3j82: Difference between revisions
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''' | ==Electron cryo-microscopy of DNGR-1 in complex with F-actin== | ||
<StructureSection load='3j82' size='340' side='right' caption='[[3j82]], [[Resolution|resolution]] 7.70Å' scene=''> | |||
== Structural highlights == | |||
<table><tr><td colspan='2'>[[3j82]] is a 4 chain structure with sequence from [http://en.wikipedia.org/wiki/ ] and [http://en.wikipedia.org/wiki/Homo_sapiens Homo sapiens]. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=3J82 OCA]. For a <b>guided tour on the structure components</b> use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=3J82 FirstGlance]. <br> | |||
</td></tr><tr id='ligand'><td class="sblockLbl"><b>[[Ligand|Ligands:]]</b></td><td class="sblockDat"><scene name='pdbligand=ADP:ADENOSINE-5-DIPHOSPHATE'>ADP</scene>, <scene name='pdbligand=CA:CALCIUM+ION'>CA</scene></td></tr> | |||
<tr id='NonStdRes'><td class="sblockLbl"><b>[[Non-Standard_Residue|NonStd Res:]]</b></td><td class="sblockDat"><scene name='pdbligand=HIC:4-METHYL-HISTIDINE'>HIC</scene></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=3j82 FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=3j82 OCA], [http://www.rcsb.org/pdb/explore.do?structureId=3j82 RCSB], [http://www.ebi.ac.uk/pdbsum/3j82 PDBsum]</span></td></tr> | |||
[[ | </table> | ||
[[Category: | == Disease == | ||
[[http://www.uniprot.org/uniprot/ACTB_HUMAN ACTB_HUMAN]] Defects in ACTB are a cause of dystonia juvenile-onset (DYTJ) [MIM:[http://omim.org/entry/607371 607371]]. DYTJ is a form of dystonia with juvenile onset. Dystonia is defined by the presence of sustained involuntary muscle contraction, often leading to abnormal postures. DYTJ patients manifest progressive, generalized, dopa-unresponsive dystonia, developmental malformations and sensory hearing loss.<ref>PMID:16685646</ref> Defects in ACTB are the cause of Baraitser-Winter syndrome type 1 (BRWS1) [MIM:[http://omim.org/entry/243310 243310]]. A rare developmental disorder characterized by the combination of congenital ptosis, high-arched eyebrows, hypertelorism, ocular colobomata, and a brain malformation consisting of anterior-predominant lissencephaly. Other typical features include postnatal short stature and microcephaly, intellectual disability, seizures, and hearing loss.<ref>PMID:22366783</ref> | |||
== Function == | |||
[[http://www.uniprot.org/uniprot/CLC9A_MOUSE CLC9A_MOUSE]] Functions as an endocytic receptor on a small subset of myeloid cells specialized for the uptake and processing of material from dead cells. Recognizes filamentous form of actin in association with particular actin-binding domains of cytoskeletal proteins, including spectrin, exposed when cell membranes are damaged, and mediate the cross-presentation of dead-cell associated antigens in a Syk-dependent manner.<ref>PMID:18408006</ref> <ref>PMID:18497879</ref> <ref>PMID:19219027</ref> <ref>PMID:22483802</ref> [[http://www.uniprot.org/uniprot/ACTB_HUMAN ACTB_HUMAN]] Actins are highly conserved proteins that are involved in various types of cell motility and are ubiquitously expressed in all eukaryotic cells. | |||
== References == | |||
<references/> | |||
__TOC__ | |||
</StructureSection> | |||
[[Category: Homo sapiens]] | |||
[[Category: Ahrens, S]] | [[Category: Ahrens, S]] | ||
[[Category: Fujii, T]] | |||
[[Category: Hanc, P]] | |||
[[Category: Huotari, J]] | [[Category: Huotari, J]] | ||
[[Category: Kjaer, S]] | |||
[[Category: Namba, K]] | |||
[[Category: Schulz, O]] | [[Category: Schulz, O]] | ||
[[Category: | [[Category: Sousa, C Reis e]] | ||
[[Category: Way, M]] | |||
[[Category: | |||
[[Category: Yamada, Y]] | [[Category: Yamada, Y]] | ||
[[Category: Actin]] | |||
[[Category: Dngr-1]] | |||
[[Category: Membrane protein-adp-binding protein complex]] | |||
[[Category: Recognition of damage-associated molecular pattern]] | |||