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1lds

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==Overview==
==Overview==
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Dissociation of human beta-2-microglobulin (beta(2)m) from the heavy chain, of the class I HLA complex is a critical first step in the formation of, amyloid fibrils from this protein. As a consequence of renal failure, the, concentration of circulating monomeric beta(2)m increases, ultimately, leading to deposition of the protein into amyloid fibrils and development, of the disorder, dialysis-related amyloidosis. Here we present the crystal, structure of a monomeric form of human beta(2)m determined at 1.8-A, resolution that reveals remarkable structural changes relative to the, HLA-bound protein. These involve the restructuring of a beta bulge that, separates two short beta strands to form a new six-residue beta strand at, one edge of this beta sandwich protein. These structural changes remove, key features proposed to have evolved to protect beta sheet proteins from, aggregation [Richardson, J. & Richardson, D. (2002) Proc. Natl. Acad. Sci., USA 99, 2754-2759] and replaces them with an aggregation-competent, surface. In combination with solution studies using (1)H NMR, we show that, the crystal structure presented here represents a rare species in solution, that could provide important clues about the mechanism of amyloid, formation from the normally highly soluble native protein.
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Dissociation of human beta-2-microglobulin (beta(2)m) from the heavy chain of the class I HLA complex is a critical first step in the formation of amyloid fibrils from this protein. As a consequence of renal failure, the concentration of circulating monomeric beta(2)m increases, ultimately leading to deposition of the protein into amyloid fibrils and development of the disorder, dialysis-related amyloidosis. Here we present the crystal structure of a monomeric form of human beta(2)m determined at 1.8-A resolution that reveals remarkable structural changes relative to the HLA-bound protein. These involve the restructuring of a beta bulge that separates two short beta strands to form a new six-residue beta strand at one edge of this beta sandwich protein. These structural changes remove key features proposed to have evolved to protect beta sheet proteins from aggregation [Richardson, J. & Richardson, D. (2002) Proc. Natl. Acad. Sci. USA 99, 2754-2759] and replaces them with an aggregation-competent surface. In combination with solution studies using (1)H NMR, we show that the crystal structure presented here represents a rare species in solution that could provide important clues about the mechanism of amyloid formation from the normally highly soluble native protein.
==Disease==
==Disease==
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[[Category: Homo sapiens]]
[[Category: Homo sapiens]]
[[Category: Single protein]]
[[Category: Single protein]]
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[[Category: Kalverda, A.P.]]
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[[Category: Kalverda, A P.]]
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[[Category: Phillips, S.E.V.]]
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[[Category: Phillips, S E.V.]]
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[[Category: Radford, S.E.]]
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[[Category: Radford, S E.]]
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[[Category: Smith, D.P.]]
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[[Category: Smith, D P.]]
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[[Category: Trinh, C.H.]]
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[[Category: Trinh, C H.]]
[[Category: NA]]
[[Category: NA]]
[[Category: immunoglobulin constant domain]]
[[Category: immunoglobulin constant domain]]
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''Page seeded by [http://oca.weizmann.ac.il/oca OCA ] on Fri Feb 15 16:17:39 2008''
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''Page seeded by [http://oca.weizmann.ac.il/oca OCA ] on Thu Feb 21 13:44:03 2008''

Revision as of 11:44, 21 February 2008


1lds, resolution 1.80Å

Drag the structure with the mouse to rotate

Crystal Structure of monomeric human beta-2-microglobulin

Contents

Overview

Dissociation of human beta-2-microglobulin (beta(2)m) from the heavy chain of the class I HLA complex is a critical first step in the formation of amyloid fibrils from this protein. As a consequence of renal failure, the concentration of circulating monomeric beta(2)m increases, ultimately leading to deposition of the protein into amyloid fibrils and development of the disorder, dialysis-related amyloidosis. Here we present the crystal structure of a monomeric form of human beta(2)m determined at 1.8-A resolution that reveals remarkable structural changes relative to the HLA-bound protein. These involve the restructuring of a beta bulge that separates two short beta strands to form a new six-residue beta strand at one edge of this beta sandwich protein. These structural changes remove key features proposed to have evolved to protect beta sheet proteins from aggregation [Richardson, J. & Richardson, D. (2002) Proc. Natl. Acad. Sci. USA 99, 2754-2759] and replaces them with an aggregation-competent surface. In combination with solution studies using (1)H NMR, we show that the crystal structure presented here represents a rare species in solution that could provide important clues about the mechanism of amyloid formation from the normally highly soluble native protein.

Disease

Known disease associated with this structure: Hypoproteinemia, hypercatabolic OMIM:[109700]

About this Structure

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

Reference

Crystal structure of monomeric human beta-2-microglobulin reveals clues to its amyloidogenic properties., Trinh CH, Smith DP, Kalverda AP, Phillips SE, Radford SE, Proc Natl Acad Sci U S A. 2002 Jul 23;99(15):9771-6. Epub 2002 Jul 15. PMID:12119416

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