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1. Full Text ITPA gene variants protect against anaemia in patients treated for chronic hepatitis C
by Ge, Dongliang and Bertelsen, Arthur H and Watson, Mark and Goldstein, David B and Albrecht, Janice and Brass, Clifford and Warner, Amelia and Gumbs, Curtis E and Thompson, Alexander J and McHutchison, John G and Shianna, Kevin V and Qiu, Ping and Sulkowski, Mark and Little, Latasha D and Fellay, Jacques and Urban, Thomas J and Muir, Andrew J
Nature, ISSN 0028-0836, 03/2010, Volume 464, Issue 7287, pp. 405 - 408
Chronic infection with the hepatitis C virus (HCV) affects 170 million people worldwide and is an important cause of liver-related morbidity and mortality. The... 
POPULATION | MULTIDISCIPLINARY SCIENCES | MISSENSE MUTATION | PHENOTYPE | WHOLE-GENOME ASSOCIATION | HEXOKINASE DEFICIENCY | RIBAVIRIN | TRIPHOSPHATE PYROPHOSPHOHYDROLASE DEFICIENCY | NONSPHEROCYTIC HEMOLYTIC-ANEMIA | INOSINE TRIPHOSPHATASE | Genome-Wide Association Study | United States | Humans | Pyrophosphatases - deficiency | Ribavirin - therapeutic use | Pyrophosphatases - genetics | Hemoglobins - metabolism | Anemia, Hemolytic - genetics | Antiviral Agents | Continental Population Groups - genetics | Hepatitis C, Chronic - complications | Hepatitis C, Chronic - drug therapy | Europe - ethnology | Pyrophosphatases - metabolism | Hemoglobins - deficiency | Anemia, Hemolytic - complications | Alleles | Polymorphism, Single Nucleotide - genetics | Anemia, Hemolytic - chemically induced | Genetic Variation - genetics | Chromosomes, Human, Pair 20 | Prevention | Anemia | Genetic variation | Development and progression | Genetic aspects | Hepatitis C | Health aspects | Risk factors | Genotype & phenotype | Genes | Quality control | African Americans | Genetics | Population | Mutation | Chromosomes | Hispanics | Blood
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2. Full Text A nonsense variant in the Hexokinase 1 gene (HK1) causing severe non‐spherocytic haemolytic anaemia: genetic analysis exemplifies ambiguity due to multiple Isoforms
by Jamwal, Manu and Aggarwal, Anu and Palodi, Arindam and Sharma, Prashant and Bansal, Deepak and Maitra, Arindam and Das, Reena
British Journal of Haematology, ISSN 0007-1048, 09/2019, Volume 186, Issue 5, pp. e142 - e145
haemolytic anaemia | inherited anaemias | hexokinase deficiency | molecular diagnosis | HEMATOLOGY | Genetic research | Anemia | Genes | Analysis | Hexokinase | Genetic analysis | Isoforms
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3. Full Text GLUT1 mutations are a cause of paroxysmal exertion-induced dyskinesias and induce hemolytic anemia by a cation leak
by Weber, Yvonne G and Storch, Alexander and Wuttke, Thomas V and Brockmann, Knut and Kempfle, Judith and Maljevic, Snezana and Margari, Lucia and Kamm, Christoph and Schneider, Susanne A and Huber, Stephan M and Pekrun, Arnulf and Roebling, Robert and Seebohm, Guiscard and Koka, Saisudha and Lang, Camelia and Kraft, Eduard and Blazevic, Dragica and Salvo-Vargas, Alberto and Fauler, Michael and Mottaghy, Felix M and Münchau, Alexander and Edwards, Mark J and Presicci, Anna and Margari, Francesco and Gasser, Thomas and Lang, Florian and Bhatia, Kailash P and Lehmann-Horn, Frank and Lerche, Holger
Journal of Clinical Investigation, ISSN 0021-9738, 06/2008, Volume 118, Issue 6, pp. 2157 - 2168
Paroxysmal dyskinesias are episodic movement disorders that can be inherited or are sporadic in nature. The pathophysiology underlying these disorders remains... 
