Structure of testis ACE glycosylation mutants and evidence for conserved domain movement

dc.contributor.authorWatermeyer, Jean M
dc.contributor.authorSewell, Trevor B
dc.contributor.authorSchwager, Sylva L
dc.contributor.authorNatesh, Ramanathan
dc.contributor.authorCorradi, Hazel R
dc.contributor.authorAcharya, Ravi K
dc.contributor.authorSturrock, Edward D
dc.date.accessioned2016-07-28T14:37:39Z
dc.date.available2016-07-28T14:37:39Z
dc.date.issued2006
dc.date.updated2016-07-28T14:31:47Z
dc.description.abstractHuman angiotensin-converting enzyme is an important drug target for which little structural information has been available until recent years. The slow progress in obtaining a crystal structure was due to the problem of surface glycosylation, a difficulty that has thus far been overcome by the use of a glucosidase-1 inhibitor in the tissue culture medium. However, the prohibitive cost of these inhibitors and incomplete glucosidase inhibition makes alternative routes to minimizing the N-glycan heterogeneity desirable. Here, glycosylation in the testis isoform (tACE) has been reduced by Asn-Gln point mutations at N-glycosylation sites, and the crystal structures of mutants having two and four intact sites have been solved to 2.0 Å and 2.8 Å, respectively. Both mutants show close structural identity with the wild-type. A hinge mechanism is proposed for substrate entry into the active cleft, based on homology to human ACE2 at the levels of sequence and flexibility. This is supported by normal-mode analysis that reveals intrinsic flexibility about the active site of tACE. Subdomain II, containing bound chloride and zinc ions, is found to have greater stability than subdomain I in the structures of three ACE homologues. Crystallizable glycosylation mutants open up new possibilities for cocrystallization studies to aid the design of novel ACE inhibitors.en_ZA
dc.identifierhttp://dx.doi.org/10.1021/bi061146z
dc.identifier.apacitationWatermeyer, J. M., Sewell, T. B., Schwager, S. L., Natesh, R., Corradi, H. R., Acharya, R. K., & Sturrock, E. D. (2006). Structure of testis ACE glycosylation mutants and evidence for conserved domain movement. <i>Biochemistry</i>, http://hdl.handle.net/11427/21004en_ZA
dc.identifier.chicagocitationWatermeyer, Jean M, Trevor B Sewell, Sylva L Schwager, Ramanathan Natesh, Hazel R Corradi, Ravi K Acharya, and Edward D Sturrock "Structure of testis ACE glycosylation mutants and evidence for conserved domain movement." <i>Biochemistry</i> (2006) http://hdl.handle.net/11427/21004en_ZA
dc.identifier.citationWatermeyer, J. M., Sewell, B. T., Schwager, S. L., Natesh, R., Corradi, H. R., Acharya, K. R., & Sturrock, E. D. (2006). Structure of testis ACE glycosylation mutants and evidence for conserved domain movement. Biochemistry, 45(42), 12654-12663.en_ZA
dc.identifier.issn0006-2960en_ZA
dc.identifier.ris TY - Journal Article AU - Watermeyer, Jean M AU - Sewell, Trevor B AU - Schwager, Sylva L AU - Natesh, Ramanathan AU - Corradi, Hazel R AU - Acharya, Ravi K AU - Sturrock, Edward D AB - Human angiotensin-converting enzyme is an important drug target for which little structural information has been available until recent years. The slow progress in obtaining a crystal structure was due to the problem of surface glycosylation, a difficulty that has thus far been overcome by the use of a glucosidase-1 inhibitor in the tissue culture medium. However, the prohibitive cost of these inhibitors and incomplete glucosidase inhibition makes alternative routes to minimizing the N-glycan heterogeneity desirable. Here, glycosylation in the testis isoform (tACE) has been reduced by Asn-Gln point mutations at N-glycosylation sites, and the crystal structures of mutants having two and four intact sites have been solved to 2.0 Å and 2.8 Å, respectively. Both mutants show close structural identity with the wild-type. A hinge mechanism is proposed for substrate entry into the active cleft, based on homology to human ACE2 at the levels of sequence and flexibility. This is supported by normal-mode analysis that reveals intrinsic flexibility about the active site of tACE. Subdomain II, containing bound chloride and zinc ions, is found to have greater stability than subdomain I in the structures of three ACE homologues. Crystallizable glycosylation mutants open up new possibilities for cocrystallization studies to aid the design of novel ACE inhibitors. DA - 2006 DB - OpenUCT DP - University of Cape Town J1 - Biochemistry LK - https://open.uct.ac.za PB - University of Cape Town PY - 2006 SM - 0006-2960 T1 - Structure of testis ACE glycosylation mutants and evidence for conserved domain movement TI - Structure of testis ACE glycosylation mutants and evidence for conserved domain movement UR - http://hdl.handle.net/11427/21004 ER - en_ZA
dc.identifier.urihttp://hdl.handle.net/11427/21004
dc.identifier.vancouvercitationWatermeyer JM, Sewell TB, Schwager SL, Natesh R, Corradi HR, Acharya RK, et al. Structure of testis ACE glycosylation mutants and evidence for conserved domain movement. Biochemistry. 2006; http://hdl.handle.net/11427/21004.en_ZA
dc.languageengen_ZA
dc.publisherAmerican Chemical Societyen_ZA
dc.publisher.institutionUniversity of Cape Town
dc.sourceBiochemistryen_ZA
dc.source.urihttp://pubs.acs.org/journal/bichaw
dc.titleStructure of testis ACE glycosylation mutants and evidence for conserved domain movementen_ZA
dc.typeJournal Articleen_ZA
uct.type.filetypeText
uct.type.filetypeImage
uct.type.publicationResearchen_ZA
uct.type.resourceArticleen_ZA
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