1lhh

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[[Image:1lhh.png|left|200px]]
 
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{{STRUCTURE_1lhh| PDB=1lhh | SCENE= }}
{{STRUCTURE_1lhh| PDB=1lhh | SCENE= }}
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===ROLE OF PROLINE RESIDUES IN HUMAN LYSOZYME STABILITY: A SCANNING CALORIMETRIC STUDY COMBINED WITH X-RAY STRUCTURE ANALYSIS OF PROLINE MUTANTS===
===ROLE OF PROLINE RESIDUES IN HUMAN LYSOZYME STABILITY: A SCANNING CALORIMETRIC STUDY COMBINED WITH X-RAY STRUCTURE ANALYSIS OF PROLINE MUTANTS===
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{{ABSTRACT_PUBMED_1643041}}
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{{ABSTRACT_PUBMED_1643041}}
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==Disease==
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[[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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==Function==
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[[http://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.
==About this Structure==
==About this Structure==
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==Reference==
==Reference==
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<ref group="xtra">PMID:001643041</ref><references group="xtra"/>
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<ref group="xtra">PMID:001643041</ref><references group="xtra"/><references/>
[[Category: Homo sapiens]]
[[Category: Homo sapiens]]
[[Category: Lysozyme]]
[[Category: Lysozyme]]

Revision as of 17:58, 24 March 2013

Template:STRUCTURE 1lhh

Contents

ROLE OF PROLINE RESIDUES IN HUMAN LYSOZYME STABILITY: A SCANNING CALORIMETRIC STUDY COMBINED WITH X-RAY STRUCTURE ANALYSIS OF PROLINE MUTANTS

Template:ABSTRACT PUBMED 1643041

Disease

[LYSC_HUMAN] Defects in LYZ are a cause of amyloidosis type 8 (AMYL8) [MIM: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.[1]

Function

[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.

About this Structure

1lhh is a 1 chain structure with sequence from Homo sapiens. Full crystallographic information is available from OCA.

See Also

Reference

  • Herning T, Yutani K, Inaka K, Kuroki R, Matsushima M, Kikuchi M. Role of proline residues in human lysozyme stability: a scanning calorimetric study combined with X-ray structure analysis of proline mutants. Biochemistry. 1992 Aug 11;31(31):7077-85. PMID:1643041
  1. ↑ Pepys MB, Hawkins PN, Booth DR, Vigushin DM, Tennent GA, Soutar AK, Totty N, Nguyen O, Blake CC, Terry CJ, et al.. Human lysozyme gene mutations cause hereditary systemic amyloidosis. Nature. 1993 Apr 8;362(6420):553-7. PMID:8464497 doi:http://dx.doi.org/10.1038/362553a0

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