1yro

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(New page: 200px<br /><applet load="1yro" size="450" color="white" frame="true" align="right" spinBox="true" caption="1yro, resolution 1.90&Aring;" /> '''Crystal structure of...)
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[[Image:1yro.gif|left|200px]]<br /><applet load="1yro" size="450" color="white" frame="true" align="right" spinBox="true"
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[[Image:1yro.gif|left|200px]]<br /><applet load="1yro" size="350" color="white" frame="true" align="right" spinBox="true"
caption="1yro, resolution 1.90&Aring;" />
caption="1yro, resolution 1.90&Aring;" />
'''Crystal structure of beta14,-galactosyltransferase mutant ARG228Lys in complex with alpha-lactalbumin in the presence of UDP-galactose and Mn'''<br />
'''Crystal structure of beta14,-galactosyltransferase mutant ARG228Lys in complex with alpha-lactalbumin in the presence of UDP-galactose and Mn'''<br />
==Overview==
==Overview==
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Beta-1,4-galactosyltransferase I (beta4Gal-T1) normally transfers Gal from, UDP-Gal to GlcNAc in the presence of Mn(2+) ion (Gal-T activity) and also, transfers Glc from UDP-Glc to GlcNAc (Glc-T activity), albeit at only 0.3%, efficiency. In addition, alpha-lactalbumin (LA) enhances this Glc-T, activity more than 25 times. Comparison of the crystal structures of, UDP-Gal- and UDP-Glc-bound beta4Gal-T1 reveals that the O4 hydroxyl group, in both Gal and Glc moieties forms a hydrogen bond with the side chain, carboxylate group of Glu317. The orientation of the O4 hydroxyl of glucose, causes a steric hindrance to the side chain carboxylate group of Glu317, accounting for the enzyme's low Glc-T activity. In this study, we show, that mutation of Arg228, a residue in the vicinity of Glu317, to lysine, (R228K-Gal-T1) results in a 15-fold higher Glc-T activity, which is, further enhanced by LA to nearly 25% of the Gal-T activity of the wild, type. The kinetic parameters indicate that the main effect of the mutation, of Arg228 to lysine is on the k(cat) of Glc-T, which increases 3-4-fold, both in the absence and in the presence of LA; simultaneously, the k(cat), for the Gal-T reaction is reduced 30-fold. The crystal structure of, R228K-Gal-T1 complexed with LA, UDP-Gal, and Mn(2+) determined at 1.9 A, resolution shows that the Asp318 side chain exhibits a minor alternate, conformation, compared to that in the wild type. This alternate, conformation now causes a steric hindrance to the O4 hydroxyl group of the, Gal moiety of UDP-Gal, probably causing the dissociation of UDP-Gal and, the reduced k(cat) of the Gal-T reaction.
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Beta-1,4-galactosyltransferase I (beta4Gal-T1) normally transfers Gal from UDP-Gal to GlcNAc in the presence of Mn(2+) ion (Gal-T activity) and also transfers Glc from UDP-Glc to GlcNAc (Glc-T activity), albeit at only 0.3% efficiency. In addition, alpha-lactalbumin (LA) enhances this Glc-T activity more than 25 times. Comparison of the crystal structures of UDP-Gal- and UDP-Glc-bound beta4Gal-T1 reveals that the O4 hydroxyl group in both Gal and Glc moieties forms a hydrogen bond with the side chain carboxylate group of Glu317. The orientation of the O4 hydroxyl of glucose causes a steric hindrance to the side chain carboxylate group of Glu317, accounting for the enzyme's low Glc-T activity. In this study, we show that mutation of Arg228, a residue in the vicinity of Glu317, to lysine (R228K-Gal-T1) results in a 15-fold higher Glc-T activity, which is further enhanced by LA to nearly 25% of the Gal-T activity of the wild type. The kinetic parameters indicate that the main effect of the mutation of Arg228 to lysine is on the k(cat) of Glc-T, which increases 3-4-fold, both in the absence and in the presence of LA; simultaneously, the k(cat) for the Gal-T reaction is reduced 30-fold. The crystal structure of R228K-Gal-T1 complexed with LA, UDP-Gal, and Mn(2+) determined at 1.9 A resolution shows that the Asp318 side chain exhibits a minor alternate conformation, compared to that in the wild type. This alternate conformation now causes a steric hindrance to the O4 hydroxyl group of the Gal moiety of UDP-Gal, probably causing the dissociation of UDP-Gal and the reduced k(cat) of the Gal-T reaction.
==About this Structure==
==About this Structure==
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1YRO is a [http://en.wikipedia.org/wiki/Protein_complex Protein complex] structure of sequences from [http://en.wikipedia.org/wiki/Bos_taurus Bos taurus] and [http://en.wikipedia.org/wiki/Mus_musculus Mus musculus] with GDU, CA, MN, UDP, MES and PG4 as [http://en.wikipedia.org/wiki/ligands ligands]. Full crystallographic information is available from [http://ispc.weizmann.ac.il/oca-bin/ocashort?id=1YRO OCA].
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1YRO is a [http://en.wikipedia.org/wiki/Protein_complex Protein complex] structure of sequences from [http://en.wikipedia.org/wiki/Bos_taurus Bos taurus] and [http://en.wikipedia.org/wiki/Mus_musculus Mus musculus] with <scene name='pdbligand=GDU:'>GDU</scene>, <scene name='pdbligand=CA:'>CA</scene>, <scene name='pdbligand=MN:'>MN</scene>, <scene name='pdbligand=UDP:'>UDP</scene>, <scene name='pdbligand=MES:'>MES</scene> and <scene name='pdbligand=PG4:'>PG4</scene> as [http://en.wikipedia.org/wiki/ligands ligands]. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=1YRO OCA].
==Reference==
==Reference==
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[[Category: Protein complex]]
[[Category: Protein complex]]
[[Category: Boeggeman, E.]]
[[Category: Boeggeman, E.]]
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[[Category: Qasba, P.K.]]
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[[Category: Qasba, P K.]]
[[Category: Ramakrishnan, B.]]
[[Category: Ramakrishnan, B.]]
[[Category: CA]]
[[Category: CA]]
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[[Category: arg228lys mutation; udp-gal complex]]
[[Category: arg228lys mutation; udp-gal complex]]
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''Page seeded by [http://ispc.weizmann.ac.il/oca OCA ] on Wed Nov 21 07:00:23 2007''
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''Page seeded by [http://oca.weizmann.ac.il/oca OCA ] on Thu Feb 21 16:08:23 2008''

