9yg0: Difference between revisions
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==Targeting PTPN22 at non-orthosteric binding sites - a fragment approach== | |||
<StructureSection load='9yg0' size='340' side='right'caption='[[9yg0]], [[Resolution|resolution]] 1.76Å' scene=''> | |||
== Structural highlights == | |||
<table><tr><td colspan='2'>[[9yg0]] is a 4 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=9YG0 OCA]. For a <b>guided tour on the structure components</b> use [https://proteopedia.org/fgij/fg.htm?mol=9YG0 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]] 1.76Å</td></tr> | |||
[[Category: | <tr id='ligand'><td class="sblockLbl"><b>[[Ligand|Ligands:]]</b></td><td class="sblockDat" id="ligandDat"><scene name='pdbligand=A1CWM:1-[(3S)-3-amino-2,3-dihydro-1H-indol-1-yl]-3-phenylpropan-1-one'>A1CWM</scene>, <scene name='pdbligand=EOH:ETHANOL'>EOH</scene>, <scene name='pdbligand=GOL:GLYCEROL'>GOL</scene>, <scene name='pdbligand=MG:MAGNESIUM+ION'>MG</scene>, <scene name='pdbligand=SO4:SULFATE+ION'>SO4</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=9yg0 FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=9yg0 OCA], [https://pdbe.org/9yg0 PDBe], [https://www.rcsb.org/pdb/explore.do?structureId=9yg0 RCSB], [https://www.ebi.ac.uk/pdbsum/9yg0 PDBsum], [https://prosat.h-its.org/prosat/prosatexe?pdbcode=9yg0 ProSAT]</span></td></tr> | |||
</table> | |||
== Disease == | |||
[https://www.uniprot.org/uniprot/PTN22_HUMAN PTN22_HUMAN] Defects in PTPN22 are a cause of susceptibility to systemic lupus erythematosus (SLE) [MIM:[https://omim.org/entry/152700 152700]. SLE is a chronic, inflammatory and often febrile multisystemic disorder of connective tissue. It affects principally the skin, joints, kidneys and serosal membranes. It is thought to represent a failure of the regulatory mechanisms of the autoimmune system.<ref>PMID:15273934</ref> | |||
== Function == | |||
[https://www.uniprot.org/uniprot/PTN22_HUMAN PTN22_HUMAN] Acts as negative regulator of T-cell receptor (TCR) signaling by direct dephosphorylation of the Src family kinases LCK and FYN, ITAMs of the TCRz/CD3 complex, as well as ZAP70, VAV, VCP and other key signaling molecules. Associates with and probably dephosphorylates CBL. Dephosphorylates LCK at its activating 'Tyr-394' residue. Dephosphorylates ZAP70 at its activating 'Tyr-493' residue. Dephosphorylates the immune system activator SKAP2.<ref>PMID:16461343</ref> <ref>PMID:18056643</ref> <ref>PMID:19167335</ref> <ref>PMID:21719704</ref> | |||
== References == | |||
<references/> | |||
__TOC__ | |||
</StructureSection> | |||
[[Category: Homo sapiens]] | |||
[[Category: Large Structures]] | |||
[[Category: Di Lello P]] | |||
[[Category: Wells MM]] | |||
Latest revision as of 14:50, 10 February 2026
Targeting PTPN22 at non-orthosteric binding sites - a fragment approach
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