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Disease on EC 2.4.1.198 - phosphatidylinositol N-acetylglucosaminyltransferase

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DISEASE
TITLE OF PUBLICATION
LINK TO PUBMED
Anemia
Paroxysmal nocturnal hemoglobinuria: new insights from murine Pig-a-deficient hematopoiesis.
Anemia, Aplastic
A cohort study of the nature of paroxysmal nocturnal hemoglobinuria clones and PIG-A mutations in patients with aplastic anemia.
Analysis of PIG-A gene in a patient who developed reciprocal translocation of chromosome 12 and paroxysmal nocturnal hemoglobinuria during follow-up of aplastic anemia.
CD59-deficient blood cells and PIG-A gene abnormalities in Japanese patients with aplastic anaemia.
Circulating PIG-A mutant T lymphocytes in healthy adults and patients with bone marrow failure syndromes.
Could aplastic anaemia be considered a pre-pre-leukaemic disorder?
Genetic defects underlying paroxysmal nocturnal hemoglobinuria that arises out of aplastic anemia.
Genotypic, immunophenotypic and clinical features of Thai patients with paroxysmal nocturnal haemoglobinuria.
High frequency of several PIG-A mutations in patients with aplastic anemia and myelodysplastic syndrome.
Pathogenesis of selective expansion of PNH clones.
PIG-A gene mutations in four Taiwanese patients with paroxysmal nocturnal haemoglobinuria following aplastic anaemia.
PIG-A mutations in paroxysmal nocturnal hemoglobinuria and in normal hematopoiesis.
The small population of PIG-A mutant cells in myelodysplastic syndromes do not arise from multipotent hematopoietic stem cells.
[Immune pathophysiology of refractory anemias]
[Paroxysmal nocturnal hemoglobinuria (PNH)]
Anemia, Hemolytic
Cloning and characterization of the mouse PIG-A gene.
Mutations in the PIG-A gene causing paroxysmal nocturnal hemoglobinuria are mainly of the frameshift type.
New insights into paroxysmal nocturnal hemoglobinuria.
Paroxysmal nocturnal hemoglobinuria and liver transplantation, a new paradigm.
Paroxysmal nocturnal hemoglobinuria: When delay in diagnosis and long therapy occurs.
Bone Marrow Failure Disorders
Circulating PIG-A mutant T lymphocytes in healthy adults and patients with bone marrow failure syndromes.
Development of paroxysmal nocturnal hemoglobinuria in CALR-positive myeloproliferative neoplasm.
Differential apoptosis and Fas expression on GPI-negative and GPI-positive stem cells: a mechanism for the evolution of paroxysmal nocturnal haemoglobinuria.
Murine models of paroxysmal nocturnal hemoglobinuria.
Paroxysmal nocturnal hemoglobinuria: When delay in diagnosis and long therapy occurs.
Breast Neoplasms
Evaluation of PIG-A-mutated granulocytes and ex-vivo binucleated micronucleated lymphocytes frequencies after breast cancer radiotherapy in humans.
Cleft Palate
Developmental abnormalities of glycosylphosphatidylinositol-anchor-deficient embryos revealed by Cre/loxP system.
COVID-19
COVID-19 infection presenting as paroxysmal nocturnal hemoglobinuria.
Down Syndrome
A novel gene, DSCR5, from the distal Down syndrome critical region on chromosome 21q22.2.
Down syndrome critical region protein 5 regulates membrane localization of Wnt receptors, Dishevelled stability and convergent extension in vertebrate embryos.
Dysregulation of growth factor receptor-bound protein 2 and fascin in hippocampus of mice polytransgenic for chromosome 21 structures.
Isolation of two novel genes, DSCR5 and DSCR6, from Down syndrome critical region on human chromosome 21q22.2.
Genetic Diseases, Inborn
The in vivo Pig-a gene mutation assay, a potential tool for regulatory safety assessment.
Hemoglobinuria
A cohort study of the nature of paroxysmal nocturnal hemoglobinuria clones and PIG-A mutations in patients with aplastic anemia.
A knock-out model of paroxysmal nocturnal hemoglobinuria: Pig-a(-) hematopoiesis is reconstituted following intercellular transfer of GPI-anchored proteins.
