6ln1: Difference between revisions
No edit summary |
No edit summary |
||
Line 1: | Line 1: | ||
==A natural inhibitor of DYRK1A for treatment of diabetes mellitus== | ==A natural inhibitor of DYRK1A for treatment of diabetes mellitus== | ||
<StructureSection load='6ln1' size='340' side='right'caption='[[6ln1]]' scene=''> | <StructureSection load='6ln1' size='340' side='right'caption='[[6ln1]], [[Resolution|resolution]] 2.70Å' scene=''> | ||
== Structural highlights == | == Structural highlights == | ||
<table><tr><td colspan='2'>Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=6LN1 OCA]. For a <b>guided tour on the structure components</b> use [https://proteopedia.org/fgij/fg.htm?mol=6LN1 FirstGlance]. <br> | <table><tr><td colspan='2'>[[6ln1]] is a 2 chain structure with sequence from [https://en.wikipedia.org/wiki/Homo_sapiens Homo sapiens]. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=6LN1 OCA]. For a <b>guided tour on the structure components</b> use [https://proteopedia.org/fgij/fg.htm?mol=6LN1 FirstGlance]. <br> | ||
</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=6ln1 FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=6ln1 OCA], [https://pdbe.org/6ln1 PDBe], [https://www.rcsb.org/pdb/explore.do?structureId=6ln1 RCSB], [https://www.ebi.ac.uk/pdbsum/6ln1 PDBsum], [https://prosat.h-its.org/prosat/prosatexe?pdbcode=6ln1 ProSAT]</span></td></tr> | </td></tr><tr id='method'><td class="sblockLbl"><b>[[Empirical_models|Method:]]</b></td><td class="sblockDat" id="methodDat">X-ray diffraction, [[Resolution|Resolution]] 2.699Å</td></tr> | ||
<tr id='ligand'><td class="sblockLbl"><b>[[Ligand|Ligands:]]</b></td><td class="sblockDat" id="ligandDat"><scene name='pdbligand=EKU:1,3,5,8-tetrakis(oxidanyl)xanthen-9-one'>EKU</scene>, <scene name='pdbligand=PTR:O-PHOSPHOTYROSINE'>PTR</scene></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=6ln1 FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=6ln1 OCA], [https://pdbe.org/6ln1 PDBe], [https://www.rcsb.org/pdb/explore.do?structureId=6ln1 RCSB], [https://www.ebi.ac.uk/pdbsum/6ln1 PDBsum], [https://prosat.h-its.org/prosat/prosatexe?pdbcode=6ln1 ProSAT]</span></td></tr> | |||
</table> | </table> | ||
== Disease == | |||
[https://www.uniprot.org/uniprot/DYR1A_HUMAN DYR1A_HUMAN] Defects in DYRK1A are the cause of mental retardation autosomal dominant type 7 (MRD7) [MIM:[https://omim.org/entry/614104 614104]. A disease characterized by primary microcephaly, severe mental retardation without speech, anxious autistic behavior, and dysmorphic features, including bitemporal narrowing, deep-set eyes, large simple ears, and a pointed nasal tip. Mental retardation is characterized by significantly below average general intellectual functioning associated with impairments in adaptative behavior and manifested during the developmental period.<ref>PMID:21294719</ref> | |||
== Function == | |||
[https://www.uniprot.org/uniprot/DYR1A_HUMAN DYR1A_HUMAN] May play a role in a signaling pathway regulating nuclear functions of cell proliferation. Phosphorylates serine, threonine and tyrosine residues in its sequence and in exogenous substrates.<ref>PMID:8769099</ref> | |||
== References == | |||
<references/> | |||
__TOC__ | __TOC__ | ||
</StructureSection> | </StructureSection> | ||
[[Category: Homo sapiens]] | |||
[[Category: Large Structures]] | [[Category: Large Structures]] | ||
[[Category: Chen JC]] | [[Category: Chen JC]] |
Revision as of 14:03, 22 November 2023
A natural inhibitor of DYRK1A for treatment of diabetes mellitusA natural inhibitor of DYRK1A for treatment of diabetes mellitus
Structural highlights
DiseaseDYR1A_HUMAN Defects in DYRK1A are the cause of mental retardation autosomal dominant type 7 (MRD7) [MIM:614104. A disease characterized by primary microcephaly, severe mental retardation without speech, anxious autistic behavior, and dysmorphic features, including bitemporal narrowing, deep-set eyes, large simple ears, and a pointed nasal tip. Mental retardation is characterized by significantly below average general intellectual functioning associated with impairments in adaptative behavior and manifested during the developmental period.[1] FunctionDYR1A_HUMAN May play a role in a signaling pathway regulating nuclear functions of cell proliferation. Phosphorylates serine, threonine and tyrosine residues in its sequence and in exogenous substrates.[2] References
|
|