The Gerbich blood group system: a review

Walker, Phyllis S.; Reid, Marion E.

doi:10.21307/immunohematology-2019-204

Cited by 30 publications

(12 citation statements)

References 51 publications

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“…This analysis uncovered regulation of surface markers (e.g. GATA1- GYPC 42 , KLF1- CD47 43 in Erythroid cells, MYCN- CD164 44 in Progenitors, etc) and others (e.g. GFI1B- E2F2 in Erythroid cells 33,45 ).…”

Section: Resultsmentioning

confidence: 96%

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Dictys: dynamic gene regulatory network dissects developmental continuum with single-cell multi-omics

Wang

Trasanidis

et al. 2022

Preprint

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Gene regulatory networks (GRNs) are key determinants of cell function and identity and are dynamically rewired during development and disease. Despite decades of advancement, challenges remain in GRN inference: dynamic rewiring, causal inference, feedback-loop modeling, and context specificity. To address them, we develop Dictys, a dynamic GRN inference and analysis method which leverages multi-omic single-cell assays of chromatin accessibility and gene expression, context specific transcription factor (TF) footprinting, stochastic process network, and efficient probabilistic modeling of scRNA-seq read counts. Dictys improves GRN reconstruction accuracy and reproducibility and enables the inference and comparative analysis of context specific and dynamic GRNs across developmental contexts. Dictys' network analyses recover unique insights in human blood and mouse skin development with cell-type specific and dynamic GRNs. Its dynamic network visualizations enable time-resolved discovery and investigation of developmental driver TFs and their regulated targets. Dictys is available as a free, open source, and user-friendly Python package.

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Section: Resultsmentioning

confidence: 96%

“…For each TF, Dictys could also uncover its cell-type specific regulatory program and mechanistic insights at gene and locus levels. In Erythroid cells, GATA1 was found to regulate erythroid-specific genes, such as the surface marker GYPC 42 and the nuclear export protein XPO7 52 ( Fig. 2f, Supplementary Table 2, Methods ).…”

Section: Resultsmentioning

confidence: 99%

Dictys: dynamic gene regulatory network dissects developmental continuum with single-cell multi-omics

Wang

Trasanidis

et al. 2022

Preprint

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“…Glycophorin C (GPC) and Glycophorin D (GPD) and are receptors for P. falciparum 1 and also carry the antigens of the Gerbich blood group system (ISBT 020). 2 GPC and GPD both are encoded by a single gene, GYPC (or GE) 3 and discriminate in alternative translation initiation sites within exon 1 and 2, resulting in a Abbreviations: BLAST, Basic Local Alignment Search Tool; DAT, direct antiglobulin test; DNA, deoxyribonucleic acid; DTT, dithiothreitol; GE, Gerbich blood group system, alternative gene name GYPC; GPC, Glycophorin C; GPD, Glycophorin D; HDFN, hemolytic disease of the newborn; IAT, indirect antiglobulin test; LISS, low Ionic Strength Saline; NCBI, National Center for Biotechnology Information; NGS, next generation sequencing; P. falciparum, Plasmodium falciparum; RBC, red blood cell; UTR, untranslated region.…”

Section: Introductionmentioning

confidence: 99%

“…4 GPC carries the Ge3 and Ge4 antigens while GPD hosts Ge2 and Ge3. 1 A complete deletion of GYPC exon 2 (allele name GE*01.-02) results in the GE:-2, 3, 4 or Yus type, whereas an exon 3 deletion (allele name GE*01.-03) induces the GE:-2,-3,4 or Gerbich type. [5][6][7] The Leach type is characterized by a truncated protein as a consequence of an exon 3 and 4 deletion associated with a gene silencing (GE*01 N.01) 8 or a missense mutation in exon 3 (GE*01N.02).…”

Section: Introductionmentioning

confidence: 99%

Compound heterozygosity induces a rare Gerbich‐negative phenotype in an immunized blood donor