A patient with paroxysmal nocturnal hemoglobinuria bearing four independent PIG-A mutant clones.
A systematic analysis of bone marrow cells by flow cytometry defines a specific phenotypic profile beyond GPI deficiency in paroxysmal nocturnal hemoglobinuria.
Abnormalities of PIG-A transcripts in granulocytes from patients with paroxysmal nocturnal hemoglobinuria.
Acute myelogenous leukemia with PIG-A gene mutation evolved from aplastic anemia-paroxysmal nocturnal hemoglobinuria syndrome.
Analysis of PIG-A gene in a patient who developed reciprocal translocation of chromosome 12 and paroxysmal nocturnal hemoglobinuria during follow-up of aplastic anemia.
Association of HLA haplotypes with paroxysmal nocturnal hemoglobinuria.
Both paroxysmal nocturnal hemoglobinuria (PNH) type II cells and PNH type III cells can arise from different point mutations involving the same codon of the PIG-A gene.
Cancer as an evolutionary process at the cell level: an epidemiological perspective.
CD52/GPI- T-Cells Are Enriched for Alloreactive Specificity and Predict Acute Graft-Versus-Host-Disease After Stem Cell Transplantation.
Characterization of alternatively spliced PIG-A transcripts in normal and paroxysmal nocturnal hemoglobinuria cells.
Characterization of genomic PIG-A gene: a gene for glycosylphosphatidylinositol-anchor biosynthesis and paroxysmal nocturnal hemoglobinuria.
Circulating PIG-A mutant T lymphocytes in healthy adults and patients with bone marrow failure syndromes.
Clinical paroxysmal nocturnal hemoglobinuria is the result of expansion of glycosyl-phosphatidyl-inositol-anchored protein-deficient clone in the condition of deficient hematopoiesis.
Clonal populations of hematopoietic cells with paroxysmal nocturnal hemoglobinuria genotype and phenotype are present in normal individuals.
Cloning and characterization of the mouse PIG-A gene.
Consensus statement for diagnosis and treatment of paroxysmal nocturnal haemoglobinuria.
Decreased susceptibility of leukemic cells with PIG-A mutation to natural killer cells in vitro.
Deficiency of the GPI anchor caused by a somatic mutation of the PIG-A gene in paroxysmal nocturnal hemoglobinuria.
Deletions of Xp22.2 including PIG-A locus lead to paroxysmal nocturnal hemoglobinuria.
Detection of somatic mutations of the PIG-A gene in Brazilian patients with paroxysmal nocturnal hemoglobinuria.
Development of paroxysmal nocturnal hemoglobinuria in CALR-positive myeloproliferative neoplasm.
Different roles of glycosylphosphatidylinositol in various hematopoietic cells as revealed by a mouse model of paroxysmal nocturnal hemoglobinuria.
Eculizumab in the management of paroxysmal nocturnal hemoglobinuria: patient selection and special considerations.
Effect of eculizumab on hemolysis and transfusion requirements in patients with paroxysmal nocturnal hemoglobinuria.
Frequent detection of T cells with mutations of the hypoxanthine-guanine phosphoribosyl transferase gene in patients with paroxysmal nocturnal hemoglobinuria.
Function and malfunction of hematopoietic stem cells in primary bone marrow failure syndromes.
Generation of glycosylphosphatidylinositol anchor protein-deficient blood cells from human induced pluripotent stem cells.
Genetic and environmental effects in paroxysmal nocturnal hemoglobinuria: this little PIG-A goes "Why? Why? Why?".
Genetic instability and the etiology of somatic PIG-A mutations in paroxysmal nocturnal hemoglobinuria.
Glycosylphosphatidylinositol-anchored protein deficiency confers resistance to apoptosis in PNH.
GPI-anchor synthesis in mammalian cells: genes, their products, and a deficiency.
Hemoglobinuria misidentified as hematuria: review of discolored urine and paroxysmal nocturnal hemoglobinuria.
Hemolytic anemia.
Heterogeneous PIG-A mutations in different cell lineages in paroxysmal nocturnal hemoglobinuria.
High frequency of several PIG-A mutations in patients with aplastic anemia and myelodysplastic syndrome.
