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Expert
Reviews in Molecular Medicine: http://www.expertreviews.org/
Accession information: Vol. 8; Issue 13; 12 June 2006 Abstract
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Location of the partial-D-causative amino acid polymorphisms
Neil D. Avent, Tracey E. Madgett, Zoe E. Lee, David J. Head, Deborah G. Maddocks and Lucy H. Skinner
Figure 2. Location of the partial-D-causative amino acid polymorphisms. This figure depicts the exofacial (i.e. on the external side of the red blood cell) location of amino acid exchanges that cause partial D phenotypes. Exofacial RhD protein loops at the top and endofacial loops at the bottom are shown in green. The positions of the 11 transmembrane helices are shown in blue and white. Note the location of the first helix [denoted M0 by Conroy et al. (Ref. 42)] cannot be modelled, because the AmtB protein, used to generate the RhD protein structure, has only 11 transmembrane domains yet RH proteins have 12 transmembrane domains. The view of the RhD protein monomer is skewed in order to reveal the six exoloops involved in RhD antigenicity. The following mutations are highlighted: Exoloop 2: DVII- L110P (Ref. 155); Exoloop 3: DFW H166P; DOL-1 M170T; Exoloop 4: DOL-1 F223V; DHR R229K; Exoloop 5: DHMi T283I; DLO S284L; Exoloop 6: DNU G353R; DII A354D; DNB G355S; DWI M358T. The RhD structure was modelled using the DeepView-Swiss PdbViewer.
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References
cited in Figure 2 155 Rouillac, C. et al. (1995) Leu110Pro substitution in the RhD polypeptide is responsible for the DVII category blood group phenotype. Am J Hematol 49, 87-88, PubMed |
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