6a48: Difference between revisions
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==Crystal structure of reelin N-terminal region== | |||
<StructureSection load='6a48' size='340' side='right'caption='[[6a48]], [[Resolution|resolution]] 2.00Å' scene=''> | |||
== Structural highlights == | |||
<table><tr><td colspan='2'>[[6a48]] is a 1 chain structure. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=6A48 OCA]. For a <b>guided tour on the structure components</b> use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=6A48 FirstGlance]. <br> | |||
</td></tr><tr id='ligand'><td class="sblockLbl"><b>[[Ligand|Ligands:]]</b></td><td class="sblockDat"><scene name='pdbligand=CA:CALCIUM+ION'>CA</scene>, <scene name='pdbligand=NAG:N-ACETYL-D-GLUCOSAMINE'>NAG</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=6a48 FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=6a48 OCA], [http://pdbe.org/6a48 PDBe], [http://www.rcsb.org/pdb/explore.do?structureId=6a48 RCSB], [http://www.ebi.ac.uk/pdbsum/6a48 PDBsum], [http://prosat.h-its.org/prosat/prosatexe?pdbcode=6a48 ProSAT]</span></td></tr> | ||
</table> | |||
== Disease == | |||
[[http://www.uniprot.org/uniprot/RELN_MOUSE RELN_MOUSE]] Note=Defects in Reln are the cause of the autosomal recessive reeler (rl) phenotype which is characterized by impaired motor coordination, tremors and ataxia. Neurons in affected mice fail to reach their correct locations in the developing brain, disrupting the organization of the cerebellar and cerebral cortices and other laminated regions. | |||
== Function == | |||
[[http://www.uniprot.org/uniprot/RELN_MOUSE RELN_MOUSE]] Extracellular matrix serine protease that plays a role in layering of neurons in the cerebral cortex and cerebellum. Regulates microtubule function in neurons and neuronal migration. Affects migration of sympathetic preganglionic neurons in the spinal cord, where it seems to act as a barrier to neuronal migration. Enzymatic activity is important for the modulation of cell adhesion. Binding to the extracellular domains of lipoprotein receptors VLDLR and LRP8/APOER2 induces tyrosine phosphorylation of DAB1 and modulation of TAU phosphorylation.<ref>PMID:10880573</ref> | |||
== References == | |||
<references/> | |||
__TOC__ | |||
</StructureSection> | |||
[[Category: Large Structures]] | |||
[[Category: Nagae, M]] | |||
[[Category: Takagi, J]] | |||
[[Category: Extracellular protein]] | |||
[[Category: Ldlr family]] | |||
[[Category: Reelin]] | |||
[[Category: Signaling protein]] | |||
Revision as of 08:49, 19 June 2019
Crystal structure of reelin N-terminal regionCrystal structure of reelin N-terminal region
Structural highlights
Disease[RELN_MOUSE] Note=Defects in Reln are the cause of the autosomal recessive reeler (rl) phenotype which is characterized by impaired motor coordination, tremors and ataxia. Neurons in affected mice fail to reach their correct locations in the developing brain, disrupting the organization of the cerebellar and cerebral cortices and other laminated regions. Function[RELN_MOUSE] Extracellular matrix serine protease that plays a role in layering of neurons in the cerebral cortex and cerebellum. Regulates microtubule function in neurons and neuronal migration. Affects migration of sympathetic preganglionic neurons in the spinal cord, where it seems to act as a barrier to neuronal migration. Enzymatic activity is important for the modulation of cell adhesion. Binding to the extracellular domains of lipoprotein receptors VLDLR and LRP8/APOER2 induces tyrosine phosphorylation of DAB1 and modulation of TAU phosphorylation.[1] References
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