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3oag

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'''Unreleased structure'''
 
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The entry 3oag is ON HOLD
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==Design and optimization of new piperidines as renin inhibitors==
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<StructureSection load='3oag' size='340' side='right'caption='[[3oag]], [[Resolution|resolution]] 2.30&Aring;' scene=''>
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== Structural highlights ==
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<table><tr><td colspan='2'>[[3oag]] 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=3OAG OCA]. For a <b>guided tour on the structure components</b> use [https://proteopedia.org/fgij/fg.htm?mol=3OAG FirstGlance]. <br>
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</td></tr><tr id='method'><td class="sblockLbl"><b>[[Empirical_models|Method:]]</b></td><td class="sblockDat" id="methodDat">X-ray diffraction, [[Resolution|Resolution]] 2.3&#8491;</td></tr>
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<tr id='ligand'><td class="sblockLbl"><b>[[Ligand|Ligands:]]</b></td><td class="sblockDat" id="ligandDat"><scene name='pdbligand=LPQ:(3R,4S)-N-{2-CHLORO-5-[(CYCLOPROPYLAMINO)METHYL]BENZYL}-N-CYCLOPROPYL-4-{6-[2-(2,6-DICHLORO-4-METHYLPHENOXY)ETHOXY]PYRIDIN-3-YL}PIPERIDINE-3-CARBOXAMIDE'>LPQ</scene>, <scene name='pdbligand=NAG:N-ACETYL-D-GLUCOSAMINE'>NAG</scene></td></tr>
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<tr id='resources'><td class="sblockLbl"><b>Resources:</b></td><td class="sblockDat"><span class='plainlinks'>[https://proteopedia.org/fgij/fg.htm?mol=3oag FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=3oag OCA], [https://pdbe.org/3oag PDBe], [https://www.rcsb.org/pdb/explore.do?structureId=3oag RCSB], [https://www.ebi.ac.uk/pdbsum/3oag PDBsum], [https://prosat.h-its.org/prosat/prosatexe?pdbcode=3oag ProSAT]</span></td></tr>
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</table>
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== Disease ==
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[https://www.uniprot.org/uniprot/RENI_HUMAN RENI_HUMAN] Defects in REN are a cause of renal tubular dysgenesis (RTD) [MIM:[https://omim.org/entry/267430 267430]. RTD is an autosomal recessive severe disorder of renal tubular development characterized by persistent fetal anuria and perinatal death, probably due to pulmonary hypoplasia from early-onset oligohydramnios (the Potter phenotype).<ref>PMID:16116425</ref> Defects in REN are the cause of familial juvenile hyperuricemic nephropathy type 2 (HNFJ2) [MIM:[https://omim.org/entry/613092 613092]. It is a renal disease characterized by juvenile onset of hyperuricemia, slowly progressive renal failure and anemia.<ref>PMID:19664745</ref>
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== Function ==
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[https://www.uniprot.org/uniprot/RENI_HUMAN RENI_HUMAN] Renin is a highly specific endopeptidase, whose only known function is to generate angiotensin I from angiotensinogen in the plasma, initiating a cascade of reactions that produce an elevation of blood pressure and increased sodium retention by the kidney.
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Authors: Prade, L.
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==See Also==
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*[[Renin|Renin]]
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Description: Design and optimization of new piperidines as renin inhibitors
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== References ==
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<references/>
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''Page seeded by [http://oca.weizmann.ac.il/oca OCA ] on Wed Aug 18 11:25:49 2010''
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__TOC__
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</StructureSection>
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[[Category: Homo sapiens]]
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[[Category: Large Structures]]
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[[Category: Prade L]]

Current revision

Design and optimization of new piperidines as renin inhibitors

PDB ID 3oag

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