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1n69

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(New page: 200px<br /> <applet load="1n69" size="450" color="white" frame="true" align="right" spinBox="true" caption="1n69, resolution 2.20&Aring;" /> '''Crystal structure o...)
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<applet load="1n69" size="450" color="white" frame="true" align="right" spinBox="true"
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caption="1n69, resolution 2.20&Aring;" />
caption="1n69, resolution 2.20&Aring;" />
'''Crystal structure of human saposin B'''<br />
'''Crystal structure of human saposin B'''<br />
==Overview==
==Overview==
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Saposin B is a small, nonenzymatic glycosphingolipid activator protein, required for the breakdown of cerebroside sulfates (sulfatides) within the, lysosome. The protein can extract target lipids from membranes, forming, soluble protein-lipid complexes that are recognized by arylsulfatase A., The crystal structure of human saposin B reveals an unusual shell-like, dimer consisting of a monolayer of alpha-helices enclosing a large, hydrophobic cavity. Although the secondary structure of saposin B is, similar to that of the known monomeric members of the saposin-like, superfamily, the helices are repacked into a different tertiary, arrangement to form the homodimer. A comparison of the two forms of the, saposin B dimer suggests that extraction of target lipids from membranes, involves a conformational change that facilitates access to the inner, cavity.
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Saposin B is a small, nonenzymatic glycosphingolipid activator protein required for the breakdown of cerebroside sulfates (sulfatides) within the lysosome. The protein can extract target lipids from membranes, forming soluble protein-lipid complexes that are recognized by arylsulfatase A. The crystal structure of human saposin B reveals an unusual shell-like dimer consisting of a monolayer of alpha-helices enclosing a large hydrophobic cavity. Although the secondary structure of saposin B is similar to that of the known monomeric members of the saposin-like superfamily, the helices are repacked into a different tertiary arrangement to form the homodimer. A comparison of the two forms of the saposin B dimer suggests that extraction of target lipids from membranes involves a conformational change that facilitates access to the inner cavity.
==Disease==
==Disease==
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Known diseases associated with this structure: Combined SAP deficiency OMIM:[[http://www.ncbi.nlm.nih.gov/entrez/dispomim.cgi?id=176801 176801]], Gaucher disease, atypical OMIM:[[http://www.ncbi.nlm.nih.gov/entrez/dispomim.cgi?id=176801 176801]], Metachromatic leukodystrophy due to deficiency of SAP-1 OMIM:[[http://www.ncbi.nlm.nih.gov/entrez/dispomim.cgi?id=176801 176801]]
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Known diseases associated with this structure: Combined SAP deficiency OMIM:[[http://www.ncbi.nlm.nih.gov/entrez/dispomim.cgi?id=176801 176801]], Gaucher disease, atypical OMIM:[[http://www.ncbi.nlm.nih.gov/entrez/dispomim.cgi?id=176801 176801]], Krabbe disease, atypical OMIM:[[http://www.ncbi.nlm.nih.gov/entrez/dispomim.cgi?id=176801 176801]], Metachromatic leukodystrophy due to SAP-b deficiency OMIM:[[http://www.ncbi.nlm.nih.gov/entrez/dispomim.cgi?id=176801 176801]]
==About this Structure==
==About this Structure==
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1N69 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 PEH as [http://en.wikipedia.org/wiki/ligand ligand]. Full crystallographic information is available from [http://ispc.weizmann.ac.il/oca-bin/ocashort?id=1N69 OCA].
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1N69 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=PEH:'>PEH</scene> as [http://en.wikipedia.org/wiki/ligand ligand]. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=1N69 OCA].
==Reference==
==Reference==
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[[Category: Homo sapiens]]
[[Category: Homo sapiens]]
[[Category: Single protein]]
[[Category: Single protein]]
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[[Category: Ahn, V.E.]]
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[[Category: Ahn, V E.]]
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[[Category: Faull, K.F.]]
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[[Category: Faull, K F.]]
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[[Category: Fluharty, A.L.]]
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[[Category: Fluharty, A L.]]
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[[Category: Prive, G.G.]]
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[[Category: Prive, G G.]]
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[[Category: Whitelegge, J.P.]]
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[[Category: Whitelegge, J P.]]
[[Category: PEH]]
[[Category: PEH]]
[[Category: glycosphingolipid activator protein]]
[[Category: glycosphingolipid activator protein]]
[[Category: lipid binding protein]]
[[Category: lipid binding protein]]
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''Page seeded by [http://ispc.weizmann.ac.il/oca OCA ] on Mon Nov 12 18:18:00 2007''
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''Page seeded by [http://oca.weizmann.ac.il/oca OCA ] on Thu Feb 21 14:02:41 2008''

Revision as of 12:02, 21 February 2008


1n69, resolution 2.20Å

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Crystal structure of human saposin B

Contents

Overview

Saposin B is a small, nonenzymatic glycosphingolipid activator protein required for the breakdown of cerebroside sulfates (sulfatides) within the lysosome. The protein can extract target lipids from membranes, forming soluble protein-lipid complexes that are recognized by arylsulfatase A. The crystal structure of human saposin B reveals an unusual shell-like dimer consisting of a monolayer of alpha-helices enclosing a large hydrophobic cavity. Although the secondary structure of saposin B is similar to that of the known monomeric members of the saposin-like superfamily, the helices are repacked into a different tertiary arrangement to form the homodimer. A comparison of the two forms of the saposin B dimer suggests that extraction of target lipids from membranes involves a conformational change that facilitates access to the inner cavity.

Disease

Known diseases associated with this structure: Combined SAP deficiency OMIM:[176801], Gaucher disease, atypical OMIM:[176801], Krabbe disease, atypical OMIM:[176801], Metachromatic leukodystrophy due to SAP-b deficiency OMIM:[176801]

About this Structure

1N69 is a Single protein structure of sequence from Homo sapiens with as ligand. Full crystallographic information is available from OCA.

Reference

Crystal structure of saposin B reveals a dimeric shell for lipid binding., Ahn VE, Faull KF, Whitelegge JP, Fluharty AL, Prive GG, Proc Natl Acad Sci U S A. 2003 Jan 7;100(1):38-43. Epub 2002 Dec 23. PMID:12518053

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