ArticleBlood2016
CRISPR/Cas9-mediated conversion of human platelet alloantigen allotypes.
Article in Blood, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
24 citing papers in PubMed, 47 citations in OpenAlex.
- The Use of Bioengineered Induced Pluripotent Stem Cell-Derived Human Megakaryocytes to Diagnose and Characterize Platelet Allo-, Auto-, and Iso-Immune Disorders.Methods in molecular biology (Clifton, N.J.) · 2026Article
- The Immunology of Transfusion Medicine: Past, Present, and Future.Methods in molecular biology (Clifton, N.J.) · 2026Review
- Article
- Megakaryocyte-induced contraction of plasma clots: cellular mechanisms and structural mechanobiology.Blood · 2024Article
- Article
- Toward in Vitro Production of Platelet from Induced Pluripotent Stem Cells.Stem cell reviews and reports · 2022Review
- Conditional CRISPR-mediated deletion of Lyn kinase enhances differentiation and function of iPSC-derived megakaryocytes.Journal of thrombosis and haemostasis : JTH · 2022Article
- Generation and manipulation of human iPSC-derived platelets.Cellular and molecular life sciences : CMLS · 2021Review
- Platelet Proteomes, Pathways, and Phenotypes as Informants of Vascular Wellness and Disease.Arteriosclerosis, thrombosis, and vascular biology · 2021Review
- CRISPR/Cas9 mediated knock-out of VPREB1 gene induces a cytotoxic effect in myeloma cells.PloS one · 2021Article
- Lung development, repair and cancer: A study on the role of MMP20 gene in adenocarcinoma.PloS one · 2021Article
- Profiling the Genetic and Molecular Characteristics of Glanzmann Thrombasthenia: Can It Guide Current and Future Therapies?Journal of blood medicine · 2021Review
- [Cultured platelets].Bulletin de l'Academie nationale de medecine · 2020Review
- [Novel platelet pharming using human induced pluripotent stem cells].Bulletin de l'Academie nationale de medecine · 2020Review
- iPSC-Derived Platelets Depleted of HLA Class I Are Inert to Anti-HLA Class I and Natural Killer Cell Immunity.Stem cell reports · 2020Article
- Platelet alloantibody detection: moving ahead.Blood · 2019Article
- Anti-apoptoticHaematologica · 2019Article
- Genome editing: A perspective on the application of CRISPR/Cas9 to study human diseases (Review).International journal of molecular medicine · 2019Review
- Rare Opportunities: CRISPR/Cas-Based Therapy Development for Rare Genetic Diseases.Molecular diagnosis & therapy · 2019Review
- On the Way toFrontiers in medicine · 2018Review
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Authors and funding
8 authors at 4 institutions in 1 country.
Funding
Abstract
Human platelet alloantigens (HPAs) reside on functionally important platelet membrane glycoproteins and are caused by single nucleotide polymorphisms in the genes that encode them. Antibodies that form against HPAs are responsible for several clinically important alloimmune bleeding disorders, including fetal and neonatal alloimmune thrombocytopenia and posttransfusion purpura. The HPA-1a/HPA-1b alloantigen system, also known as the Pl(A1)/Pl(A2) polymorphism, is the most frequently implicated HPA among whites, and a single Leu33Pro amino acid polymorphism within the integrin β3 subunit is responsible for generating the HPA-1a/HPA-1b alloantigenic epitopes. HPA-1b/b platelets, like those bearing other low-frequency platelet-specific alloantigens, are relatively rare in the population and difficult to obtain for purposes of transfusion therapy and diagnostic testing. We used CRISPR/Cas9 (clustered regularly interspaced short palindromic repeats/CRISPR associated protein 9) gene-editing technology to transform Leu33 (+) megakaryocytelike DAMI cells and induced pluripotent stem cells (iPSCs) to the Pro33 allotype. CD41(+) megakaryocyte progenitors derived from these cells expressed the HPA-1b (Pl(A2)) alloantigenic epitope, as reported by diagnostic NciI restriction enzyme digestion, DNA sequencing, and western blot analysis using HPA-1b-specific human maternal alloantisera. Application of CRISPR/Cas9 technology to genetically edit this and other clinically-important HPAs holds great potential for production of designer platelets for diagnostic, investigative, and, ultimately, therapeutic use.
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What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.