3wuq
From Proteopedia
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| - | '''Unreleased structure''' | ||
| - | + | ==Structure of the entire stalk region of the dynein motor domain== | |
| + | <StructureSection load='3wuq' size='340' side='right'caption='[[3wuq]], [[Resolution|resolution]] 3.50Å' scene=''> | ||
| + | == Structural highlights == | ||
| + | <table><tr><td colspan='2'>[[3wuq]] is a 1 chain structure with sequence from [https://en.wikipedia.org/wiki/Mus_musculus Mus musculus]. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=3WUQ OCA]. For a <b>guided tour on the structure components</b> use [https://proteopedia.org/fgij/fg.htm?mol=3WUQ FirstGlance]. <br> | ||
| + | </td></tr><tr id='method'><td class="sblockLbl"><b>[[Empirical_models|Method:]]</b></td><td class="sblockDat" id="methodDat">X-ray diffraction, [[Resolution|Resolution]] 3.5Å</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=3wuq FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=3wuq OCA], [https://pdbe.org/3wuq PDBe], [https://www.rcsb.org/pdb/explore.do?structureId=3wuq RCSB], [https://www.ebi.ac.uk/pdbsum/3wuq PDBsum], [https://prosat.h-its.org/prosat/prosatexe?pdbcode=3wuq ProSAT]</span></td></tr> | ||
| + | </table> | ||
| + | == Disease == | ||
| + | [https://www.uniprot.org/uniprot/DYHC1_MOUSE DYHC1_MOUSE] Defects in Dync1h1 are the cause of the 'Legs at odd angles' (LOA) phenotype, an autosomal dominant trait where affected animals display unusual twisting of the body and clenching of the hindlimbs when suspended by the tail. Heterozygotes suffer age-related progressive loss of muscle tone and locomotor ability without major reduction in life-span while homozygotes show a more severe phenotype with an inability to move or feed, and die within 24 hours of birth. LOA mutants display defects in migration of facial motor neuron cell bodies and impaired retrograde transport in spinal cord motor neurons. Defects in Dync1h1 are the cause of the Cramping 1 (Cra1) phenotype, an autosomal dominant trait where affected animals display unusual twisting of the body and clenching of the hindlimbs when suspended by the tail. Heterozygotes suffer age-related progressive loss of muscle tone and locomotor ability without major reduction in life-span while homozygotes show a more severe phenotype with an inability to move or feed, and die within 24 hours of birth. | ||
| + | == Function == | ||
| + | [https://www.uniprot.org/uniprot/DYHC1_MOUSE DYHC1_MOUSE] Cytoplasmic dynein 1 acts as a motor for the intracellular retrograde motility of vesicles and organelles along microtubules. Dynein has ATPase activity; the force-producing power stroke is thought to occur on release of ADP. | ||
| - | + | ==See Also== | |
| - | + | *[[Dynein 3D structures|Dynein 3D structures]] | |
| - | + | __TOC__ | |
| + | </StructureSection> | ||
| + | [[Category: Large Structures]] | ||
| + | [[Category: Mus musculus]] | ||
| + | [[Category: Kamiya N]] | ||
| + | [[Category: Kon T]] | ||
| + | [[Category: Kurisu G]] | ||
| + | [[Category: Nakamura H]] | ||
| + | [[Category: Nishikawa Y]] | ||
| + | [[Category: Oyama T]] | ||
| + | [[Category: Toyoshima YY]] | ||
Current revision
Structure of the entire stalk region of the dynein motor domain
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Categories: Large Structures | Mus musculus | Kamiya N | Kon T | Kurisu G | Nakamura H | Nishikawa Y | Oyama T | Toyoshima YY
