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Emile Van Den Akker - One of the best experts on this subject based on the ideXlab platform.
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a variant rhag protein encoded by the rhag 572a allele causes serological weak d expression while maintaining normal rhce phenotypes
Transfusion, 2019Co-Authors: Jizhi Wen, O. J. H. M. Verhagen, Shuangshuang Jia, Qian-ni Liang, Zhen Wang, Ling Wei, Hong Luo, Guangping Luo, Gestur Vidarsson, Emile Van Den AkkerAbstract:BACKGROUND: The molecular events resulting in a weak D phenotype include missense mutations, in-frame insertion, or deletion mutations of the RHD Gene and hybrid RHD-CE-D hybrid alleles. Mutations in Genes encoding the proteins that are required for proper membrane expression of Rh proteins, such as RhAG and ankyrin 1, can lead to absent or weakened expression of Rh antigens. STUDY DESIGN AND METHODS: Blood sample from a Chinese blood donor with a serological weak D phenotype was collected. RhAG antigen expression, RHD, and RhCE phenotypes were determined. Analysis of the RHD and RHCE genotypes by RH multiplex ligation-dependent probe amplification (MLPA), Sanger sequencing of the RHD exons, and next-Generation sequencing (NGS) of the RHAG and ANK1 exons were performed. Expression studies in vitro were conducted by lentivirally transducing the mutant RHAG*572A or wild-type RHAG, in combination with either RHD or RHCE constructs, into HEK 293 T cells. The expression of RhAG, RHD, and RhCE antigens was analyzed by flow cytometry. RESULTS: Serological weak D and normal C + c-E–e + phenotypes, normal CCDDee genotype determined by RH-MLPA, and normal sequence of the RHD Gene by Sanger sequencing were demonstrated. A homozygous variant (c.572G > A, p.Arg191Gln) of the RHAG Gene was revealed by NGS analysis. Normal RhAG, weak RHD, and normal RhCE antigens were detected in cells transduced with the mutant RHAG*572A, the mutant RHAG*572A and RHD, and the mutant RHAG*572A and RHCE constructs, respectively. CONCLUSION: The homozygous presence of RHAG*572A allele results in weak D expression. It does not affect RhCE expression.
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A variant RhAG protein encoded by the RHAG*572A allele causes serological weak D expression while maintaining normal RhCE phenotypes.
Transfusion, 2018Co-Authors: Jizhi Wen, O. J. H. M. Verhagen, Shuangshuang Jia, Qian-ni Liang, Zhen Wang, Ling Wei, Hong Luo, Guangping Luo, Gestur Vidarsson, Emile Van Den AkkerAbstract:BACKGROUND: The molecular events resulting in a weak D phenotype include missense mutations, in-frame insertion, or deletion mutations of the RHD Gene and hybrid RHD-CE-D hybrid alleles. Mutations in Genes encoding the proteins that are required for proper membrane expression of Rh proteins, such as RhAG and ankyrin 1, can lead to absent or weakened expression of Rh antigens. STUDY DESIGN AND METHODS: Blood sample from a Chinese blood donor with a serological weak D phenotype was collected. RhAG antigen expression, RHD, and RhCE phenotypes were determined. Analysis of the RHD and RHCE genotypes by RH multiplex ligation-dependent probe amplification (MLPA), Sanger sequencing of the RHD exons, and next-Generation sequencing (NGS) of the RHAG and ANK1 exons were performed. Expression studies in vitro were conducted by lentivirally transducing the mutant RHAG*572A or wild-type RHAG, in combination with either RHD or RHCE constructs, into HEK 293 T cells. The expression of RhAG, RHD, and RhCE antigens was analyzed by flow cytometry. RESULTS: Serological weak D and normal C + c-E–e + phenotypes, normal CCDDee genotype determined by RH-MLPA, and normal sequence of the RHD Gene by Sanger sequencing were demonstrated. A homozygous variant (c.572G > A, p.Arg191Gln) of the RHAG Gene was revealed by NGS analysis. Normal RhAG, weak RHD, and normal RhCE antigens were detected in cells transduced with the mutant RHAG*572A, the mutant RHAG*572A and RHD, and the mutant RHAG*572A and RHCE constructs, respectively. CONCLUSION: The homozygous presence of RHAG*572A allele results in weak D expression. It does not affect RhCE expression.