Petermann,

Mayer,

Carbol

et al. 2024

Transfusion

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BackgroundAntibodies to Gerbich blood group antigens are exceedingly rare and can cause moderate transfusion reactions. Several deletional variants of the GE‐gene, that harbors long sequence repeats, enable alloimmunization and formation of naturally occurring antibodies.Subject and MethodsA female blood donor and soldier of the German Army without history of pregnancy or transfusion showed an antibody reactive with all test cells except for GE:‐2‐3 RBC. Thus, anti‐Ge2 was suspected. Molecular analysis including fragment length specific PCR, Sanger sequencing and NGS should reveal the molecular background of the deficiency. Segregation of the variant alleles should be demonstrated by family analysis.ResultsCompound heterozygosity for GYPC exon 2 (GE*01.‐02) and exon 3 (GE*01.‐03) deletion was detected in the donor and her sister. The mother had one exon 3 amplicon of reduced length, while the father heterozygously exhibited a truncated GYPC exon 2. NGS clearly demonstrated reduced coverages within the deletional fragments within each family member. The donor and her sister showed the complete absence of a 640 bp fragment.Discussion and ConclusionRare GE deletion variants can induce naturally occurring anti‐Ge2 in Caucasians. Because of an enhanced risk of injury as soldier autologous RBC of the donor were cryopreserved. The donor and her sibling can give blood for each other because of identical ABO, Rh, and K antigen blood types.

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“…The Gerbich (GE) blood system (ISBT 020) consists of 13 antigens carried on single‐pass type I membrane glycoproteins, called glycophorin C (GPC) and glycophorin D (GPD) [1]. Rare Gerbich phenotypes such as Yus (GE:−2,3,4), Gerbich (GE:−2,−3,4) and Leach (GE:−2,−3,−4) are related to the development of antibodies against high‐prevalence antigens [2]. As there are no commercial antisera for typing Gerbich antigens, antibody identification depends on the availability of rare red cells and sera with antibodies from individuals previously alloimmunized [3].…”

Section: Introductionmentioning

confidence: 99%

Genetic diversity of Gerbich alleles in Brazilians reveals an unexpected prevalence of the GE:−2,−3,4 phenotype

Arnoni

Silva

et al. 2023

Vox Sanguinis

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Background and ObjectivesGerbich (GE) blood group system carries high‐frequency antigens and the absence of them leads to rare phenotypes: GE:−2,3,4, GE:−2,−3,4 and GE:−2,−3,−4. Their serological differentiation is limited and misclassification of Gerbich phenotypes may occur, but this can be avoided by molecular characterization. This study aimed to characterize the molecular background responsible for rare Gerbich phenotypes in Brazilian population.Materials and MethodsWe selected eight samples from patients with anti‐Ge, six from their relatives and nine samples with normal expression of Gerbich antigens. Serological tests were performed in gel and red blood cells (RBCs) were tested with anti‐Ge2 and anti‐Ge3. Monocyte monolayer assay (MMA) was performed. Molecular investigation was performed with allele‐specific polymerase chain reaction and DNA sequencing.ResultsPatient plasma samples reacted with all commercial RBCs. Patient RBCs showed negative results with anti‐Ge2 and anti‐Ge3. Using MMA two of eight antibodies were clinically significant. Exon 3 was not amplified in any of the patient samples and in two samples from relatives, suggesting the presence of GE*01.‐03/GE*01.‐03. By sequencing, we identified the genetic variability that interferes with the definition of deletion breakpoints, thus two options of genetic structure were suggested to be responsible for the GE:−2,−3,4 phenotype.ConclusionThis study showed for the first time the genetic diversity of GYPC alleles for carriers of Gerbich‐negative phenotypes in a Brazilian population and showed an unexpected prevalence of the GE:−2,−3,4 phenotype. It also demonstrated the importance of using molecular tools to correctly classify Gerbich phenotypes for selection of variants in antigen‐matched transfusions.

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The Gerbich blood group system: a review

Cited by 30 publications

References 51 publications

Dictys: dynamic gene regulatory network dissects developmental continuum with single-cell multi-omics

Dictys: dynamic gene regulatory network dissects developmental continuum with single-cell multi-omics

Compound heterozygosity induces a rare Gerbich‐negative phenotype in an immunized blood donor

Genetic diversity of Gerbich alleles in Brazilians reveals an unexpected prevalence of the GE:−2,−3,4 phenotype

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