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2js7
From Proteopedia
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| - | + | ==Solution NMR structure of human myeloid differentiation primary response (MyD88). Northeast Structural Genomics target HR2869A== | |
| - | + | <StructureSection load='2js7' size='340' side='right' caption='[[2js7]], [[NMR_Ensembles_of_Models | 20 NMR models]]' scene=''> | |
| - | + | == Structural highlights == | |
| - | ==Disease== | + | <table><tr><td colspan='2'>[[2js7]] is a 1 chain structure with sequence from [http://en.wikipedia.org/wiki/Homo_sapiens Homo sapiens]. Full experimental information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=2JS7 OCA]. For a <b>guided tour on the structure components</b> use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=2JS7 FirstGlance]. <br> |
| - | [[http://www.uniprot.org/uniprot/MYD88_HUMAN MYD88_HUMAN]] Defects in MYD88 are the cause of MYD88 deficiency (MYD88D) [MIM:[http://omim.org/entry/612260 612260]]; also known as recurrent pyogenic bacterial infections due to MYD88 deficiency. Patients suffer from autosomal recessive, life-threatening, often recurrent pyogenic bacterial infections, including invasive pneumococcal disease, and die between 1 and 11 months of age. Surviving patients are otherwise healthy, with normal resistance to other microbes, and their clinical status improved with age.<ref>PMID:19506249</ref><ref>PMID:18669862</ref> | + | </td></tr><tr><td class="sblockLbl"><b>[[Gene|Gene:]]</b></td><td class="sblockDat">MYD88 ([http://www.ncbi.nlm.nih.gov/Taxonomy/Browser/wwwtax.cgi?mode=Info&srchmode=5&id=9606 Homo sapiens])</td></tr> |
| - | + | <tr><td class="sblockLbl"><b>Resources:</b></td><td class="sblockDat"><span class='plainlinks'>[http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=2js7 FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=2js7 OCA], [http://www.rcsb.org/pdb/explore.do?structureId=2js7 RCSB], [http://www.ebi.ac.uk/pdbsum/2js7 PDBsum], [http://www.topsan.org/Proteins/NESGC/2js7 TOPSAN]</span></td></tr> | |
| - | ==Function== | + | <table> |
| - | [[http://www.uniprot.org/uniprot/MYD88_HUMAN MYD88_HUMAN]] Adapter protein involved in the Toll-like receptor and IL-1 receptor signaling pathway in the innate immune response. Acts via IRAK1, IRAK2, IRF7 and TRAF6, leading to NF-kappa-B activation, cytokine secretion and the inflammatory response. Increases IL-8 transcription. Involved in IL-18-mediated signaling pathway. Activates IRF1 resulting in its rapid migration into the nucleus to mediate an efficient induction of IFN-beta, NOS2/INOS, and IL12A genes (By similarity).<ref>PMID:9013863</ref><ref>PMID:15361868</ref><ref>PMID:18292575</ref><ref>PMID:19506249</ref> | + | == Disease == |
| - | + | [[http://www.uniprot.org/uniprot/MYD88_HUMAN MYD88_HUMAN]] Defects in MYD88 are the cause of MYD88 deficiency (MYD88D) [MIM:[http://omim.org/entry/612260 612260]]; also known as recurrent pyogenic bacterial infections due to MYD88 deficiency. Patients suffer from autosomal recessive, life-threatening, often recurrent pyogenic bacterial infections, including invasive pneumococcal disease, and die between 1 and 11 months of age. Surviving patients are otherwise healthy, with normal resistance to other microbes, and their clinical status improved with age.<ref>PMID:19506249</ref> <ref>PMID:18669862</ref> | |
| - | == | + | == Function == |
| - | [[ | + | [[http://www.uniprot.org/uniprot/MYD88_HUMAN MYD88_HUMAN]] Adapter protein involved in the Toll-like receptor and IL-1 receptor signaling pathway in the innate immune response. Acts via IRAK1, IRAK2, IRF7 and TRAF6, leading to NF-kappa-B activation, cytokine secretion and the inflammatory response. Increases IL-8 transcription. Involved in IL-18-mediated signaling pathway. Activates IRF1 resulting in its rapid migration into the nucleus to mediate an efficient induction of IFN-beta, NOS2/INOS, and IL12A genes (By similarity).<ref>PMID:9013863</ref> <ref>PMID:15361868</ref> <ref>PMID:18292575</ref> <ref>PMID:19506249</ref> |
| - | + | == Evolutionary Conservation == | |
| - | == | + | [[Image:Consurf_key_small.gif|200px|right]] |
| - | <references | + | Check<jmol> |
| + | <jmolCheckbox> | ||
| + | <scriptWhenChecked>select protein; define ~consurf_to_do selected; consurf_initial_scene = true; script "/wiki/ConSurf/js/2js7_consurf.spt"</scriptWhenChecked> | ||
| + | <scriptWhenUnchecked>script /wiki/extensions/Proteopedia/spt/initialview01.spt</scriptWhenUnchecked> | ||
| + | <text>to colour the structure by Evolutionary Conservation</text> | ||
| + | </jmolCheckbox> | ||
| + | </jmol>, as determined by [http://consurfdb.tau.ac.il/ ConSurfDB]. You may read the [[Conservation%2C_Evolutionary|explanation]] of the method and the full data available from [http://bental.tau.ac.il/new_ConSurfDB/chain_selection.php?pdb_ID=2ata ConSurf]. | ||
| + | <div style="clear:both"></div> | ||
| + | == References == | ||
| + | <references/> | ||
| + | __TOC__ | ||
| + | </StructureSection> | ||
[[Category: Homo sapiens]] | [[Category: Homo sapiens]] | ||
[[Category: Acton, T B.]] | [[Category: Acton, T B.]] | ||
Revision as of 10:24, 30 September 2014
Solution NMR structure of human myeloid differentiation primary response (MyD88). Northeast Structural Genomics target HR2869A
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Categories: Homo sapiens | Acton, T B. | Ciano, M. | Ho, C. | Kennedy, M A. | Ma, L-C. | Montelione, G T. | NESG, Northeast Structural Genomics Consortium. | Ramelot, T A. | Rossi, P. | Tao, X. | Tong, L. | Xiao, R. | Innate immune signaling | Myd88 human | Nesg | Northeast structural genomics consortium | Protein structure initiative | Psi-2 | Signaling protein | Structural genomic | Tir domain | Toll like receptor adaptor domain