Jean-pierre Cartron - One of the best experts on this subject based on the ideXlab platform.
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Mice Expressing RHAG and RHD Human Blood Group Genes
PLoS ONE, 2013Co-Authors: Dominique Goossens, Isabelle Mouro-chanteloup, Nelly Da Silva, Sylvain Metral, Ulrich Cortes, Isabelle Callebaut, Julien Picot, Jean-pierre CartronAbstract:Anti-RHD prophylaxis of haemolytic disease of the fetus and newborn (HDFN) is highly effective, but as the suppressive mechanism remains uncertain, a mouse model would be of interest. Here we have Generated transgenic mice expressing human RhAG and RHD erythrocyte membrane proteins in the presence and, for human RhAG, in the absence, of mouse Rhag. Human RhAG associates with mouse Rh but not mouse Rhag on red blood cells. In Rhag knockout mice transgenic for human RHAG, the mouse Rh protein is " rescued " (re-expressed), and co-immunoprecipitates with human RhAG, indicating the presence of hetero-complexes which associate mouse and human proteins. RHD antigen was expressed from a human RHD Gene on a BAC or from RHD cDNA under control of β-globin regulatory elements. RHD was never observed alone, strongly indicative that its expression absolutely depends on the presence of transgenic human RhAG. This first expression of RHD in mice is an important step in the creation of a mouse model of RHD allo-immunisation and HDFN, in conjunction with the Rh-Rhag knockout mice we have developed previously.
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Shift from Rh-positive to Rh-negative phenotype caused by a somatic mutation within the RHD Gene in a patient with chronic myelocytic leukaemia
British journal of haematology, 1998Co-Authors: Baya Chérif-zahar, Pierre Gane, Virginie Raynal, Viviane Bony, Rudi Steffensen, Dominique Goosens, Jens Skaaning Laursen, Kim Varming, Casper Jersild, Jean-pierre CartronAbstract:We report a female patient whose Rh phenotype shifted from RHD-positive to RHD-negative over a 3-year period (1991–94), during which time she was treated with mastectomy (1992) and local irradiation for a low-grade recurrent breast cancer. She was diagnosed with chronic myeloid leukaemia in 1994, and has since then received chemotherapy. The patient was repeatedly typed as O, RHD-positive between 1965 and 1991 and was repeatedly found RHD-negative after 1994. Bcr-Abl transcripts typical of Ph1 chromosome were detected. Molecular analysis indicated that the patient was heterozygous at the RH locus, carrying one haplotype in which the RHD Gene exhibited a single nucleotide deletion (G600) resulting in a frameshift and premature stop codon, and a normal RHCE Gene (allele Ce). The second haplotype contained only the RHCE Gene (allele ce) and was normal. Further analysis carried out on total leucocytes, purified neutrophils, EBV-lymphoblastoid cell line and cultured erythroblasts indicated that the G600 deletion was restricted to the myeloid lineage. No modification of other blood group antigens could be detected. These findings suggest a somatic mutation which most probably occurred in a stem cell common to the myeloid lineage.
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Single-cell analysis of the RHD blood type for use in preimplantation diagnosis in the prevention of severe hemolytic disease of the newborn☆
American Journal of Obstetrics and Gynecology, 1995Co-Authors: Ignatia B. Van Den Veyver, Jean-pierre Cartron, Yves Colin, Samuel S. Chong, Juan Cota, Phillip R. Bennett, Nicholas M. Fisk, Alan H. Handyside, Caroline Le Van Kim, Michael C. SnabesAbstract:Abstract OBJECTIVE: Our purpose was to develop a molecular assay to determine the fetal RHD blood type on single diploid cells, including blastomeres. STUDY DESIGN: Polymerase chain reaction amplification of a 99 bp deoxyribonucleic acid fragment of the RHD Gene or a 113 bp fragment from the RhCE Gene was performed from 20 venous blood samples and 20 amniotic fluid samples and from 60 single-cultured lymphoblasts and 12 media blanks mixed in a blinded fashion. This reaction was similarly tested after whole-genome amplification on 10 lymphoblasts and seven human blastomeres. RESULTS: Deoxyribonucleic acid amplification was successful and correct from all genomic deoxyribonucleic acid samples. Ninety-seven percent of single cells amplified: correct diagnosis was made in 96%. Five blastomeres successfully amplified. No media blanks produced amplified, contaminating deoxyribonucleic acid. CONCLUSIONS: The RHD blood type can be determined reliably from single cells and can be used for preimplantation Genetic diagnosis for the prevention of rhesus hemolytic disease.
