3err
From Proteopedia
(Difference between revisions)
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== Structural highlights == | == Structural highlights == | ||
<table><tr><td colspan='2'>[[3err]] is a 2 chain structure with sequence from [http://en.wikipedia.org/wiki/Mus_musculus Mus musculus]. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=3ERR OCA]. For a <b>guided tour on the structure components</b> use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=3ERR FirstGlance]. <br> | <table><tr><td colspan='2'>[[3err]] is a 2 chain structure with sequence from [http://en.wikipedia.org/wiki/Mus_musculus Mus musculus]. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=3ERR OCA]. For a <b>guided tour on the structure components</b> use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=3ERR FirstGlance]. <br> | ||
| - | </td></tr><tr><td class="sblockLbl"><b>[[Ligand|Ligands:]]</b></td><td class="sblockDat"><scene name='pdbligand=AMP:ADENOSINE+MONOPHOSPHATE'>AMP</scene>< | + | </td></tr><tr id='ligand'><td class="sblockLbl"><b>[[Ligand|Ligands:]]</b></td><td class="sblockDat"><scene name='pdbligand=AMP:ADENOSINE+MONOPHOSPHATE'>AMP</scene></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=3err FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=3err OCA], [http://www.rcsb.org/pdb/explore.do?structureId=3err RCSB], [http://www.ebi.ac.uk/pdbsum/3err PDBsum]</span></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=3err FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=3err OCA], [http://www.rcsb.org/pdb/explore.do?structureId=3err RCSB], [http://www.ebi.ac.uk/pdbsum/3err PDBsum]</span></td></tr> |
| - | <table> | + | </table> |
== Disease == | == Disease == | ||
[[http://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. | [[http://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. | ||
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</StructureSection> | </StructureSection> | ||
[[Category: Mus musculus]] | [[Category: Mus musculus]] | ||
| - | [[Category: Carter, A P | + | [[Category: Carter, A P]] |
[[Category: Dynein]] | [[Category: Dynein]] | ||
[[Category: Fusion protein]] | [[Category: Fusion protein]] | ||
[[Category: Ligase]] | [[Category: Ligase]] | ||
[[Category: Microtubule binding domain]] | [[Category: Microtubule binding domain]] | ||
Revision as of 11:47, 20 January 2015
Microtubule binding domain from mouse cytoplasmic dynein as a fusion with seryl-tRNA synthetase
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