ArticleExperimental hematology2009
Silencing of genes required for glycosylphosphatidylinositol anchor biosynthesis in Burkitt lymphoma.
Article in Experimental hematology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 20 citations in OpenAlex.
- An epigenetic GPI anchor defect impairs TLR4 signaling in the B cell transdifferentiation model for primary human monocytes BLaER1.Scientific reports · 2021Article
- Development of an in vitro PIG-A gene mutation assay in human cells.Mutagenesis · 2017Article
- Glycosylphosphatidylinositol Anchor Modification Machinery Deficiency Is Responsible for the Formation of Pro-Prion Protein (PrP) in BxPC-3 Protein and Increases Cancer Cell Motility.The Journal of biological chemistry · 2016Article
- Both PIGA and PIGL mutations cause GPI-a deficient isolates in the Tk6 cell line.Environmental and molecular mutagenesis · 2015Article
- Generation of glycosylphosphatidylinositol anchor protein-deficient blood cells from human induced pluripotent stem cells.Stem cells translational medicine · 2013Article
- Leukemic blasts with the paroxysmal nocturnal hemoglobinuria phenotype in children with acute lymphoblastic leukemia.The American journal of pathology · 2012Article
- The small population of PIG-A mutant cells in myelodysplastic syndromes do not arise from multipotent hematopoietic stem cells.Haematologica · 2012Article
- Paroxysmal nocturnal hemoglobinuria from bench to bedside.Clinical and translational science · 2011Review
- Global gene expression profiling of a population exposed to a range of benzene levels.Environmental health perspectives · 2011Article
- A quantitative analysis of genomic instability in lymphoid and plasma cell neoplasms based on the PIG-A gene.Mutation research · 2010Article
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Authors and funding
9 authors at 4 institutions in 2 countries.
Funding
Abstract
objectiveTo investigate the mechanism of glycosylphosphatidylinositol (GPI) anchor deficiency in Burkitt lymphoma cell lines.
methodsWe identified a large GPI anchor protein deficient population in three different Burkitt lymphoma cell lines through proaerolysin treatment of the cells and flow cytometry analysis using a proaerolysin variant (FLAER). The mechanism of GPI anchor protein deficiency was studied by DNA gene sequencing, a cell-free assay to investigate the GPI anchor biosynthetic pathway, microarray analysis, and quantitative real-time polymerase chain reaction.
resultsBurkitt lymphoma cell lines harbor large populations of FLAER(neg) cells, which are resistant to proaerolysin. In all three cell lines, silencing of a gene involved in an early step in GPI-anchor biosynthesis was responsible for the lack of GPI-anchored proteins on the cell surface. Quantitative polymerase chain reaction and microarray analysis demonstrate that the level of mRNA for PIGL and PIGY is lower in the FLAER(neg) Ramos cells and that mRNA levels of PIGY are reduced in the Akata and Daudi cells. Hypermethylation of these genes was associated with the low levels of mRNA and treatment of the cells with 5-aza-2' deoxycytidine restored cell surface GPI-anchored proteins to the FLAER(neg) cells.
conclusionGPI-anchored protein deficiency in Burkitt lymphoma cells is not due to a genetic mutation (e.g., PIGA); rather, the lack of GPI-anchored proteins results from transcriptional silencing of PIGL and PIGY.
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