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rearrangements of the blood group RHD Gene associated with the dvi category phenotype
Blood, 1994Co-Authors: I Mouro, Jean-pierre Cartron, D. J. Van Rhenen, Le C Van Kim, C Rouillac, P Le Y Pennec, Pascal Bailly, Yves ColinAbstract:The Rh (Rhesus) blood group antigens, D, Cc, and Ee, are carried by three unglycosylated membrane proteins of the human erythrocytes encoded by two highly related Genes, D and CcEe. The major antigen, D, is a mosaic composed of at least nine determinants (epD1 through epD9). The lack of expression of some of these D epitopes at the surface of variant red blood cells defines the so-called D category phenotypes. In this report, we have determined the molecular basis of the DVI category phenotype characterized by the lack of epitopes D1, D2, D5, D6/7, and D8. Southern blot analysis and mRNA sequencing showed that the DVI phenotype is associated with two types of rearrangement of the D Gene. Of 10 DVI genomes investigated, 8 exhibited a segmental DNA replacement (Gene conversion) between the D fragment encompassing exons 4, 5, and 6 and the equivalent region of the CcEe Gene. In the two other variants, these three exons are deleted. In both cases, the genomic rearrangement did not alter the reading frame of the variant RHD transcripts that are translated in 417 and 266 amino acid polypeptides, respectively. A heteroGeneity of category DVI samples based on variable reactivity of the red blood cells with anti-D antibodies was previously found to be associated with the CDVIe or cDVIE haplotypes. Interestingly, our present results indicated that this serologic subdivision of the DVI category is correlated to two types of genomic rearrangements of the D Gene.
C. E. Van Der Schoot - One of the best experts on this subject based on the ideXlab platform.
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systemic analysis and zygosity determination of the RHD Gene in a d negative chinese han population reveals a novel d negative RHD Gene
Vox Sanguinis, 2005Co-Authors: X Qun, Martine G H M Grootkerktax, P Maaskantvan A Wijk, C. E. Van Der SchootAbstract:Background and Objectives The aim of this study was to systemically analyse the Genetic background of D negativity in a Chinese Han population. Materials and Methods DNA of 74 D-negative samples was analysed by using an RHD multiplex polymerase chain reaction (MPX PCR) for the presence of RHD and by PCR–restriction fragment length polymorphism (PCR–RFLP) for RHD zygosity determination. Sixty-five samples were additionally analysed by using real-time quantitative PCR on RHD exon 7. RHD exon-specific sequencing was performed on discrepant samples. Results Forty-six samples (62%) showed the absence of RHD-specific exons by RHD MPX PCR and homozygous RHD negativity by PCR–RFLP. Twenty-two samples (30%) showed a 1227G>A mutation, characteristic for the Del phenotype. Five (7%) samples showed all characteristics of the RHD(1–2)-CE(3–9)-D(10) hybrid Gene. One sample (1·4%) showed a novel 933C>A nonsense mutation in RHD exon 6, which resulted in a premature stop codon. Conclusions The RHD Gene deletion, RHD-CE-D hybrid Genes and one novel 93C>A mutation were found to be the three mechanisms that cause D negativity in our samples. The 1227G>A Del mutation was found to be the major cause of discrepant results between genotyping and phenotyping strategies, favouring genotyping of D-negative samples.