Revision as of 14:08, 21 February 2008


1yro, resolution 1.90Å

Drag the structure with the mouse to rotate

Crystal structure of beta14,-galactosyltransferase mutant ARG228Lys in complex with alpha-lactalbumin in the presence of UDP-galactose and Mn

Overview

Beta-1,4-galactosyltransferase I (beta4Gal-T1) normally transfers Gal from UDP-Gal to GlcNAc in the presence of Mn(2+) ion (Gal-T activity) and also transfers Glc from UDP-Glc to GlcNAc (Glc-T activity), albeit at only 0.3% efficiency. In addition, alpha-lactalbumin (LA) enhances this Glc-T activity more than 25 times. Comparison of the crystal structures of UDP-Gal- and UDP-Glc-bound beta4Gal-T1 reveals that the O4 hydroxyl group in both Gal and Glc moieties forms a hydrogen bond with the side chain carboxylate group of Glu317. The orientation of the O4 hydroxyl of glucose causes a steric hindrance to the side chain carboxylate group of Glu317, accounting for the enzyme's low Glc-T activity. In this study, we show that mutation of Arg228, a residue in the vicinity of Glu317, to lysine (R228K-Gal-T1) results in a 15-fold higher Glc-T activity, which is further enhanced by LA to nearly 25% of the Gal-T activity of the wild type. The kinetic parameters indicate that the main effect of the mutation of Arg228 to lysine is on the k(cat) of Glc-T, which increases 3-4-fold, both in the absence and in the presence of LA; simultaneously, the k(cat) for the Gal-T reaction is reduced 30-fold. The crystal structure of R228K-Gal-T1 complexed with LA, UDP-Gal, and Mn(2+) determined at 1.9 A resolution shows that the Asp318 side chain exhibits a minor alternate conformation, compared to that in the wild type. This alternate conformation now causes a steric hindrance to the O4 hydroxyl group of the Gal moiety of UDP-Gal, probably causing the dissociation of UDP-Gal and the reduced k(cat) of the Gal-T reaction.

About this Structure

1YRO is a Protein complex structure of sequences from Bos taurus and Mus musculus with , , , , and as ligands. Full crystallographic information is available from OCA.

Reference

Mutation of arginine 228 to lysine enhances the glucosyltransferase activity of bovine beta-1,4-galactosyltransferase I., Ramakrishnan B, Boeggeman E, Qasba PK, Biochemistry. 2005 Mar 8;44(9):3202-10. PMID:15736931

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