How do PIG-A mutant paroxysmal nocturnal hemoglobinuria stem cells achieve clonal dominance?
Identification of a PIG-A related processed gene on chromosome 12.
Immune pathogenesis of paroxysmal nocturnal hemoglobinuria.
Impaired hematopoiesis in paroxysmal nocturnal hemoglobinuria/aplastic anemia is not associated with a selective proliferative defect in the glycosylphosphatidylinositol-anchored protein-deficient clone.
Increased resistance of PIG-A- bone marrow progenitors to tumor necrosis factor a and interferon gamma: possible implications for the in vivo dominance of paroxysmal nocturnal hemoglobinuria clones.
Laboratory studies for paroxysmal nocturnal hemoglobinuria, with emphasis on flow cytometry.
Leukemia arising out of paroxysmal nocturnal hemoglobinuria.
Long-term support of hematopoiesis by a single stem cell clone in patients with paroxysmal nocturnal hemoglobinuria.
Mean fluorescence intensity rate is a useful marker in the detection of paroxysmal nocturnal hemoglobinuria clones.
Molecular cloning of murine pig-a, a gene for GPI-anchor biosynthesis, and demonstration of interspecies conservation of its structure, function, and genetic locus.
Murine embryonic stem cells without pig-a gene activity are competent for hematopoiesis with the PNH phenotype but not for clonal expansion.
Mutations in the PIG-A gene causing paroxysmal nocturnal hemoglobinuria are mainly of the frameshift type.
New insights into paroxysmal nocturnal hemoglobinuria.
New somatic mutation in the PIG-A gene emerges at relapse of paroxysmal nocturnal hemoglobinuria.
On the origin of multiple mutant clones in paroxysmal nocturnal hemoglobinuria.
Paroxysmal nocturnal hemoglobinuria and liver transplantation, a new paradigm.
Paroxysmal nocturnal hemoglobinuria and myelodysplastic syndrome: a case report.
Paroxysmal nocturnal hemoglobinuria and the age of therapeutic complement inhibition.
Paroxysmal nocturnal hemoglobinuria: analysis of the effects of mutant PIG-A on gene expression.
Paroxysmal nocturnal hemoglobinuria: molecular pathogenesis and molecular therapeutic approaches.
Paroxysmal nocturnal hemoglobinuria: significant association with specific HLA-A, -B, -C, and -DR alleles in an Italian population.
Paroxysmal nocturnal hemoglobinuria: Test to monitor the action of eculizumab treatment.
Paroxysmal nocturnal hemoglobinuria: When delay in diagnosis and long therapy occurs.
Pathogenesis of selective expansion of PNH clones.
Phenotypes and phosphatidylinositol glycan-class A gene abnormalities during cell differentiation and maturation from precursor cells to mature granulocytes in patients with paroxysmal nocturnal hemoglobinuria.
PIG-A gene abnormalities in Thai patients with paroxysmal nocturnal hemoglobinuria.
PIG-A mutations in paroxysmal nocturnal hemoglobinuria and in normal hematopoiesis.
PIG-B, a membrane protein of the endoplasmic reticulum with a large lumenal domain, is involved in transferring the third mannose of the GPI anchor.
Postpartum thrombotic complication in a patient with paroxysmal nocturnal hemoglobinuria.
Proliferative capacity of single isolated CD34+ hematopoietic stem/progenitor cells in paroxysmal nocturnal hemoglobinuria.
Rare Hematological Disease of Paroxysmal Nocturnal Hemoglobinuria With Profound Implications for a Gastroenterologist: A Case Report and Literature Review.
Resistance to apoptosis caused by PIG-A gene mutations in paroxysmal nocturnal hemoglobinuria.
Response of paroxysmal nocturnal hemoglobinuria clone with aplastic anemia to rituximab.
Role of phosphatidylinositol-linked proteins in paroxysmal nocturnal hemoglobinuria pathogenesis.
Somatic mutation and clonal selection in the pathogenesis and in the control of paroxysmal nocturnal hemoglobinuria.
Somatic mutations and the hierarchy of hematopoiesis.
Somatic mutations of PIG-A in Thai patients with paroxysmal nocturnal hemoglobinuria.