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lower antigen site density and weak d immunogenicity cannot be explained by structural genomic abnormalities or regulatory defects of the RHD Gene
Transfusion, 1997Co-Authors: Erik A M Beckers, B. H. W. Faas, M. A. M. Overbeeke, C. E. Van Der Schoot, Peter C Ligthart, A E G K Von Dem Borne, D. J. Van RhenenAbstract:BACKGROUND: The weak D phenotype is characterized serologically by a weak or negative agglutination reaction with polyclonal anti-D in an immediate-spin test. Agglutination is enhanced in the indirect antiglobulin test. Red cells that are typed weak D have a much lower number of apparently complete D antigens at their cell surface and are associated with considerably weaker immunogenicity than are red cells with normal D. In a previous study, the number of D sites per cell was determined in eight unrelated weak D individuals to range from 490 to 1870 D sites per cell, which corresponded to 4 to 14.2 percent of the number of D sites in CcDee samples. STUDY DESIGN AND METHODS: The RHD Gene was investigated for structural abnormalities by Southern blot experiments and polymerase chain reaction-based RHD typing in these individuals. In addition, abnormalities in the transcription process were studied by sequence analysis of RH transcripts and by comparing the relative amounts of RHD mRNA in weak D to those in CcDee, CcDEe, and -D- samples by using a semiquantitative reverse transcriptase- polymerase chain reaction analysis. RESULTS: The RHD Gene in weak D phenotypes does not show any abnormalities at either the genomic or the transcriptional level when compared to the RHD Gene in normal D phenotypes. CONCLUSION: The weaker immunogenicity of weak D is not explained by structural difference in the RHD Gene itself. The weaker expression of D might be caused by factors involved in the Rh-related complex or by an as yet unidentified suppressor Gene. This study supports the concept that weak D phenotypes carry complete D polypeptides and reflect a quantitative rather than a qualitative variation of D.
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characterization of the hybrid RHD Gene leading to the partial d category iiic phenotype
Transfusion, 1996Co-Authors: Erik A M Beckers, B. H. W. Faas, M. A. M. Overbeeke, D. J. Van Rhenen, Peter C Ligthart, A E G K Von Dem Borne, S Simsek, C. E. Van Der SchootAbstract:A D-positive white woman was found to have produced alloanti-D leading to hemolytic disease of the newborn in her third D-positive child. The maternal D was identified as the partial D category IIIc antigen (DIIIc). The molecular basis of this phenotype was studied. The proposita and her relatives were phenotyped for Rh system antigens with standard reagents. D(IIIc) typing of D-positive red cells was done with serum that contained anti-D from the proposita. Southern blot analysis and RHD-specific polymerase chain reactions were performed with genomic DNA. Rh transcripts were cloned and sequenced. Six relatives of the proposita were found to express the DIIIc phenotype, which traveled with Ce. The DIIIc phenotype was inherited in a Mendelian fashion. Southern blot analysis showed an identical digestion pattern in D(IIIc) individuals and in DD controls. Three different Rh transcripts were found. Two Rh transcripts were derived from RHCE (RHce and RHCe). The RHD-derived Rh transcript was the same as that of the published RHD sequence, apart from exon 3, which appeared to be exon 3 of RHCE. At the genomic level, RHD exon 3 was missing in all individuals expressing D(IIIc). This study shows the characteristics of a new hybrid D-CE-D allele encoding D(IIIc). It may be concluded that exon 3 of RHD is not involved in the formation of any of the D epitopes known at present, but rather encodes a new D epitope or D epitopes, as yet undefined by monoclonal anti-D reagents
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The R0Har Rh:33 phenotype results from substitution of exon 5 of the RHCE Gene by the corresponding exon of the RHD Gene
British journal of haematology, 1996Co-Authors: E. A. M. Beckers, B. H. W. Faas, M. A. M. Overbeeke, D. J. Van Rhenen, A. E. G. Krvon Dem Borne, C. E. Van Der SchootAbstract:The highly polymorphic Rh (Rhesus) system is encoded by two homologous Genes, one encoding the D polypeptide and the other the CcEe polypeptides. Partial D antigens may be caused by Gene rearrangements, deletions or point mutations. In this study the molecular basis of R 0 Har Rh :33, a Rh phenotype of low frequency, is described. The R 0 Har Rh :33 phenotype is characterized by partial expression of D, altered expression of e, absence of G and the presence of two antigens of low frequency : Rh33 and FPTT. Southern blot analysis, RHD typing by PCR and sequence analysis of Rh transcripts revealed that the RHD Gene is absent in subjects with this phenotype. Apart from the expected RHCE transcripts, a new Rh transcript, RHc(D)(e). was identified in three unrelated individuals expressing R 0 Har Rh :33. The RHc(D)(e) transcript showed the same sequence as the RHce transcript, with the exception of exon 5, which was substituted by the corresponding exon of the RHD Gene. A method for PCR-based genotyping was developed to determine specifically the c(D)(e) haplotype. The c(I))(e) PCR proved to be a reliable alternative method for R 0 Har Rh :33 typing.
