5a6c

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'''Unreleased structure'''
 
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The entry 5a6c is ON HOLD until Paper Publication
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==Concomitant binding of Afadin to LGN and F-actin directs planar spindle orientation==
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<StructureSection load='5a6c' size='340' side='right'caption='[[5a6c]], [[Resolution|resolution]] 2.90&Aring;' scene=''>
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== Structural highlights ==
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<table><tr><td colspan='2'>[[5a6c]] is a 2 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=5A6C OCA]. For a <b>guided tour on the structure components</b> use [https://proteopedia.org/fgij/fg.htm?mol=5A6C FirstGlance]. <br>
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</td></tr><tr id='method'><td class="sblockLbl"><b>[[Empirical_models|Method:]]</b></td><td class="sblockDat" id="methodDat">X-ray diffraction, [[Resolution|Resolution]] 2.901&#8491;</td></tr>
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<tr id='ligand'><td class="sblockLbl"><b>[[Ligand|Ligands:]]</b></td><td class="sblockDat" id="ligandDat"><scene name='pdbligand=SO4:SULFATE+ION'>SO4</scene></td></tr>
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<tr id='resources'><td class="sblockLbl"><b>Resources:</b></td><td class="sblockDat"><span class='plainlinks'>[https://proteopedia.org/fgij/fg.htm?mol=5a6c FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=5a6c OCA], [https://pdbe.org/5a6c PDBe], [https://www.rcsb.org/pdb/explore.do?structureId=5a6c RCSB], [https://www.ebi.ac.uk/pdbsum/5a6c PDBsum], [https://prosat.h-its.org/prosat/prosatexe?pdbcode=5a6c ProSAT]</span></td></tr>
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</table>
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== Disease ==
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[https://www.uniprot.org/uniprot/AFAD_HUMAN AFAD_HUMAN] Note=A chromosomal aberration involving MLLT4 is associated with acute leukemias. Translocation t(6;11)(q27;q23) with MLL/HRX. The result is a rogue activator protein.[https://www.uniprot.org/uniprot/GPSM2_HUMAN GPSM2_HUMAN] Autosomal recessive nonsyndromic sensorineural deafness type DFNB;Chudley-McCullough syndrome. Chudley-McCullough syndrome (CMCS) [MIM:[https://omim.org/entry/604213 604213]: An autosomal recessive neurologic disorder characterized by early-onset sensorineural deafness and specific brain anomalies on MRI, including hypoplasia of the corpus callosum, enlarged cysterna magna with mild focal cerebellar dysplasia, and nodular heterotopia. Some patients have hydrocephalus. Psychomotor development is normal. Note=The disease is caused by mutations affecting the gene represented in this entry.<ref>PMID:20602914</ref> <ref>PMID:22578326</ref>
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== Function ==
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[https://www.uniprot.org/uniprot/AFAD_HUMAN AFAD_HUMAN] Belongs to an adhesion system, probably together with the E-cadherin-catenin system, which plays a role in the organization of homotypic, interneuronal and heterotypic cell-cell adherens junctions (AJs). Nectin- and actin-filament-binding protein that connects nectin to the actin cytoskeleton.[https://www.uniprot.org/uniprot/GPSM2_HUMAN GPSM2_HUMAN] Plays an important role in spindle pole orientation. Interacts and contributes to the functional activity of G(i) alpha proteins. Acts to stabilize the apical complex during neuroblast divisions.<ref>PMID:15632202</ref>
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<div style="background-color:#fffaf0;">
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== Publication Abstract from PubMed ==
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Polarized epithelia form by oriented cell divisions in which the mitotic spindle aligns parallel to the epithelial plane. To orient the mitotic spindle, cortical cues trigger the recruitment of NuMA-dynein-based motors, which pull on astral microtubules via the protein LGN. We demonstrate that the junctional protein Afadin is required for spindle orientation and correct epithelial morphogenesis of Caco-2 cysts. Molecularly, Afadin binds directly and concomitantly to F-actin and to LGN. We determined the crystallographic structure of human Afadin in complex with LGN and show that it resembles the LGN-NuMA complex. In mitosis, Afadin is necessary for cortical accumulation of LGN and NuMA above the spindle poles, in an F-actin-dependent manner. Collectively, our results depict Afadin as a molecular hub governing the enrichment of LGN and NuMA at the cortex. To our knowledge, Afadin is the first-described mechanical anchor between dynein and cortical F-actin.
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Authors: Carminati, M., Gallini, S., Pirovano, L., Alfieri, A., Bisi, S., Mapelli, M.
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Concomitant binding of Afadin to LGN and F-actin directs planar spindle orientation.,Carminati M, Gallini S, Pirovano L, Alfieri A, Bisi S, Mapelli M Nat Struct Mol Biol. 2016 Jan 11. doi: 10.1038/nsmb.3152. PMID:26751642<ref>PMID:26751642</ref>
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Description: Concomitant binding of Afadin to LGN and F-actin directs planar spindle orientation
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From MEDLINE&reg;/PubMed&reg;, a database of the U.S. National Library of Medicine.<br>
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[[Category: Unreleased Structures]]
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</div>
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[[Category: Pirovano, L]]
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<div class="pdbe-citations 5a6c" style="background-color:#fffaf0;"></div>
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[[Category: Alfieri, A]]
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== References ==
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[[Category: Mapelli, M]]
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<references/>
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[[Category: Bisi, S]]
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__TOC__
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[[Category: Gallini, S]]
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</StructureSection>
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[[Category: Carminati, M]]
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[[Category: Homo sapiens]]
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[[Category: Large Structures]]
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[[Category: Alfieri A]]
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[[Category: Bisi S]]
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[[Category: Carminati M]]
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[[Category: Gallini S]]
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[[Category: Mapelli M]]
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[[Category: Pirovano L]]

Current revision

Concomitant binding of Afadin to LGN and F-actin directs planar spindle orientation

PDB ID 5a6c

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