific cytokine responses with engineered interleukin-4 superkines.,Junttila IS, Creusot RJ, Moraga I, Bates DL, Wong MT, Alonso MN, Suhoski MM, Lupardus P, Meier-Schellersheim M, Engleman EG, Utz PJ, Fathman CG, Paul WE, Garcia KC Nat Chem Biol. 2012 Oct 28. doi: 10.1038/nchembio.1096. PMID:23103943[2] From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine. See AlsoReferences
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