1b5x: Difference between revisions
No edit summary |
No edit summary |
||
| Line 1: | Line 1: | ||
{{STRUCTURE_1b5x| PDB=1b5x | SCENE= }} | {{STRUCTURE_1b5x| PDB=1b5x | SCENE= }} | ||
===Contribution of hydrogen bonds to the conformational stability of human lysozyme: calorimetry and x-ray analysis of six ser->ala mutants=== | |||
{{ABSTRACT_PUBMED_10350481}} | |||
=== | ==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> | |||
==Function== | |||
[[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== | ||
| Line 14: | Line 16: | ||
==Reference== | ==Reference== | ||
<ref group="xtra">PMID:010350481</ref><references group="xtra"/> | <ref group="xtra">PMID:010350481</ref><references group="xtra"/><references/> | ||
[[Category: Homo sapiens]] | [[Category: Homo sapiens]] | ||
[[Category: Lysozyme]] | [[Category: Lysozyme]] | ||
Revision as of 14:11, 24 March 2013
Contribution of hydrogen bonds to the conformational stability of human lysozyme: calorimetry and x-ray analysis of six ser->ala mutantsContribution of hydrogen bonds to the conformational stability of human lysozyme: calorimetry and x-ray analysis of six ser->ala mutants
Template:ABSTRACT PUBMED 10350481
DiseaseDisease
[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]
FunctionFunction
[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 StructureAbout this Structure
1b5x is a 1 chain structure with sequence from Homo sapiens. Full crystallographic information is available from OCA.
See AlsoSee Also
ReferenceReference
- ↑ Takano K, Yamagata Y, Kubota M, Funahashi J, Fujii S, Yutani K. Contribution of hydrogen bonds to the conformational stability of human lysozyme: calorimetry and X-ray analysis of six Ser --> Ala mutants. Biochemistry. 1999 May 18;38(20):6623-9. PMID:10350481 doi:10.1021/bi9901228
- ↑ 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