5ybv: Difference between revisions
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The entry | ==The structure of the KANK2 ankyrin domain with the KIF21A peptide== | ||
<StructureSection load='5ybv' size='340' side='right' caption='[[5ybv]], [[Resolution|resolution]] 2.12Å' scene=''> | |||
== Structural highlights == | |||
<table><tr><td colspan='2'>[[5ybv]] is a 4 chain structure. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=5YBV OCA]. For a <b>guided tour on the structure components</b> use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=5YBV FirstGlance]. <br> | |||
</td></tr><tr id='ligand'><td class="sblockLbl"><b>[[Ligand|Ligands:]]</b></td><td class="sblockDat"><scene name='pdbligand=GOL:GLYCEROL'>GOL</scene>, <scene name='pdbligand=SO4:SULFATE+ION'>SO4</scene></td></tr> | |||
[[Category: | <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=5ybv FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=5ybv OCA], [http://pdbe.org/5ybv PDBe], [http://www.rcsb.org/pdb/explore.do?structureId=5ybv RCSB], [http://www.ebi.ac.uk/pdbsum/5ybv PDBsum], [http://prosat.h-its.org/prosat/prosatexe?pdbcode=5ybv ProSAT]</span></td></tr> | ||
</table> | |||
== Disease == | |||
[[http://www.uniprot.org/uniprot/KI21A_HUMAN KI21A_HUMAN]] Congenital fibrosis of extraocular muscles. The disease is caused by mutations affecting the gene represented in this entry. | |||
== Function == | |||
[[http://www.uniprot.org/uniprot/KANK2_HUMAN KANK2_HUMAN]] Involved in transcription regulation by sequestering nuclear receptor coactivators, such as NCOA1, NCOA2 and NCOA3, in the cytoplasm; the function is deregulated by phosphorylation. May be involved in the control of cytoskeleton formation by regulating actin polymerization. Involved in regulation of caspase-independent apoptosis; proposed to sequester AIFM1 in mitochondria and apoptotic stimuli lead to its proteasomal degradation allowing the release of AIFM1 to the nucleus. May be involved in promotion of cell proliferation.<ref>PMID:17476305</ref> <ref>PMID:22371500</ref> [[http://www.uniprot.org/uniprot/KI21A_HUMAN KI21A_HUMAN]] Microtubule-binding motor protein probably involved in neuronal axonal transport. In vitro, has a plus-end directed motor activity (By similarity). | |||
== References == | |||
<references/> | |||
__TOC__ | |||
</StructureSection> | |||
[[Category: Guo, Q]] | |||
[[Category: Liao, S]] | |||
[[Category: Min, J]] | |||
[[Category: Structural genomic]] | |||
[[Category: Xu, C]] | |||
[[Category: Cell adhesion]] | |||
Revision as of 10:22, 6 December 2017
The structure of the KANK2 ankyrin domain with the KIF21A peptideThe structure of the KANK2 ankyrin domain with the KIF21A peptide
Structural highlights
Disease[KI21A_HUMAN] Congenital fibrosis of extraocular muscles. The disease is caused by mutations affecting the gene represented in this entry. Function[KANK2_HUMAN] Involved in transcription regulation by sequestering nuclear receptor coactivators, such as NCOA1, NCOA2 and NCOA3, in the cytoplasm; the function is deregulated by phosphorylation. May be involved in the control of cytoskeleton formation by regulating actin polymerization. Involved in regulation of caspase-independent apoptosis; proposed to sequester AIFM1 in mitochondria and apoptotic stimuli lead to its proteasomal degradation allowing the release of AIFM1 to the nucleus. May be involved in promotion of cell proliferation.[1] [2] [KI21A_HUMAN] Microtubule-binding motor protein probably involved in neuronal axonal transport. In vitro, has a plus-end directed motor activity (By similarity). References
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