Somatic mutations of the PIG-A gene found in Japanese patients with paroxysmal nocturnal hemoglobinuria.
Structural and functional analysis of the Pig-a protein that is mutated in paroxysmal nocturnal hemoglobinuria.
Successful unrelated donor bone marrow transplantation for paroxysmal nocturnal hemoglobinuria.
The distribution of PIG-A gene abnormalities in paroxysmal nocturnal hemoglobinuria granulocytes and cultured erythroblasts.
The mutation rate in PIG-A is normal in patients with paroxysmal nocturnal hemoglobinuria (PNH).
The Patterns of MHC Association in Aplastic and Non-aplastic Paroxysmal Nocturnal Hemoglobinuria.
The PIG-A gene somatic mutation responsible for paroxysmal nocturnal hemoglobinuria.
The PIG-A mutation and absence of glycosylphosphatidylinositol-linked proteins do not confer resistance to apoptosis in paroxysmal nocturnal hemoglobinuria.
The small population of PIG-A mutant cells in myelodysplastic syndromes do not arise from multipotent hematopoietic stem cells.
The spectrum of PIG-A gene mutations in aplastic anemia/paroxysmal nocturnal hemoglobinuria (AA/PNH): a high incidence of multiple mutations and evidence of a mutational hot spot.
The spectrum of somatic mutations in the PIG-A gene in paroxysmal nocturnal hemoglobinuria includes large deletions and small duplications.
The yeast spt14 gene is homologous to the human PIG-A gene and is required for GPI anchor synthesis.
[Eculizumab in paroxysmal nocturnal hemoglobinuria]
[Gene diagnosis of hemolytic anemia]
[Immune pathophysiology of refractory anemias]
[Mutations in the PIG-A gene lead to GPI-deficiency in paroxysmal nocturnal hemoglobinuria]
[Paroxysmal nocturnal hemoglobinuria--consequences of a missing anchor]
[Paroxysmal nocturnal hemoglobinuria.]
[PIG-A gene mutation and paroxysmal nocturnal hemoglobinuria]
[Somatic mutations of PIG-A gene in Chinese patients with paroxysmal nocturnal hemoglobinuria]
[Spontaneous recovery from pancytopenia in a young female patient with paroxysmal nocturnal hemoglobinuria(PNH): changes in the GPI-anchor expression on peripheral blood cells]
[The evaluation and comparative characteristic of detection of clone of paroxysmal nocturnal hemoglobinuria on reticulocytes using the technique of flow cytometry].
Hemoglobinuria, Paroxysmal
A cohort study of the nature of paroxysmal nocturnal hemoglobinuria clones and PIG-A mutations in patients with aplastic anemia.
A knock-out model of paroxysmal nocturnal hemoglobinuria: Pig-a(-) hematopoiesis is reconstituted following intercellular transfer of GPI-anchored proteins.
A patient with paroxysmal nocturnal hemoglobinuria bearing four independent PIG-A mutant clones.
A systematic analysis of bone marrow cells by flow cytometry defines a specific phenotypic profile beyond GPI deficiency in paroxysmal nocturnal hemoglobinuria.
Abnormalities of PIG-A transcripts in granulocytes from patients with paroxysmal nocturnal hemoglobinuria.
Analysis of PIG-A gene in a patient who developed reciprocal translocation of chromosome 12 and paroxysmal nocturnal hemoglobinuria during follow-up of aplastic anemia.
Association of HLA haplotypes with paroxysmal nocturnal hemoglobinuria.
Both paroxysmal nocturnal hemoglobinuria (PNH) type II cells and PNH type III cells can arise from different point mutations involving the same codon of the PIG-A gene.
Cancer as an evolutionary process at the cell level: an epidemiological perspective.
CD52/GPI- T-Cells Are Enriched for Alloreactive Specificity and Predict Acute Graft-Versus-Host-Disease After Stem Cell Transplantation.
Characterization of alternatively spliced PIG-A transcripts in normal and paroxysmal nocturnal hemoglobinuria cells.
Characterization of genomic PIG-A gene: a gene for glycosylphosphatidylinositol-anchor biosynthesis and paroxysmal nocturnal hemoglobinuria.
Circulating PIG-A mutant T lymphocytes in healthy adults and patients with bone marrow failure syndromes.
