3ln2: Difference between revisions
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<StructureSection load='3ln2' size='340' side='right'caption='[[3ln2]], [[Resolution|resolution]] 2.04Å' scene=''> | <StructureSection load='3ln2' size='340' side='right'caption='[[3ln2]], [[Resolution|resolution]] 2.04Å' scene=''> | ||
== Structural highlights == | == Structural highlights == | ||
<table><tr><td colspan='2'>[[3ln2]] is a 2 chain structure with sequence from [https://en.wikipedia.org/wiki/ | <table><tr><td colspan='2'>[[3ln2]] 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=3LN2 OCA]. For a <b>guided tour on the structure components</b> use [https://proteopedia.org/fgij/fg.htm?mol=3LN2 FirstGlance]. <br> | ||
</td></tr><tr id=' | </td></tr><tr id='method'><td class="sblockLbl"><b>[[Empirical_models|Method:]]</b></td><td class="sblockDat" id="methodDat">X-ray diffraction, [[Resolution|Resolution]] 2.037Å</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=3ln2 FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=3ln2 OCA], [https://pdbe.org/3ln2 PDBe], [https://www.rcsb.org/pdb/explore.do?structureId=3ln2 RCSB], [https://www.ebi.ac.uk/pdbsum/3ln2 PDBsum], [https://prosat.h-its.org/prosat/prosatexe?pdbcode=3ln2 ProSAT]</span></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=3ln2 FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=3ln2 OCA], [https://pdbe.org/3ln2 PDBe], [https://www.rcsb.org/pdb/explore.do?structureId=3ln2 RCSB], [https://www.ebi.ac.uk/pdbsum/3ln2 PDBsum], [https://prosat.h-its.org/prosat/prosatexe?pdbcode=3ln2 ProSAT]</span></td></tr> | ||
</table> | </table> | ||
== Disease == | == Disease == | ||
[https://www.uniprot.org/uniprot/LYSC_HUMAN LYSC_HUMAN] Defects in LYZ are a cause of amyloidosis type 8 (AMYL8) [MIM:[https://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> | |||
== Function == | == Function == | ||
[https://www.uniprot.org/uniprot/LYSC_HUMAN LYSC_HUMAN] Lysozymes have primarily a bacteriolytic function; those in tissues and body fluids are associated with the monocyte-macrophage system and enhance the activity of immunoagents. | |||
<div style="background-color:#fffaf0;"> | <div style="background-color:#fffaf0;"> | ||
== Publication Abstract from PubMed == | == Publication Abstract from PubMed == | ||
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__TOC__ | __TOC__ | ||
</StructureSection> | </StructureSection> | ||
[[Category: | [[Category: Homo sapiens]] | ||
[[Category: Large Structures]] | [[Category: Large Structures]] | ||
[[Category: Gill A]] | |||
[[Category: Gill | [[Category: Griswold KE]] | ||
[[Category: Griswold | [[Category: Scanlon TC]] | ||
[[Category: Scanlon | |||