MEDICINE, RESEARCH & EXPERIMENTAL | CYSTEINE-SCANNING MUTAGENESIS | MOVEMENT-DISORDER | GENE | GLUCOSE-TRANSPORTER | RED-CELLS | EXERCISE-INDUCED DYSTONIA | EPILEPSY | FAMILIAL INFANTILE CONVULSIONS | BLOOD-BRAIN-BARRIER | DEFICIENCY SYNDROME | Xenopus | Amino Acid Sequence | Humans | Molecular Sequence Data | Male | Anemia, Hemolytic - genetics | Chorea - pathology | Animals | Glucose Transporter Type 1 - genetics | Models, Biological | Erythrocytes - metabolism | Glucose Transporter Type 1 - physiology | Glucose - metabolism | Adult | Female | Cations | Chorea - genetics | Anemia, Hemolytic - etiology | Physical Exertion | Care and treatment | Hemolytic anemia | Gene mutations | Diagnosis | Research | Risk factors | Movement disorders
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4. Full Text Mutations in Krüppel-like factor 1 cause transfusion-dependent hemolytic anemia and persistence of embryonic globin gene expression
by Viprakasit, Vip and Ekwattanakit, Supachai and Riolueang, Suchada and Chalaow, Nipon and Fisher, Chris and Lower, Karen and Kanno, Hitoshi and Tachavanich, Kalaya and Bejrachandra, Sasithorn and Saipin, Jariya and Juntharaniyom, Monthana and Sanpakit, Kleebsabai and Tanphaichitr, Voravarn S and Songdej, Duantida and Babbs, Christian and Gibbons, Richard J and Philipsen, Sjaak and Higgs, Douglas R
Blood, ISSN 0006-4971, 03/2014, Volume 123, Issue 10, pp. 1586 - 1595
In this study, we report on 8 compound heterozygotes for mutations in the key erythroid transcription factor Kruppel-like factor 1 in patients who presented... 
TRANSCRIPTION FACTOR KLF1 | ALPHA-THALASSEMIA | ERYTHROPOIESIS | FETAL-HEMOGLOBIN | ERYTHROID-CELLS | MICE | CONGENITAL DYSERYTHROPOIETIC ANEMIA | BETA-THALASSEMIA | IDENTIFICATION | HEMATOLOGY | HAPLOINSUFFICIENCY | Humans | Child, Preschool | Molecular Sequence Data | Erythrocyte Indices | Infant | Male | Anemia, Hemolytic - genetics | Young Adult | Fetal Hemoglobin - chemistry | Conserved Sequence | Adult | Female | Protein Interaction Domains and Motifs | Child | Gene Order | Anemia, Hemolytic - etiology | Amino Acid Sequence | Gene Expression Regulation | Transfusion Reaction | Sequence Alignment | beta-Globins - metabolism | Adolescent | Erythrocytes - metabolism | Fetal Hemoglobin - genetics | Protein Binding | Mutation | Anemia, Hemolytic - blood | Kruppel-Like Transcription Factors - genetics | alpha-Globins - metabolism
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5. Full Text Gene disruption of dematin causes precipitous loss of erythrocyte membrane stability and severe hemolytic anemia
by Lu, Yunzhe and Hanada, Toshihiko and Fujiwara, Yuko and Nwankwo, Jennifer O and Wieschhaus, Adam J and Hartwig, John and Huang, Sha and Han, Jongyoon and Chishti, Athar H
Blood, ISSN 0006-4971, 07/2016, Volume 128, Issue 1, pp. 93 - 103
Dematin is a relatively low abundance actin binding and bundling protein associated with the spectrin-actin junctions of mature erythrocytes. Primary structure... 