Clinical paroxysmal nocturnal hemoglobinuria is the result of expansion of glycosyl-phosphatidyl-inositol-anchored protein-deficient clone in the condition of deficient hematopoiesis.
Clonal populations of hematopoietic cells with paroxysmal nocturnal hemoglobinuria genotype and phenotype are present in normal individuals.
Cloning and characterization of the mouse PIG-A gene.
Consensus statement for diagnosis and treatment of paroxysmal nocturnal haemoglobinuria.
Decreased susceptibility of leukemic cells with PIG-A mutation to natural killer cells in vitro.
Deficiency of the GPI anchor caused by a somatic mutation of the PIG-A gene in paroxysmal nocturnal hemoglobinuria.
Deletions of Xp22.2 including PIG-A locus lead to paroxysmal nocturnal hemoglobinuria.
Detection of somatic mutations of the PIG-A gene in Brazilian patients with paroxysmal nocturnal hemoglobinuria.
Development of paroxysmal nocturnal hemoglobinuria in CALR-positive myeloproliferative neoplasm.
Different roles of glycosylphosphatidylinositol in various hematopoietic cells as revealed by a mouse model of paroxysmal nocturnal hemoglobinuria.
Eculizumab in the management of paroxysmal nocturnal hemoglobinuria: patient selection and special considerations.
Effect of eculizumab on hemolysis and transfusion requirements in patients with paroxysmal nocturnal hemoglobinuria.
Frequent detection of T cells with mutations of the hypoxanthine-guanine phosphoribosyl transferase gene in patients with paroxysmal nocturnal hemoglobinuria.
Function and malfunction of hematopoietic stem cells in primary bone marrow failure syndromes.
Generation of glycosylphosphatidylinositol anchor protein-deficient blood cells from human induced pluripotent stem cells.
Genetic and environmental effects in paroxysmal nocturnal hemoglobinuria: this little PIG-A goes "Why? Why? Why?".
Genetic instability and the etiology of somatic PIG-A mutations in paroxysmal nocturnal hemoglobinuria.
Glycosylphosphatidylinositol-anchored protein deficiency confers resistance to apoptosis in PNH.
GPI-anchor synthesis in mammalian cells: genes, their products, and a deficiency.
Hemoglobinuria misidentified as hematuria: review of discolored urine and paroxysmal nocturnal hemoglobinuria.
Hemolytic anemia.
Heterogeneous PIG-A mutations in different cell lineages in paroxysmal nocturnal hemoglobinuria.
High frequency of several PIG-A mutations in patients with aplastic anemia and myelodysplastic syndrome.
How do PIG-A mutant paroxysmal nocturnal hemoglobinuria stem cells achieve clonal dominance?
Identification of a PIG-A related processed gene on chromosome 12.
Immune pathogenesis of paroxysmal nocturnal hemoglobinuria.
Impaired hematopoiesis in paroxysmal nocturnal hemoglobinuria/aplastic anemia is not associated with a selective proliferative defect in the glycosylphosphatidylinositol-anchored protein-deficient clone.
Increased resistance of PIG-A- bone marrow progenitors to tumor necrosis factor a and interferon gamma: possible implications for the in vivo dominance of paroxysmal nocturnal hemoglobinuria clones.
Laboratory studies for paroxysmal nocturnal hemoglobinuria, with emphasis on flow cytometry.
Leukemia arising out of paroxysmal nocturnal hemoglobinuria.
Long-term support of hematopoiesis by a single stem cell clone in patients with paroxysmal nocturnal hemoglobinuria.
Mean fluorescence intensity rate is a useful marker in the detection of paroxysmal nocturnal hemoglobinuria clones.
Molecular cloning of murine pig-a, a gene for GPI-anchor biosynthesis, and demonstration of interspecies conservation of its structure, function, and genetic locus.
Murine embryonic stem cells without pig-a gene activity are competent for hematopoiesis with the PNH phenotype but not for clonal expansion.
Mutations in the PIG-A gene causing paroxysmal nocturnal hemoglobinuria are mainly of the frameshift type.
New insights into paroxysmal nocturnal hemoglobinuria.
