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Our data demonstrate a near twofold increase in the expression of D antigen in subjects homozygous for RHD when compared with RHD hemizygotes (Fig. 3). This copy number ��dose effect�� of RHD was perhaps predictable but not previously documented does not fully explain expression variability since considerable variation in D antigen expression was still noted within both the DD and the Dd cohorts (Fig. 3). The potential impact of minor Rh antigen expression (Cc and Ee) on D antigen expression was suggested by previous reports [16, 17]. We not only confirmed that the presence of C antigen or e antigen was associated with reduced D antigen expression but also suggest that the presence of c or E antigen may be associated with increased D antigen expression http://www.selleckchem.com/products/r428.html (Table II). When both C and c were present, D antigen expression remained high suggesting the positive effects of c antigen appear to outweigh the negative or potentially suppressive effects of C antigen expression. Although significant advances have been made in the understanding of Rh protein structure and function [1, 38, 39], the interactions between D antigen and C/c or E/e antigens that could alter membrane expression of D antigen are not clear. As tandem duplicated genes, it is possible that RHCE expression has a direct suppressive effect on RHD transcription. Alternatively, RHCE expression could influence RHD mRNA translation, or be involved with post-translational modifications. Finally, given the tight trimeric structure of the Rh protein superfamily [38], it is possible that coexpression of D http://www.selleckchem.com/products/PF-2341066.html and C antigens results in more steric hindrance on the RBC membrane, thereby reducing D antigen expression. There are several http://www.selleck.cn/products/3-methyladenine.html potential limitations of this report. First, our samples came from pediatric patients rather than normal adult controls; this was primarily for convenience, and our data should be applicable to all patient groups. Second, our sample size was relatively small, yet 107 samples provided us with enough data to identify clear differences in D antigen expression by flow cytometry and also significant influences from the RhCcEe phenotype. Larger studies should be able to validate and extend our findings and allow better evaluation of the effects of E antigen expression. Third, an incorrect assignment of RHD zygosity status is possible for subjects with a silenced but not deleted RHD, particularly in non-Caucasian subjects [25]. Despite our attempts at confirming RHD zygosity by using two complementary assays, it is possible with an inactivating mutation as described in the literature [25, 27] are misassigned DD status due to inability to identify these mutations by PCR-RFLP or RQ-PCR [25, 27]. In our report, there are two DD samples (both African American) shown as outliers in Fig. 3 with