Jizhi Wen - One of the best experts on this subject based on the ideXlab platform.
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a variant rhag protein encoded by the rhag 572a allele causes serological weak d expression while maintaining normal rhce phenotypes
Transfusion, 2019Co-Authors: Jizhi Wen, O. J. H. M. Verhagen, Shuangshuang Jia, Qian-ni Liang, Zhen Wang, Ling Wei, Hong Luo, Guangping Luo, Gestur Vidarsson, Emile Van Den AkkerAbstract:BACKGROUND: The molecular events resulting in a weak D phenotype include missense mutations, in-frame insertion, or deletion mutations of the RHD Gene and hybrid RHD-CE-D hybrid alleles. Mutations in Genes encoding the proteins that are required for proper membrane expression of Rh proteins, such as RhAG and ankyrin 1, can lead to absent or weakened expression of Rh antigens. STUDY DESIGN AND METHODS: Blood sample from a Chinese blood donor with a serological weak D phenotype was collected. RhAG antigen expression, RHD, and RhCE phenotypes were determined. Analysis of the RHD and RHCE genotypes by RH multiplex ligation-dependent probe amplification (MLPA), Sanger sequencing of the RHD exons, and next-Generation sequencing (NGS) of the RHAG and ANK1 exons were performed. Expression studies in vitro were conducted by lentivirally transducing the mutant RHAG*572A or wild-type RHAG, in combination with either RHD or RHCE constructs, into HEK 293 T cells. The expression of RhAG, RHD, and RhCE antigens was analyzed by flow cytometry. RESULTS: Serological weak D and normal C + c-E–e + phenotypes, normal CCDDee genotype determined by RH-MLPA, and normal sequence of the RHD Gene by Sanger sequencing were demonstrated. A homozygous variant (c.572G > A, p.Arg191Gln) of the RHAG Gene was revealed by NGS analysis. Normal RhAG, weak RHD, and normal RhCE antigens were detected in cells transduced with the mutant RHAG*572A, the mutant RHAG*572A and RHD, and the mutant RHAG*572A and RHCE constructs, respectively. CONCLUSION: The homozygous presence of RHAG*572A allele results in weak D expression. It does not affect RhCE expression.
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A variant RhAG protein encoded by the RHAG*572A allele causes serological weak D expression while maintaining normal RhCE phenotypes.
Transfusion, 2018Co-Authors: Jizhi Wen, O. J. H. M. Verhagen, Shuangshuang Jia, Qian-ni Liang, Zhen Wang, Ling Wei, Hong Luo, Guangping Luo, Gestur Vidarsson, Emile Van Den AkkerAbstract:BACKGROUND: The molecular events resulting in a weak D phenotype include missense mutations, in-frame insertion, or deletion mutations of the RHD Gene and hybrid RHD-CE-D hybrid alleles. Mutations in Genes encoding the proteins that are required for proper membrane expression of Rh proteins, such as RhAG and ankyrin 1, can lead to absent or weakened expression of Rh antigens. STUDY DESIGN AND METHODS: Blood sample from a Chinese blood donor with a serological weak D phenotype was collected. RhAG antigen expression, RHD, and RhCE phenotypes were determined. Analysis of the RHD and RHCE genotypes by RH multiplex ligation-dependent probe amplification (MLPA), Sanger sequencing of the RHD exons, and next-Generation sequencing (NGS) of the RHAG and ANK1 exons were performed. Expression studies in vitro were conducted by lentivirally transducing the mutant RHAG*572A or wild-type RHAG, in combination with either RHD or RHCE constructs, into HEK 293 T cells. The expression of RhAG, RHD, and RhCE antigens was analyzed by flow cytometry. RESULTS: Serological weak D and normal C + c-E–e + phenotypes, normal CCDDee genotype determined by RH-MLPA, and normal sequence of the RHD Gene by Sanger sequencing were demonstrated. A homozygous variant (c.572G > A, p.Arg191Gln) of the RHAG Gene was revealed by NGS analysis. Normal RhAG, weak RHD, and normal RhCE antigens were detected in cells transduced with the mutant RHAG*572A, the mutant RHAG*572A and RHD, and the mutant RHAG*572A and RHCE constructs, respectively. CONCLUSION: The homozygous presence of RHAG*572A allele results in weak D expression. It does not affect RhCE expression.