New somatic mutation in the PIG-A gene emerges at relapse of paroxysmal nocturnal hemoglobinuria.
On the origin of multiple mutant clones in paroxysmal nocturnal hemoglobinuria.
Paroxysmal nocturnal hemoglobinuria and liver transplantation, a new paradigm.
Paroxysmal nocturnal hemoglobinuria and myelodysplastic syndrome: a case report.
Paroxysmal nocturnal hemoglobinuria and the age of therapeutic complement inhibition.
Paroxysmal nocturnal hemoglobinuria: analysis of the effects of mutant PIG-A on gene expression.
Paroxysmal nocturnal hemoglobinuria: molecular pathogenesis and molecular therapeutic approaches.
Paroxysmal nocturnal hemoglobinuria: significant association with specific HLA-A, -B, -C, and -DR alleles in an Italian population.
Paroxysmal nocturnal hemoglobinuria: Test to monitor the action of eculizumab treatment.
Paroxysmal nocturnal hemoglobinuria: When delay in diagnosis and long therapy occurs.
Pathogenesis of selective expansion of PNH clones.
Phenotypes and phosphatidylinositol glycan-class A gene abnormalities during cell differentiation and maturation from precursor cells to mature granulocytes in patients with paroxysmal nocturnal hemoglobinuria.
PIG-A gene abnormalities in Thai patients with paroxysmal nocturnal hemoglobinuria.
PIG-A mutations in paroxysmal nocturnal hemoglobinuria and in normal hematopoiesis.
PIG-B, a membrane protein of the endoplasmic reticulum with a large lumenal domain, is involved in transferring the third mannose of the GPI anchor.
Postpartum thrombotic complication in a patient with paroxysmal nocturnal hemoglobinuria.
Proliferative capacity of single isolated CD34+ hematopoietic stem/progenitor cells in paroxysmal nocturnal hemoglobinuria.
Rare Hematological Disease of Paroxysmal Nocturnal Hemoglobinuria With Profound Implications for a Gastroenterologist: A Case Report and Literature Review.
Resistance to apoptosis caused by PIG-A gene mutations in paroxysmal nocturnal hemoglobinuria.
Response of paroxysmal nocturnal hemoglobinuria clone with aplastic anemia to rituximab.
Role of phosphatidylinositol-linked proteins in paroxysmal nocturnal hemoglobinuria pathogenesis.
Somatic mutation and clonal selection in the pathogenesis and in the control of paroxysmal nocturnal hemoglobinuria.
Somatic mutations and the hierarchy of hematopoiesis.
Somatic mutations of PIG-A in Thai patients with paroxysmal nocturnal hemoglobinuria.
Somatic mutations of the PIG-A gene found in Japanese patients with paroxysmal nocturnal hemoglobinuria.
Structural and functional analysis of the Pig-a protein that is mutated in paroxysmal nocturnal hemoglobinuria.
Successful unrelated donor bone marrow transplantation for paroxysmal nocturnal hemoglobinuria.
The distribution of PIG-A gene abnormalities in paroxysmal nocturnal hemoglobinuria granulocytes and cultured erythroblasts.
The mutation rate in PIG-A is normal in patients with paroxysmal nocturnal hemoglobinuria (PNH).
The Patterns of MHC Association in Aplastic and Non-aplastic Paroxysmal Nocturnal Hemoglobinuria.
The PIG-A gene somatic mutation responsible for paroxysmal nocturnal hemoglobinuria.
The PIG-A mutation and absence of glycosylphosphatidylinositol-linked proteins do not confer resistance to apoptosis in paroxysmal nocturnal hemoglobinuria.
The small population of PIG-A mutant cells in myelodysplastic syndromes do not arise from multipotent hematopoietic stem cells.
The spectrum of somatic mutations in the PIG-A gene in paroxysmal nocturnal hemoglobinuria includes large deletions and small duplications.
The yeast spt14 gene is homologous to the human PIG-A gene and is required for GPI anchor synthesis.
[Eculizumab in paroxysmal nocturnal hemoglobinuria]
[Gene diagnosis of hemolytic anemia]
[Immune pathophysiology of refractory anemias]
[Mutations in the PIG-A gene lead to GPI-deficiency in paroxysmal nocturnal hemoglobinuria]
[Paroxysmal nocturnal hemoglobinuria--consequences of a missing anchor]
[Paroxysmal nocturnal hemoglobinuria.]
