9y3w: Difference between revisions
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==Crystal structure of NRas-G12D in complex with GDP and compound 13== | |||
<StructureSection load='9y3w' size='340' side='right'caption='[[9y3w]], [[Resolution|resolution]] 1.56Å' scene=''> | |||
== Structural highlights == | |||
<table><tr><td colspan='2'>[[9y3w]] 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=9Y3W OCA]. For a <b>guided tour on the structure components</b> use [https://proteopedia.org/fgij/fg.htm?mol=9Y3W 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]] 1.56Å</td></tr> | |||
[[Category: | <tr id='ligand'><td class="sblockLbl"><b>[[Ligand|Ligands:]]</b></td><td class="sblockDat" id="ligandDat"><scene name='pdbligand=A1CSD:(4P)-4-{3-[(1R,5S,6r)-3-azabicyclo[3.1.0]hexan-6-yl]-1-cyclopropyl-7-fluoro-4-(propan-2-yl)-1H-pyrazolo[4,3-c]pyridin-6-yl}-5-ethynyl-6-fluoronaphthalen-2-ol'>A1CSD</scene>, <scene name='pdbligand=CIT:CITRIC+ACID'>CIT</scene>, <scene name='pdbligand=GDP:GUANOSINE-5-DIPHOSPHATE'>GDP</scene>, <scene name='pdbligand=MG:MAGNESIUM+ION'>MG</scene></td></tr> | ||
[[Category: Cross | <tr id='resources'><td class="sblockLbl"><b>Resources:</b></td><td class="sblockDat"><span class='plainlinks'>[https://proteopedia.org/fgij/fg.htm?mol=9y3w FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=9y3w OCA], [https://pdbe.org/9y3w PDBe], [https://www.rcsb.org/pdb/explore.do?structureId=9y3w RCSB], [https://www.ebi.ac.uk/pdbsum/9y3w PDBsum], [https://prosat.h-its.org/prosat/prosatexe?pdbcode=9y3w ProSAT]</span></td></tr> | ||
[[Category: Johnson | </table> | ||
== Disease == | |||
[https://www.uniprot.org/uniprot/RASN_HUMAN RASN_HUMAN] Defects in NRAS are a cause of juvenile myelomonocytic leukemia (JMML) [MIM:[https://omim.org/entry/607785 607785]. JMML is a pediatric myelodysplastic syndrome that constitutes approximately 30% of childhood cases of myelodysplastic syndrome (MDS) and 2% of leukemia. Defects in NRAS are the cause of Noonan syndrome type 6 (NS6) [MIM:[https://omim.org/entry/613224 613224]. A syndrome characterized by facial dysmorphic features such as hypertelorism, a downward eyeslant and low-set posteriorly rotated ears. Other features can include short stature, a short neck with webbing or redundancy of skin, cardiac anomalies, deafness, motor delay and variable intellectual deficits.<ref>PMID:19966803</ref> Defects in NRAS are the cause of autoimmune lymphoproliferative syndrome type 4 (ALPS4) [MIM:[https://omim.org/entry/614470 614470]. A disorder of apoptosis, characterized by chronic accumulation of non-malignant lymphocytes, defective lymphocyte apoptosis, and an increased risk for the development of hematologic malignancies.<ref>PMID:17517660</ref> | |||
== Function == | |||
[https://www.uniprot.org/uniprot/RASN_HUMAN RASN_HUMAN] Ras proteins bind GDP/GTP and possess intrinsic GTPase activity. | |||
== References == | |||
<references/> | |||
__TOC__ | |||
</StructureSection> | |||
[[Category: Homo sapiens]] | |||
[[Category: Large Structures]] | |||
[[Category: Cross JB]] | |||
[[Category: Johnson TA]] | |||