HEADPIECE DOMAIN | ADDUCIN | TARGETED DISRUPTION | IN-VITRO | SPECTRIN | PROTEIN-KINASE | GLYCOPHORIN-C | RED-BLOOD-CELLS | MICE | HEMATOLOGY | SKELETON | Calmodulin-Binding Proteins - genetics | Cytoskeleton - pathology | Cytoskeletal Proteins - genetics | Anemia, Hemolytic - pathology | Cytoskeleton - genetics | Erythrocyte Membrane - metabolism | Erythrocyte Membrane - pathology | Male | Anemia, Hemolytic - genetics | Calmodulin-Binding Proteins - metabolism | Mice, Knockout | Animals | Erythrocyte Membrane - genetics | Gene Deletion | Anemia, Hemolytic - metabolism | Cytoskeleton - metabolism | Cytoskeletal Proteins - metabolism | Female | Spectrin - genetics | Mice | Spectrin - metabolism | Red Cells, Iron, and Erythropoiesis
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6. Full Text G6PD deficiency: a classic example of pharmacogenetics with on‐going clinical implications
by Luzzatto, Lucio and Seneca, Elisa
British Journal of Haematology, ISSN 0007-1048, 02/2014, Volume 164, Issue 4, pp. 469 - 480
That primaquine and other drugs can trigger acute haemolytic anaemia in subjects who have an inherited mutation of the glucose 6‐phosphate dehydrogenase (G6 PD... 
Clinical Implications | pharmacogenetics | G6PD | Pharmacogenetics | METHYLENE-BLUE | CHLORPROGUANIL-DAPSONE-ARTESUNATE | INDUCED HEMOLYTIC-ANEMIA | RED-CELLS | PLASMODIUM-FALCIPARUM MALARIA | PHASE-III TRIAL | AFRICAN CHILDREN | DOUBLE-BLIND | GLUCOSE-6-PHOSPHATE-DEHYDROGENASE DEFICIENCY | INDUCED METHEMOGLOBINEMIA | HEMATOLOGY | Dapsone - adverse effects | Antimalarials - adverse effects | Humans | Male | Anemia, Hemolytic - genetics | Glucosephosphate Dehydrogenase Deficiency - pathology | Anemia, Hemolytic - enzymology | Animals | Anemia, Hemolytic - chemically induced | Female | Primaquine - adverse effects | Hemolysis - genetics | Glucosephosphate Dehydrogenase Deficiency - genetics | Reviews
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7. Full Text A Rare Cause of Neonatal Hemolytic Anemia: Glutathione Synthetase Deficiency
by Ustkoyuncu, Pembe Soylu and Mutlu, Fatma Türkan and Kiraz, Aslihan and Tag Balkis, Zuhal and Yel, Sibel
Journal of Pediatric Hematology/Oncology, ISSN 1077-4114, 2018, Volume 40, Issue 1, pp. e45 - e49
Background: Isolated hemolysis or hemolytic anemia and 5-oxoprolinuria are 2 distinct medical conditions in the clinical spectrum associated with glutathione... 
Anemia | Metabolic acidosis | Glutathione synthetase deficiency | 5-OXOPROLINURIA | metabolic acidosis | VITAMIN-E | glutathione synthetase deficiency | METABOLIC-ACIDOSIS | ONCOLOGY | PEDIATRICS | MUTATIONS | HEMATOLOGY | anemia | Amino Acid Metabolism, Inborn Errors - complications | Glutathione Synthase - deficiency | Diagnosis, Differential | Infant, Newborn, Diseases - diagnosis | Humans | Anemia, Hemolytic - genetics | Anemia, Hemolytic, Congenital - genetics | Amino Acid Metabolism, Inborn Errors - diagnosis | Anemia, Hemolytic, Congenital - etiology | Amino Acid Metabolism, Inborn Errors - genetics | Female | Infant, Newborn, Diseases - genetics | Glutathione Synthase - genetics | Mutation | Anemia, Hemolytic - etiology | Infant, Newborn
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8. Full Text CD59 deficiency is associated with chronic hemolysis and childhood relapsing immune-mediated polyneuropathy
by Nevo, Yoram and Ben-Zeev, Bruria and Tabib, Adi and Straussberg, Rachel and Anikster, Yair and Shorer, Zamir and Fattal-Valevski, Aviva and Ta-Shma, Asaf and Aharoni, Sharon and Rabie, Malcolm and Zenvirt, Shamir and Goldshmidt, Hanoch and Fellig, Yakov and Shaag, Avraham and Mevorach, Dror and Elpeleg, Orly
Blood, ISSN 0006-4971, 01/2013, Volume 121, Issue 1, pp. 129 - 135
CD59 deficiency is a common finding in RBCs and WBCs in patients with chronic hemolysis suffering from paroxysmal nocturnal hemoglobinuria in which the... 