[PIG-A gene mutation and paroxysmal nocturnal hemoglobinuria]
[Somatic mutations of PIG-A gene in Chinese patients with paroxysmal nocturnal hemoglobinuria]
[Spontaneous recovery from pancytopenia in a young female patient with paroxysmal nocturnal hemoglobinuria(PNH): changes in the GPI-anchor expression on peripheral blood cells]
[The evaluation and comparative characteristic of detection of clone of paroxysmal nocturnal hemoglobinuria on reticulocytes using the technique of flow cytometry].
[THE METHODICAL APPROACHES TO DIAGNOSTIC OF NIGHT PAROXYSMAL HEMOGLOBINURIA].
Ichthyosis, Lamellar
Epidermal-specific defect of GPI anchor in Pig-a null mice results in Harlequin ichthyosis-like features.
Inflammatory Bowel Diseases
Dextran sulfate sodium mouse model of inflammatory bowel disease evaluated for systemic genotoxicity via blood micronucleus and Pig-a gene mutation assays.
The potential application of human PIG-A assay on azathioprine-treated inflammatory bowel disease patients.
Leukemia
N-RAS gene mutation in patients with aplastic anemia and aplastic anemia/ paroxysmal nocturnal hemoglobinuria during evolution to clonal disease.
Leukemia, Myelogenous, Chronic, BCR-ABL Positive
Somatic mutations and the hierarchy of hematopoiesis.
Leukemia, Myeloid, Acute
Acute myelogenous leukemia with PIG-A gene mutation evolved from aplastic anemia-paroxysmal nocturnal hemoglobinuria syndrome.
Lymphoma
The development of an in vitro Pig-a assay in L5178Y cells.
Malnutrition
Moderate malnutrition in rats induces somatic gene mutations.
Myelodysplastic Syndromes
High frequency of several PIG-A mutations in patients with aplastic anemia and myelodysplastic syndrome.
Pathogenesis of selective expansion of PNH clones.
The small population of PIG-A mutant cells in myelodysplastic syndromes do not arise from multipotent hematopoietic stem cells.
[Clinical and laboratory characteristics in patients of myelodysplastic syndrome with PNH clones].
Myeloproliferative Disorders
Development of paroxysmal nocturnal hemoglobinuria in CALR-positive myeloproliferative neoplasm.
Neoplasms
A quantitative analysis of genomic instability in lymphoid and plasma cell neoplasms based on the PIG-A gene.
Biological and molecular characterization of PNH-like lymphocytes emerging after Campath-1H therapy.
Monitoring genotoxicity in patients receiving chemotherapy for cancer: application of the PIG-A assay.
Monitoring humans for somatic mutation in the endogenous pig-a gene using red blood cells.
Neoplasms, Plasma Cell
A quantitative analysis of genomic instability in lymphoid and plasma cell neoplasms based on the PIG-A gene.
Obesity
Diet-induced obesity increases the frequency of Pig-a mutant erythrocytes in male C57BL/6J mice.
Protein Deficiency
Glycosylphosphatidylinositol (GPI) anchored protein deficiency serves as a reliable reporter of Pig-a gene Mutation: Support from an in vitro assay based on L5178Y/Tk
Seizures
Generation of glycosylphosphatidylinositol anchor protein-deficient blood cells from human induced pluripotent stem cells.
Starvation
The PIG-A mutation and absence of glycosylphosphatidylinositol-linked proteins do not confer resistance to apoptosis in paroxysmal nocturnal hemoglobinuria.
Thrombophilia
Rare Hematological Disease of Paroxysmal Nocturnal Hemoglobinuria With Profound Implications for a Gastroenterologist: A Case Report and Literature Review.
Thrombosis
Development of paroxysmal nocturnal hemoglobinuria in CALR-positive myeloproliferative neoplasm.
Paroxysmal nocturnal hemoglobinuria: When delay in diagnosis and long therapy occurs.
Thymoma
Direct evidence of involvement of glycosylphosphatidylinositol-anchored proteins in the heavy metal-mediated signal delivery into T lymphocytes.