4amt

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== Structural highlights ==
== Structural highlights ==
<table><tr><td colspan='2'>[[4amt]] is a 1 chain structure with sequence from [http://en.wikipedia.org/wiki/Human Human]. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=4AMT OCA]. For a <b>guided tour on the structure components</b> use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=4AMT FirstGlance]. <br>
<table><tr><td colspan='2'>[[4amt]] is a 1 chain structure with sequence from [http://en.wikipedia.org/wiki/Human Human]. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=4AMT OCA]. For a <b>guided tour on the structure components</b> use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=4AMT FirstGlance]. <br>
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</td></tr><tr><td class="sblockLbl"><b>[[Ligand|Ligands:]]</b></td><td class="sblockDat"><scene name='pdbligand=BMA:BETA-D-MANNOSE'>BMA</scene>, <scene name='pdbligand=SO4:SULFATE+ION'>SO4</scene>, <scene name='pdbligand=FUC:ALPHA-L-FUCOSE'>FUC</scene>, <scene name='pdbligand=NAG:N-ACETYL-D-GLUCOSAMINE'>NAG</scene><br>
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</td></tr><tr id='ligand'><td class="sblockLbl"><b>[[Ligand|Ligands:]]</b></td><td class="sblockDat"><scene name='pdbligand=BMA:BETA-D-MANNOSE'>BMA</scene>, <scene name='pdbligand=SO4:SULFATE+ION'>SO4</scene>, <scene name='pdbligand=FUC:ALPHA-L-FUCOSE'>FUC</scene>, <scene name='pdbligand=NAG:N-ACETYL-D-GLUCOSAMINE'>NAG</scene></td></tr>
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<tr><td class="sblockLbl"><b>[[Related_structure|Related:]]</b></td><td class="sblockDat">[[1bbs|1bbs]], [[1bil|1bil]], [[1bim|1bim]], [[1hrn|1hrn]], [[1rne|1rne]], [[2bks|2bks]], [[2bkt|2bkt]], [[2fs4|2fs4]], [[2g1n|2g1n]], [[2g1o|2g1o]], [[2g1r|2g1r]], [[2g1s|2g1s]], [[2g1y|2g1y]], [[2g20|2g20]], [[2g21|2g21]], [[2g22|2g22]], [[2g24|2g24]], [[2g26|2g26]], [[2g27|2g27]], [[2ren|2ren]], [[2v0z|2v0z]], [[2v10|2v10]], [[2v11|2v11]], [[2v12|2v12]], [[2v13|2v13]], [[2v16|2v16]], [[2x0b|2x0b]]</td></tr>
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<tr id='related'><td class="sblockLbl"><b>[[Related_structure|Related:]]</b></td><td class="sblockDat">[[1bbs|1bbs]], [[1bil|1bil]], [[1bim|1bim]], [[1hrn|1hrn]], [[1rne|1rne]], [[2bks|2bks]], [[2bkt|2bkt]], [[2fs4|2fs4]], [[2g1n|2g1n]], [[2g1o|2g1o]], [[2g1r|2g1r]], [[2g1s|2g1s]], [[2g1y|2g1y]], [[2g20|2g20]], [[2g21|2g21]], [[2g22|2g22]], [[2g24|2g24]], [[2g26|2g26]], [[2g27|2g27]], [[2ren|2ren]], [[2v0z|2v0z]], [[2v10|2v10]], [[2v11|2v11]], [[2v12|2v12]], [[2v13|2v13]], [[2v16|2v16]], [[2x0b|2x0b]]</td></tr>
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<tr><td class="sblockLbl"><b>Activity:</b></td><td class="sblockDat"><span class='plainlinks'>[http://en.wikipedia.org/wiki/Renin Renin], with EC number [http://www.brenda-enzymes.info/php/result_flat.php4?ecno=3.4.23.15 3.4.23.15] </span></td></tr>
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<tr id='activity'><td class="sblockLbl"><b>Activity:</b></td><td class="sblockDat"><span class='plainlinks'>[http://en.wikipedia.org/wiki/Renin Renin], with EC number [http://www.brenda-enzymes.info/php/result_flat.php4?ecno=3.4.23.15 3.4.23.15] </span></td></tr>
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<tr><td class="sblockLbl"><b>Resources:</b></td><td class="sblockDat"><span class='plainlinks'>[http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=4amt FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=4amt OCA], [http://www.rcsb.org/pdb/explore.do?structureId=4amt RCSB], [http://www.ebi.ac.uk/pdbsum/4amt PDBsum]</span></td></tr>
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<tr id='resources'><td class="sblockLbl"><b>Resources:</b></td><td class="sblockDat"><span class='plainlinks'>[http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=4amt FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=4amt OCA], [http://www.rcsb.org/pdb/explore.do?structureId=4amt RCSB], [http://www.ebi.ac.uk/pdbsum/4amt PDBsum]</span></td></tr>
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<table>
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</table>
== Disease ==
== Disease ==
[[http://www.uniprot.org/uniprot/RENI_HUMAN RENI_HUMAN]] Defects in REN are a cause of renal tubular dysgenesis (RTD) [MIM:[http://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:[http://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>
[[http://www.uniprot.org/uniprot/RENI_HUMAN RENI_HUMAN]] Defects in REN are a cause of renal tubular dysgenesis (RTD) [MIM:[http://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:[http://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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[[Category: Human]]
[[Category: Human]]
[[Category: Renin]]
[[Category: Renin]]
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[[Category: Zhou, A.]]
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[[Category: Zhou, A]]
[[Category: Hormone]]
[[Category: Hormone]]
[[Category: Hydrolase]]
[[Category: Hydrolase]]

Revision as of 14:09, 4 January 2015

The crystal structure at 2.6A of human prorenin

4amt, resolution 2.60Å

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