4ml7
From Proteopedia
(Difference between revisions)
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== Structural highlights == | == Structural highlights == | ||
<table><tr><td colspan='2'>[[4ml7]] is a 4 chain structure. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=4ML7 OCA]. For a <b>guided tour on the structure components</b> use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=4ML7 FirstGlance]. <br> | <table><tr><td colspan='2'>[[4ml7]] is a 4 chain structure. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=4ML7 OCA]. For a <b>guided tour on the structure components</b> use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=4ML7 FirstGlance]. <br> | ||
- | </td></tr><tr><td class="sblockLbl"><b>Activity:</b></td><td class="sblockDat"><span class='plainlinks'>[http://en.wikipedia.org/wiki/Lysozyme Lysozyme], with EC number [http://www.brenda-enzymes.info/php/result_flat.php4?ecno=3.2.1.17 3.2.1.17] </span></td></tr> | + | </td></tr><tr id='activity'><td class="sblockLbl"><b>Activity:</b></td><td class="sblockDat"><span class='plainlinks'>[http://en.wikipedia.org/wiki/Lysozyme Lysozyme], with EC number [http://www.brenda-enzymes.info/php/result_flat.php4?ecno=3.2.1.17 3.2.1.17] </span></td></tr> |
- | <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=4ml7 FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=4ml7 OCA], [http://www.rcsb.org/pdb/explore.do?structureId=4ml7 RCSB], [http://www.ebi.ac.uk/pdbsum/4ml7 PDBsum]</span></td></tr> | + | <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=4ml7 FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=4ml7 OCA], [http://www.rcsb.org/pdb/explore.do?structureId=4ml7 RCSB], [http://www.ebi.ac.uk/pdbsum/4ml7 PDBsum]</span></td></tr> |
- | <table> | + | </table> |
== Disease == | == Disease == | ||
[[http://www.uniprot.org/uniprot/LYSC_HUMAN LYSC_HUMAN]] Defects in LYZ are a cause of amyloidosis type 8 (AMYL8) [MIM:[http://omim.org/entry/105200 105200]]; also known as systemic non-neuropathic amyloidosis or Ostertag-type amyloidosis. AMYL8 is a hereditary generalized amyloidosis due to deposition of apolipoprotein A1, fibrinogen and lysozyme amyloids. Viscera are particularly affected. There is no involvement of the nervous system. Clinical features include renal amyloidosis resulting in nephrotic syndrome, arterial hypertension, hepatosplenomegaly, cholestasis, petechial skin rash.<ref>PMID:8464497</ref> | [[http://www.uniprot.org/uniprot/LYSC_HUMAN LYSC_HUMAN]] Defects in LYZ are a cause of amyloidosis type 8 (AMYL8) [MIM:[http://omim.org/entry/105200 105200]]; also known as systemic non-neuropathic amyloidosis or Ostertag-type amyloidosis. AMYL8 is a hereditary generalized amyloidosis due to deposition of apolipoprotein A1, fibrinogen and lysozyme amyloids. Viscera are particularly affected. There is no involvement of the nervous system. Clinical features include renal amyloidosis resulting in nephrotic syndrome, arterial hypertension, hepatosplenomegaly, cholestasis, petechial skin rash.<ref>PMID:8464497</ref> | ||
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</StructureSection> | </StructureSection> | ||
[[Category: Lysozyme]] | [[Category: Lysozyme]] | ||
- | [[Category: Ha, N C | + | [[Category: Ha, N C]] |
- | [[Category: Kim, J S | + | [[Category: Kim, J S]] |
- | [[Category: Um, S H | + | [[Category: Um, S H]] |
[[Category: Hydrolase]] | [[Category: Hydrolase]] | ||
[[Category: Inhibitor]] | [[Category: Inhibitor]] | ||
- | [[Category: Lysozyme]] |
Revision as of 12:37, 5 January 2015
Crystal structure of Brucella abortus PliC in complex with human lysozyme
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