5vrp: Difference between revisions
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<StructureSection load='5vrp' size='340' side='right'caption='[[5vrp]], [[Resolution|resolution]] 3.22Å' scene=''> | <StructureSection load='5vrp' size='340' side='right'caption='[[5vrp]], [[Resolution|resolution]] 3.22Å' scene=''> | ||
== Structural highlights == | == Structural highlights == | ||
<table><tr><td colspan='2'>[[5vrp]] is a 2 chain structure with sequence from [ | <table><tr><td colspan='2'>[[5vrp]] 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=5VRP OCA]. For a <b>guided tour on the structure components</b> use [https://proteopedia.org/fgij/fg.htm?mol=5VRP FirstGlance]. <br> | ||
</td></tr><tr id='ligand'><td class="sblockLbl"><b>[[Ligand|Ligands:]]</b></td><td class="sblockDat" id="ligandDat"><scene name='pdbligand=9JD:methyl+[(4S)-4-{(3R)-1-[(3S)-4-amino-3-hydroxybutanoyl]piperidin-3-yl}-4-(3-ethyl-6-fluoro[1,1-biphenyl]-2-yl)-4-hydroxybutyl]carbamate'>9JD</scene>, <scene name='pdbligand=NAG:N-ACETYL-D-GLUCOSAMINE'>NAG</scene>, <scene name='pdbligand=SO4:SULFATE+ION'>SO4</scene | </td></tr><tr id='method'><td class="sblockLbl"><b>[[Empirical_models|Method:]]</b></td><td class="sblockDat" id="methodDat">X-ray diffraction, [[Resolution|Resolution]] 3.22Å</td></tr> | ||
<tr id='ligand'><td class="sblockLbl"><b>[[Ligand|Ligands:]]</b></td><td class="sblockDat" id="ligandDat"><scene name='pdbligand=9JD:methyl+[(4S)-4-{(3R)-1-[(3S)-4-amino-3-hydroxybutanoyl]piperidin-3-yl}-4-(3-ethyl-6-fluoro[1,1-biphenyl]-2-yl)-4-hydroxybutyl]carbamate'>9JD</scene>, <scene name='pdbligand=NAG:N-ACETYL-D-GLUCOSAMINE'>NAG</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=5vrp FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=5vrp OCA], [https://pdbe.org/5vrp PDBe], [https://www.rcsb.org/pdb/explore.do?structureId=5vrp RCSB], [https://www.ebi.ac.uk/pdbsum/5vrp PDBsum], [https://prosat.h-its.org/prosat/prosatexe?pdbcode=5vrp ProSAT]</span></td></tr> | |||
<tr id='resources'><td class="sblockLbl"><b>Resources:</b></td><td class="sblockDat"><span class='plainlinks'>[ | |||
</table> | </table> | ||
== Disease == | == Disease == | ||
[ | [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> | ||
== Function == | == Function == | ||
[ | [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. | ||
<div style="background-color:#fffaf0;"> | <div style="background-color:#fffaf0;"> | ||
== Publication Abstract from PubMed == | == Publication Abstract from PubMed == | ||
| Line 30: | Line 28: | ||
__TOC__ | __TOC__ | ||
</StructureSection> | </StructureSection> | ||
[[Category: | [[Category: Homo sapiens]] | ||
[[Category: Large Structures]] | [[Category: Large Structures]] | ||
[[Category: Concha N]] | |||
[[Category: Concha | [[Category: Zhao B]] | ||
[[Category: Zhao | |||
Latest revision as of 13:55, 30 October 2024
Crystal Structure of Human Renin in Complex with a biphenylpipderidinylcarbinolCrystal Structure of Human Renin in Complex with a biphenylpipderidinylcarbinol
Structural highlights
DiseaseRENI_HUMAN Defects in REN are a cause of renal tubular dysgenesis (RTD) [MIM: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).[1] Defects in REN are the cause of familial juvenile hyperuricemic nephropathy type 2 (HNFJ2) [MIM:613092. It is a renal disease characterized by juvenile onset of hyperuricemia, slowly progressive renal failure and anemia.[2] FunctionRENI_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. Publication Abstract from PubMedDiscovery of potent renin inhibitors which contain a simplified alkylamino Asp-binding group and exhibit improved selectivity for renin over Cyp3A4 is described. Structure-function results in this series are rationalized based on analysis of selected compounds bound to renin, and the contribution of each molecular feature leading to the reduced P450 inhibition is quantified. Discovery of renin inhibitors containing a simple aspartate binding moiety that imparts reduced P450 inhibition.,Lawhorn BG, Tran T, Hong VS, Morgan LA, Le BT, Harpel MR, Jolivette L, Diaz E, Schwartz B, Gross JW, Tomaszek T, Semus S, Concha N, Smallwood A, Holt DA, Kallander LS Bioorg Med Chem Lett. 2017 Sep 23. pii: S0960-894X(17)30954-X. doi:, 10.1016/j.bmcl.2017.09.046. PMID:28985999[3] From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine. See AlsoReferences
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