Gestur Vidarsson - One of the best experts on this subject based on the ideXlab platform.
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a variant rhag protein encoded by the rhag 572a allele causes serological weak d expression while maintaining normal rhce phenotypes
Transfusion, 2019Co-Authors: Jizhi Wen, O. J. H. M. Verhagen, Shuangshuang Jia, Qian-ni Liang, Zhen Wang, Ling Wei, Hong Luo, Guangping Luo, Gestur Vidarsson, Emile Van Den AkkerAbstract:BACKGROUND: The molecular events resulting in a weak D phenotype include missense mutations, in-frame insertion, or deletion mutations of the RHD Gene and hybrid RHD-CE-D hybrid alleles. Mutations in Genes encoding the proteins that are required for proper membrane expression of Rh proteins, such as RhAG and ankyrin 1, can lead to absent or weakened expression of Rh antigens. STUDY DESIGN AND METHODS: Blood sample from a Chinese blood donor with a serological weak D phenotype was collected. RhAG antigen expression, RHD, and RhCE phenotypes were determined. Analysis of the RHD and RHCE genotypes by RH multiplex ligation-dependent probe amplification (MLPA), Sanger sequencing of the RHD exons, and next-Generation sequencing (NGS) of the RHAG and ANK1 exons were performed. Expression studies in vitro were conducted by lentivirally transducing the mutant RHAG*572A or wild-type RHAG, in combination with either RHD or RHCE constructs, into HEK 293 T cells. The expression of RhAG, RHD, and RhCE antigens was analyzed by flow cytometry. RESULTS: Serological weak D and normal C + c-E–e + phenotypes, normal CCDDee genotype determined by RH-MLPA, and normal sequence of the RHD Gene by Sanger sequencing were demonstrated. A homozygous variant (c.572G > A, p.Arg191Gln) of the RHAG Gene was revealed by NGS analysis. Normal RhAG, weak RHD, and normal RhCE antigens were detected in cells transduced with the mutant RHAG*572A, the mutant RHAG*572A and RHD, and the mutant RHAG*572A and RHCE constructs, respectively. CONCLUSION: The homozygous presence of RHAG*572A allele results in weak D expression. It does not affect RhCE expression.
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A variant RhAG protein encoded by the RHAG*572A allele causes serological weak D expression while maintaining normal RhCE phenotypes.
Transfusion, 2018Co-Authors: Jizhi Wen, O. J. H. M. Verhagen, Shuangshuang Jia, Qian-ni Liang, Zhen Wang, Ling Wei, Hong Luo, Guangping Luo, Gestur Vidarsson, Emile Van Den AkkerAbstract:BACKGROUND: The molecular events resulting in a weak D phenotype include missense mutations, in-frame insertion, or deletion mutations of the RHD Gene and hybrid RHD-CE-D hybrid alleles. Mutations in Genes encoding the proteins that are required for proper membrane expression of Rh proteins, such as RhAG and ankyrin 1, can lead to absent or weakened expression of Rh antigens. STUDY DESIGN AND METHODS: Blood sample from a Chinese blood donor with a serological weak D phenotype was collected. RhAG antigen expression, RHD, and RhCE phenotypes were determined. Analysis of the RHD and RHCE genotypes by RH multiplex ligation-dependent probe amplification (MLPA), Sanger sequencing of the RHD exons, and next-Generation sequencing (NGS) of the RHAG and ANK1 exons were performed. Expression studies in vitro were conducted by lentivirally transducing the mutant RHAG*572A or wild-type RHAG, in combination with either RHD or RHCE constructs, into HEK 293 T cells. The expression of RhAG, RHD, and RhCE antigens was analyzed by flow cytometry. RESULTS: Serological weak D and normal C + c-E–e + phenotypes, normal CCDDee genotype determined by RH-MLPA, and normal sequence of the RHD Gene by Sanger sequencing were demonstrated. A homozygous variant (c.572G > A, p.Arg191Gln) of the RHAG Gene was revealed by NGS analysis. Normal RhAG, weak RHD, and normal RhCE antigens were detected in cells transduced with the mutant RHAG*572A, the mutant RHAG*572A and RHD, and the mutant RHAG*572A and RHCE constructs, respectively. CONCLUSION: The homozygous presence of RHAG*572A allele results in weak D expression. It does not affect RhCE expression.