1dgk: Difference between revisions

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[[Image:1dgk.png|left|200px]]
{{STRUCTURE_1dgk|  PDB=1dgk  |  SCENE=  }}  
{{STRUCTURE_1dgk|  PDB=1dgk  |  SCENE=  }}  
===MUTANT MONOMER OF RECOMBINANT HUMAN HEXOKINASE TYPE I WITH GLUCOSE AND ADP IN THE ACTIVE SITE===
===MUTANT MONOMER OF RECOMBINANT HUMAN HEXOKINASE TYPE I WITH GLUCOSE AND ADP IN THE ACTIVE SITE===
{{ABSTRACT_PUBMED_10686099}}


{{ABSTRACT_PUBMED_10686099}}
==Disease==
[[http://www.uniprot.org/uniprot/HXK1_HUMAN HXK1_HUMAN]] Defects in HK1 are the cause of hexokinase deficiency (HK deficiency) [MIM:[http://omim.org/entry/235700 235700]]. HK deficiency is a rare autosomal recessive disease with nonspherocytic hemolytic anemia as the predominant clinical feature.


==About this Structure==
==About this Structure==
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==Reference==
==Reference==
<ref group="xtra">PMID:010686099</ref><references group="xtra"/>
<ref group="xtra">PMID:010686099</ref><references group="xtra"/><references/>
[[Category: Hexokinase]]
[[Category: Hexokinase]]
[[Category: Homo sapiens]]
[[Category: Homo sapiens]]

Revision as of 20:51, 24 March 2013

Template:STRUCTURE 1dgk

MUTANT MONOMER OF RECOMBINANT HUMAN HEXOKINASE TYPE I WITH GLUCOSE AND ADP IN THE ACTIVE SITE

Template:ABSTRACT PUBMED 10686099

Disease

[HXK1_HUMAN] Defects in HK1 are the cause of hexokinase deficiency (HK deficiency) [MIM:235700]. HK deficiency is a rare autosomal recessive disease with nonspherocytic hemolytic anemia as the predominant clinical feature.

About this Structure

1dgk is a 1 chain structure with sequence from Homo sapiens. The February 2004 RCSB PDB Molecule of the Month feature on The Glycolytic Enzymes by David S. Goodsell is 10.2210/rcsb_pdb/mom_2004_2. Full crystallographic information is available from OCA.

See Also

Reference

  1. Aleshin AE, Kirby C, Liu X, Bourenkov GP, Bartunik HD, Fromm HJ, Honzatko RB. Crystal structures of mutant monomeric hexokinase I reveal multiple ADP binding sites and conformational changes relevant to allosteric regulation. J Mol Biol. 2000 Mar 3;296(4):1001-15. PMID:10686099 doi:10.1006/jmbi.1999.3494

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