MEMBRANE ATTACK | COMPLEMENT | ACTIVATION | ERYTHROCYTES | GENE | TERM-FOLLOW-UP | INFLAMMATORY DEMYELINATING POLYNEUROPATHY | PAROXYSMAL-NOCTURNAL HEMOGLOBINURIA | HEMATOLOGY | Polyradiculoneuropathy, Chronic Inflammatory Demyelinating - blood | Hemoglobinuria - ethnology | Hemoglobinuria - genetics | Polyradiculoneuropathy, Chronic Inflammatory Demyelinating - cerebrospinal fluid | Humans | Child, Preschool | Molecular Sequence Data | Infant | Male | Anemia, Hemolytic - genetics | Mutation, Missense | Libya - ethnology | Jews - genetics | Membrane Proteins - analysis | Founder Effect | Morocco - ethnology | Anemia, Hemolytic - cerebrospinal fluid | Female | Anemia, Hemolytic - ethnology | Amino Acid Sequence | CD59 Antigens - genetics | Protein Transport | Hemoglobinuria - cerebrospinal fluid | Point Mutation | Pedigree | Polyradiculoneuropathy, Chronic Inflammatory Demyelinating - ethnology | Age of Onset | Hemoglobinuria - blood | CD59 Antigens - metabolism | Polyradiculoneuropathy, Chronic Inflammatory Demyelinating - genetics | Anemia, Hemolytic - blood
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9. Full Text LRBA gene deletion in a patient presenting with autoimmunity without hypogammaglobulinemia
by Burns, Siobhan O., MD, PhD and Zenner, Helen L., PhD and Plagnol, Vincent, PhD and Curtis, James, BSc and Mok, Kin, MBBS, MSc and Eisenhut, Michael, MD and Kumararatne, Dinakantha, MD and Doffinger, Rainer, PhD and Thrasher, Adrian J., MD, PhD and Nejentsev, Sergey, MD, PhD
Journal of Allergy and Clinical Immunology, The, ISSN 0091-6749, 2012, Volume 130, Issue 6, pp. 1428 - 1432
  [...]she received several courses of steroids, rituximab (with prophylactic immunoglobulin replacement), and mycophenolate mofetil. Because of further chest... 
Allergy and Immunology | ALLERGY | IMMUNOLOGY | Autoimmune Diseases - physiopathology | Agammaglobulinemia - complications | Agammaglobulinemia - genetics | Humans | Autoimmune Diseases - complications | Child, Preschool | Anemia, Hemolytic - genetics | Agammaglobulinemia - physiopathology | Autoimmune Diseases - genetics | Homozygote | Exome - genetics | Erythema Nodosum - genetics | DNA Mutational Analysis | Erythema Nodosum - complications | Erythema Nodosum - physiopathology | Anemia, Hemolytic - complications | Adaptor Proteins, Signal Transducing - genetics | Anemia, Hemolytic - physiopathology | Female | Consanguinity | Child | Cell Line, Transformed | Sequence Deletion - genetics | Autoimmunity | Children's hospitals | Genes | Genetic research | Children | Universities and colleges | Health aspects | Diseases | Proteins | Lymphocytes | Mutation | Vaccines | Tetanus | Age | Immune system | Streptococcus infections | CVID | exome sequencing | autoimmunity | deletion | gene | Primary immunodeficiency
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10. Full Text Deficiency of nicotinamide mononucleotide adenylyltransferase 3 (Nmnat3) causes hemolytic anemia by altering the glycolytic flow in mature erythrocytes
by Hikosaka, Keisuke and Ikutani, Masashi and Shito, Masayuki and Kazuma, Kohei and Gulshan, Maryam and Nagai, Yoshinori and Takatsu, Kiyoshi and Konno, Katsuhiro and Tobe, Kazuyuki and Kanno, Hitoshi and Nakagawa, Takashi
Journal of Biological Chemistry, ISSN 0021-9258, 1782, Volume 289, Issue 21, pp. 14796 - 14811
NAD biosynthesis is of substantial interest because of its important roles in regulating various biological processes. Nicotinamide mononucleotide... 
