2nwd
From Proteopedia
(Difference between revisions)
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== Structural highlights == | == Structural highlights == | ||
<table><tr><td colspan='2'>[[2nwd]] is a 1 chain structure. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=2NWD OCA]. For a <b>guided tour on the structure components</b> use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=2NWD FirstGlance]. <br> | <table><tr><td colspan='2'>[[2nwd]] is a 1 chain structure. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=2NWD OCA]. For a <b>guided tour on the structure components</b> use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=2NWD 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=2nwd FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=2nwd OCA], [http://www.rcsb.org/pdb/explore.do?structureId=2nwd RCSB], [http://www.ebi.ac.uk/pdbsum/2nwd 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=2nwd FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=2nwd OCA], [http://www.rcsb.org/pdb/explore.do?structureId=2nwd RCSB], [http://www.ebi.ac.uk/pdbsum/2nwd 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: Durek, T | + | [[Category: Durek, T]] |
- | [[Category: Kent, S B.H | + | [[Category: Kent, S B.H]] |
- | [[Category: Torbeev, V Y | + | [[Category: Torbeev, V Y]] |
[[Category: Chemical protein synthesis]] | [[Category: Chemical protein synthesis]] | ||
[[Category: Convergent synthesis]] | [[Category: Convergent synthesis]] | ||
[[Category: Hydrolase]] | [[Category: Hydrolase]] | ||
[[Category: Native chemical ligation]] | [[Category: Native chemical ligation]] |
Revision as of 14:11, 19 January 2015
Structure of chemically synthesized human lysozyme at 1 Angstrom resolution
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