3bpl: Difference between revisions

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==Crystal structure of the IL4-IL4R-Common Gamma ternary complex==
==Crystal structure of the IL4-IL4R-Common Gamma ternary complex==
<StructureSection load='3bpl' size='340' side='right' caption='[[3bpl]], [[Resolution|resolution]] 2.93&Aring;' scene=''>
<StructureSection load='3bpl' size='340' side='right'caption='[[3bpl]], [[Resolution|resolution]] 2.93&Aring;' scene=''>
== Structural highlights ==
== Structural highlights ==
<table><tr><td colspan='2'>[[3bpl]] is a 3 chain structure with sequence from [http://en.wikipedia.org/wiki/Human Human]. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=3BPL OCA]. For a <b>guided tour on the structure components</b> use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=3BPL FirstGlance]. <br>
<table><tr><td colspan='2'>[[3bpl]] is a 3 chain structure with sequence from [https://en.wikipedia.org/wiki/Human Human]. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=3BPL OCA]. For a <b>guided tour on the structure components</b> use [https://proteopedia.org/fgij/fg.htm?mol=3BPL FirstGlance]. <br>
</td></tr><tr id='ligand'><td class="sblockLbl"><b>[[Ligand|Ligands:]]</b></td><td class="sblockDat"><scene name='pdbligand=FUC:ALPHA-L-FUCOSE'>FUC</scene>, <scene name='pdbligand=NAG:N-ACETYL-D-GLUCOSAMINE'>NAG</scene></td></tr>
</td></tr><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=FUC:ALPHA-L-FUCOSE'>FUC</scene></td></tr>
<tr id='related'><td class="sblockLbl"><b>[[Related_structure|Related:]]</b></td><td class="sblockDat">[[3bpn|3bpn]], [[3bpo|3bpo]]</td></tr>
<tr id='related'><td class="sblockLbl"><b>[[Related_structure|Related:]]</b></td><td class="sblockDat"><div style='overflow: auto; max-height: 3em;'>[[3bpn|3bpn]], [[3bpo|3bpo]]</div></td></tr>
<tr id='gene'><td class="sblockLbl"><b>[[Gene|Gene:]]</b></td><td class="sblockDat">IL4 ([http://www.ncbi.nlm.nih.gov/Taxonomy/Browser/wwwtax.cgi?mode=Info&srchmode=5&id=9606 HUMAN]), IL4R, 582J2.1, IL4RA ([http://www.ncbi.nlm.nih.gov/Taxonomy/Browser/wwwtax.cgi?mode=Info&srchmode=5&id=9606 HUMAN]), IL2RG ([http://www.ncbi.nlm.nih.gov/Taxonomy/Browser/wwwtax.cgi?mode=Info&srchmode=5&id=9606 HUMAN])</td></tr>
<tr id='gene'><td class="sblockLbl"><b>[[Gene|Gene:]]</b></td><td class="sblockDat">IL4 ([https://www.ncbi.nlm.nih.gov/Taxonomy/Browser/wwwtax.cgi?mode=Info&srchmode=5&id=9606 HUMAN]), IL4R, 582J2.1, IL4RA ([https://www.ncbi.nlm.nih.gov/Taxonomy/Browser/wwwtax.cgi?mode=Info&srchmode=5&id=9606 HUMAN]), IL2RG ([https://www.ncbi.nlm.nih.gov/Taxonomy/Browser/wwwtax.cgi?mode=Info&srchmode=5&id=9606 HUMAN])</td></tr>
<tr id='resources'><td class="sblockLbl"><b>Resources:</b></td><td class="sblockDat"><span class='plainlinks'>[http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=3bpl FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=3bpl OCA], [http://pdbe.org/3bpl PDBe], [http://www.rcsb.org/pdb/explore.do?structureId=3bpl RCSB], [http://www.ebi.ac.uk/pdbsum/3bpl PDBsum], [http://prosat.h-its.org/prosat/prosatexe?pdbcode=3bpl ProSAT]</span></td></tr>
<tr id='resources'><td class="sblockLbl"><b>Resources:</b></td><td class="sblockDat"><span class='plainlinks'>[https://proteopedia.org/fgij/fg.htm?mol=3bpl FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=3bpl OCA], [https://pdbe.org/3bpl PDBe], [https://www.rcsb.org/pdb/explore.do?structureId=3bpl RCSB], [https://www.ebi.ac.uk/pdbsum/3bpl PDBsum], [https://prosat.h-its.org/prosat/prosatexe?pdbcode=3bpl ProSAT]</span></td></tr>
</table>
</table>
== Disease ==
== Disease ==
[[http://www.uniprot.org/uniprot/IL4_HUMAN IL4_HUMAN]] Genetic variations in IL4 may be a cause of susceptibility to ischemic stroke (ISCHSTR) [MIM:[http://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>  [[http://www.uniprot.org/uniprot/IL2RG_HUMAN IL2RG_HUMAN]] Defects in IL2RG are the cause of severe combined immunodeficiency X-linked T-cell-negative/B-cell-positive/NK-cell-negative (XSCID) [MIM:[http://omim.org/entry/300400 300400]]; also known as agammaglobulinemia Swiss type. A form of severe combined immunodeficiency (SCID), a genetically and clinically heterogeneous group of rare congenital disorders characterized by impairment of both humoral and cell-mediated immunity, leukopenia, and low or absent antibody levels. Patients present in infancy recurrent, persistent infections by opportunistic organisms. The common characteristic of all types of SCID is absence of T-cell-mediated cellular immunity due to a defect in T-cell development.