ArticleThe Journal of experimental medicine2001
FES-Cre targets phosphatidylinositol glycan class A (PIGA) inactivation to hematopoietic stem cells in the bone marrow.
Article in The Journal of experimental medicine, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 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
22 citing papers in PubMed, 63 citations in OpenAlex.
- A Pig-a conditional knock-out mice model mediated by Vav-iCre: stable GPI-deficient and mild hemolysis.Experimental hematology & oncology · 2022Article
- Inhibition of the DNA damage response phosphatase PPM1D reprograms neutrophils to enhance anti-tumor immune responses.Nature communications · 2021Article
- Insights Into the Emergence of Paroxysmal Nocturnal Hemoglobinuria.Frontiers in immunology · 2021Review
- The Glycosylphosphatidylinositol biosynthesis pathway in human diseases.Orphanet journal of rare diseases · 2020Review
- Analyzing clinical and genetic characteristics of a cohort with multiple congenital anomalies-hypotonia-seizures syndrome (MCAHS).Orphanet journal of rare diseases · 2020Article
- Analysis ofExperimental hematology & oncology · 2019Article
- The mutational landscape of paroxysmal nocturnal hemoglobinuria revealed: new insights into clonal dominance.The Journal of clinical investigation · 2014Article
- Anti-Complement Treatment in Paroxysmal Nocturnal Hemoglobinuria: Where we Stand and Where we are Going.Translational medicine @ UniSa · 2014Article
- The rate of spontaneous mutations in human myeloid cells.Mutation research · 2013Article
- Leukemic blasts with the paroxysmal nocturnal hemoglobinuria phenotype in children with acute lymphoblastic leukemia.The American journal of pathology · 2012Article
- The phenotype of a germline mutation in PIGA: the gene somatically mutated in paroxysmal nocturnal hemoglobinuria.American journal of human genetics · 2012Article
- Transcription intermediary factor 1γ is a tumor suppressor in mouse and human chronic myelomonocytic leukemia.The Journal of clinical investigation · 2011Article
- Accelerated hematopoietic stem cell aging in a mouse model of dyskeratosis congenita responds to antioxidant treatment.Aging cell · 2011Article
- A quantitative analysis of genomic instability in lymphoid and plasma cell neoplasms based on the PIG-A gene.Mutation research · 2010Article
- Phenotypic and functional characterization of a mouse model of targeted Pig-a deletion in hematopoietic cells.Haematologica · 2010Article
- Convergent extension movements in growth plate chondrocytes require gpi-anchored cell surface proteins.Development (Cambridge, England) · 2009Article
- Neutral evolution in paroxysmal nocturnal hemoglobinuria.Proceedings of the National Academy of Sciences of the United States of America · 2008Article
- Article
- Paroxysmal nocturnal hemoglobinuria: pathophysiology, natural history and treatment options in the era of biological agents.Biologics : targets & therapy · 2008Article
- Trophoblast differentiation defect in human embryonic stem cells lacking PIG-A and GPI-anchored cell-surface proteins.Cell stem cell · 2008Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 3 institutions in 2 countries.
Funding
Abstract
A somatic mutation in the X-linked phosphatidylinositol glycan class A (PIGA) gene causes the loss of glycosyl phosphatidylinositol (GPI)-linked proteins on blood cells from patients with paroxysmal nocturnal hemoglobinuria. Because all blood cell lineages may be affected it is thought that the mutation occurs in a hematopoietic stem cell. In transgenic mice, germline transmission of an inactive Piga gene is embryonic lethal. To inactivate the murine Piga gene in early hematopoiesis we therefore chose conditional gene inactivation using the Cre/loxP system. We expressed Cre recombinase under the transcription regulatory sequences of the human c-fes gene. FES-Cre inactivated PIGA in hematopoietic cells of mice carrying a floxed Piga allele (LF mice). PIGA(-) cells were found in all hematopoietic lineages of definitive but not primitive hematopoiesis. Their proportions were low in newborn mice but subsequently increased continuously to produce for the first time mice that have almost exclusively PIGA(-) blood cells. The loss of GPI-linked proteins occurred mainly in c-kit(+)CD34(+)Lin(-) progenitor cells before the CFU-GEMM stage. Using bone marrow reconstitution experiments with purified PIGA(-) cells we demonstrate that LF mice have long-term bone marrow repopulating cells that lack GPI-linked proteins, indicating that recombination of the floxed Piga allele occurs in the hematopoietic stem cell.
Indexed as
Identifiers
What Socratic 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 Socratic graph.