1g96

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(New page: 200px<br /> <applet load="1g96" size="450" color="white" frame="true" align="right" spinBox="true" caption="1g96, resolution 2.5&Aring;" /> '''HUMAN CYSTATIN C; DI...)
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caption="1g96, resolution 2.5&Aring;" />
'''HUMAN CYSTATIN C; DIMERIC FORM WITH 3D DOMAIN SWAPPING'''<br />
'''HUMAN CYSTATIN C; DIMERIC FORM WITH 3D DOMAIN SWAPPING'''<br />
==Overview==
==Overview==
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The crystal structure of human cystatin C, a protein with amyloidogenic, properties and a potent inhibitor of cysteine proteases, reveals how the, protein refolds to produce very tight two-fold symmetric dimers while, retaining the secondary structure of the monomeric form. The dimerization, occurs through three-dimensional domain swapping, a mechanism for forming, oligomeric proteins. The reconstituted monomer-like domains are similar to, chicken cystatin except for one inhibitory loop that unfolds to form the, 'open interface' of the dimer. The structure explains the tendency of, human cystatin C to dimerize and suggests a mechanism for its aggregation, in the brain arteries of elderly people with amyloid angiopathy. A more, severe 'conformational disease' is associated with the L68Q mutant of, human cystatin C, which causes massive amyloidosis, cerebral hemorrhage, and death in young adults. The structure of the three-dimensional, domain-swapped dimers shows how the L68Q mutation destabilizes the, monomers and makes the partially unfolded intermediate less unstable., Higher aggregates may arise through the three-dimensional domain-swapping, mechanism occurring in an open-ended fashion in which partially unfolded, molecules are linked into infinite chains.
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The crystal structure of human cystatin C, a protein with amyloidogenic properties and a potent inhibitor of cysteine proteases, reveals how the protein refolds to produce very tight two-fold symmetric dimers while retaining the secondary structure of the monomeric form. The dimerization occurs through three-dimensional domain swapping, a mechanism for forming oligomeric proteins. The reconstituted monomer-like domains are similar to chicken cystatin except for one inhibitory loop that unfolds to form the 'open interface' of the dimer. The structure explains the tendency of human cystatin C to dimerize and suggests a mechanism for its aggregation in the brain arteries of elderly people with amyloid angiopathy. A more severe 'conformational disease' is associated with the L68Q mutant of human cystatin C, which causes massive amyloidosis, cerebral hemorrhage and death in young adults. The structure of the three-dimensional domain-swapped dimers shows how the L68Q mutation destabilizes the monomers and makes the partially unfolded intermediate less unstable. Higher aggregates may arise through the three-dimensional domain-swapping mechanism occurring in an open-ended fashion in which partially unfolded molecules are linked into infinite chains.
==About this Structure==
==About this Structure==
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1G96 is a [http://en.wikipedia.org/wiki/Single_protein Single protein] structure of sequence from [http://en.wikipedia.org/wiki/Homo_sapiens Homo sapiens] with CL and GOL as [http://en.wikipedia.org/wiki/ligands ligands]. Full crystallographic information is available from [http://ispc.weizmann.ac.il/oca-bin/ocashort?id=1G96 OCA].
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1G96 is a [http://en.wikipedia.org/wiki/Single_protein Single protein] structure of sequence from [http://en.wikipedia.org/wiki/Homo_sapiens Homo sapiens] with <scene name='pdbligand=CL:'>CL</scene> and <scene name='pdbligand=GOL:'>GOL</scene> as [http://en.wikipedia.org/wiki/ligands ligands]. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=1G96 OCA].
==Reference==
==Reference==
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[[Category: inhibitor of c1 and c13 cysteine proteases]]
[[Category: inhibitor of c1 and c13 cysteine proteases]]
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''Page seeded by [http://ispc.weizmann.ac.il/oca OCA ] on Mon Nov 12 17:01:55 2007''
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''Page seeded by [http://oca.weizmann.ac.il/oca OCA ] on Thu Feb 21 12:47:31 2008''

Revision as of 10:47, 21 February 2008


1g96, resolution 2.5Å

Drag the structure with the mouse to rotate

HUMAN CYSTATIN C; DIMERIC FORM WITH 3D DOMAIN SWAPPING

Overview

The crystal structure of human cystatin C, a protein with amyloidogenic properties and a potent inhibitor of cysteine proteases, reveals how the protein refolds to produce very tight two-fold symmetric dimers while retaining the secondary structure of the monomeric form. The dimerization occurs through three-dimensional domain swapping, a mechanism for forming oligomeric proteins. The reconstituted monomer-like domains are similar to chicken cystatin except for one inhibitory loop that unfolds to form the 'open interface' of the dimer. The structure explains the tendency of human cystatin C to dimerize and suggests a mechanism for its aggregation in the brain arteries of elderly people with amyloid angiopathy. A more severe 'conformational disease' is associated with the L68Q mutant of human cystatin C, which causes massive amyloidosis, cerebral hemorrhage and death in young adults. The structure of the three-dimensional domain-swapped dimers shows how the L68Q mutation destabilizes the monomers and makes the partially unfolded intermediate less unstable. Higher aggregates may arise through the three-dimensional domain-swapping mechanism occurring in an open-ended fashion in which partially unfolded molecules are linked into infinite chains.

About this Structure

1G96 is a Single protein structure of sequence from Homo sapiens with and as ligands. Full crystallographic information is available from OCA.

Reference

Human cystatin C, an amyloidogenic protein, dimerizes through three-dimensional domain swapping., Janowski R, Kozak M, Jankowska E, Grzonka Z, Grubb A, Abrahamson M, Jaskolski M, Nat Struct Biol. 2001 Apr;8(4):316-20. PMID:11276250

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