<ref>PMID:8401490</ref> <ref>PMID:8299698</ref> <ref>PMID:8088810</ref> <ref>PMID:8027558</ref> <ref>PMID:7937790</ref> <ref>PMID:7668284</ref> <ref>PMID:7557965</ref> <ref>PMID:7860773</ref> <ref>PMID:8900089</ref> <ref>PMID:9150740</ref>  Defects in IL2RG are the cause of X-linked combined immunodeficiency (XCID) [MIM:[http://omim.org/entry/312863 312863]]. XCID is a less severe form of X-linked immunodeficiency with a less severe degree of deficiency in cellular and humoral immunity than that seen in XSCID.<ref>PMID:7883965</ref> <ref>PMID:9399950</ref>   
[[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>  [[https://www.uniprot.org/uniprot/IL2RG_HUMAN IL2RG_HUMAN]] Defects in IL2RG are the cause of severe combined immunodeficiency X-linked T-cell-negative/B-cell-positive/NK-cell-negative (XSCID) [MIM:[https://omim.org/entry/300400 300400]]; also known as agammaglobulinemia Swiss type. A form of severe combined immunodeficiency (SCID), a genetically and clinically heterogeneous group of rare congenital disorders characterized by impairment of both humoral and cell-mediated immunity, leukopenia, and low or absent antibody levels. Patients present in infancy recurrent, persistent infections by opportunistic organisms. The common characteristic of all types of SCID is absence of T-cell-mediated cellular immunity due to a defect in T-cell development.<ref>PMID:8401490</ref> <ref>PMID:8299698</ref> <ref>PMID:8088810</ref> <ref>PMID:8027558</ref> <ref>PMID:7937790</ref> <ref>PMID:7668284</ref> <ref>PMID:7557965</ref> <ref>PMID:7860773</ref> <ref>PMID:8900089</ref> <ref>PMID:9150740</ref>  Defects in IL2RG are the cause of X-linked combined immunodeficiency (XCID) [MIM:[https://omim.org/entry/312863 312863]]. XCID is a less severe form of X-linked immunodeficiency with a less severe degree of deficiency in cellular and humoral immunity than that seen in XSCID.<ref>PMID:7883965</ref> <ref>PMID:9399950</ref>   
== Function ==
== Function ==
[[http://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. [[http://www.uniprot.org/uniprot/IL2RG_HUMAN IL2RG_HUMAN]] Common subunit for the receptors for a variety of interleukins. [[http://www.uniprot.org/uniprot/IL4RA_HUMAN IL4RA_HUMAN]] Receptor for both interleukin 4 and interleukin 13. Couples to the JAK1/2/3-STAT6 pathway. The IL4 response is involved in promoting Th2 differentiation. The IL4/IL13 responses are involved in regulating IgE production and, chemokine and mucus production at sites of allergic inflammation. In certain cell types, can signal through activation of insulin receptor substrates, IRS1/IRS2.<ref>PMID:8124718</ref>  Soluble IL4R (sIL4R) inhibits IL4-mediated cell proliferation and IL5 up-regulation by T-cells.<ref>PMID:8124718</ref>   
[[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. [[https://www.uniprot.org/uniprot/IL2RG_HUMAN IL2RG_HUMAN]] Common subunit for the receptors for a variety of interleukins. [[https://www.uniprot.org/uniprot/IL4RA_HUMAN IL4RA_HUMAN]] Receptor for both interleukin 4 and interleukin 13. Couples to the JAK1/2/3-STAT6 pathway. The IL4 response is involved in promoting Th2 differentiation. The IL4/IL13 responses are involved in regulating IgE production and, chemokine and mucus production at sites of allergic inflammation. In certain cell types, can signal through activation of insulin receptor substrates, IRS1/IRS2.<ref>PMID:8124718</ref>  Soluble IL4R (sIL4R) inhibits IL4-mediated cell proliferation and IL5 up-regulation by T-cells.<ref>PMID:8124718</ref>   
== Evolutionary Conservation ==
== Evolutionary Conservation ==
[[Image:Consurf_key_small.gif|200px|right]]
[[Image:Consurf_key_small.gif|200px|right]]
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==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/>
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</StructureSection>
</StructureSection>
[[Category: Human]]
[[Category: Human]]
[[Category: Large Structures]]
[[Category: Garcia, K C]]
[[Category: Garcia, K C]]
[[Category: B-cell activation]]
[[Category: B-cell activation]]

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