LEBER CONGENITAL AMAUROSIS | AXONAL DEGENERATION | NAD SYNTHESIS | METABOLISM | BIOCHEMISTRY & MOLECULAR BIOLOGY | ADENINE-DINUCLEOTIDE | SUBCELLULAR COMPARTMENTATION | PYRUVATE-KINASE DEFICIENCY | ENZYMATIC-SYNTHESIS | MICE | MUTATIONS | Cytoplasm - enzymology | Microscopy, Electron, Scanning | Splenomegaly - genetics | Nicotinamide-Nucleotide Adenylyltransferase - metabolism | Erythrocytes - ultrastructure | Anemia, Hemolytic - genetics | Splenomegaly - metabolism | Metabolomics - methods | Blotting, Western | Mice, Knockout | Nicotinamide-Nucleotide Adenylyltransferase - deficiency | Tandem Mass Spectrometry | Metabolic Networks and Pathways - genetics | Animals | Adenosine Triphosphate - metabolism | Erythrocytes - metabolism | Survival Analysis | Anemia, Hemolytic - metabolism | Chromatography, Liquid | Glycolysis | Nicotinamide-Nucleotide Adenylyltransferase - genetics | Mice | NAD - metabolism | Erythrocyte | Metabolomics | NAD Biosynthesis | Metabolism | Nicotinamide Adenine Dinucleotide (NAD)
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11. Full Text Molecular diagnosis of unexplained haemolytic anaemia using targeted next-generation sequencing panel revealed (p.Ala337Thr) novel mutation in GPI gene in two Indian patients
by Kedar, Prabhakar S and Gupta, Vinod and Dongerdiye, Rashmi and Chiddarwar, Ashish and Warang, Prashant and Madkaikar, Manisha R
Journal of Clinical Pathology, ISSN 0021-9746, 01/2019, Volume 72, Issue 1, pp. 81 - 85
Glucose-6-phosphate isomerase (GPI) deficiency is an autosomal recessive genetic disorder causing congenital haemolytic anaemia (CHA). Diagnosis of GPI... 
Molecular modeling. next-generation sequencing | Next-generation sequencing | Molecular modeling | Glycolysis | Glucose-6-phosphate isIsomerase (GPI) deficiency | Hereditary Non-spherocytic haemolytic anaemia (HNSHA) | Neurological disorders | hereditary Non-spherocytic haemolytic anaemia (HNSHA) | molecular modeling | next-generation sequencing | glycolysis | neurological disorders | PATHOLOGY | GLUCOSE-6-PHOSPHATE ISOMERASE | PHOSPHATE ISOMERASE DEFICIENCY | BONE-MARROW FAILURE | PRECISION | Humans | Erythrocytes | Anemia, Hemolytic - genetics | Mutation, Missense | Sequence Analysis, DNA | Glucose-6-Phosphate Isomerase - genetics | India | Homozygote | Anemia, Hemolytic - diagnosis | Adult | Female | High-Throughput Nucleotide Sequencing | Child | Cytokines - genetics | Pathology, Molecular | Amino Acid Substitution | Proteins | Enzymes | Motility | Hematology | Anemia | Genes | Bone marrow | Genomes | Mutation | Medical diagnosis | Patients
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12. Full Text Hemolytic anemia repressed hepcidin level without hepatocyte iron overload: Lesson from Günther disease model
by Millot, Sarah and Delaby, Constance and Moulouel, Boualem and Lefebvre, Thibaud and Pilard, Nathalie and Ducrot, Nicolas and Ged, Cécile and Lettéron, Philippe and de Franceschi, Lucia and Deybach, Jean Charles and Beaumont, Carole and Gouya, Laurent and De Verneuil, Hubert and Lyoumi, Saïd and Puy, Hervé and Karim, Zoubida
Haematologica, ISSN 0390-6078, 2017, Volume 102, Issue 2, pp. 260 - 270
Hemolysis occurring in hematologic diseases is often associated with an iron loading anemia. This iron overload is the result of a massive outflow of... 
CONGENITAL ERYTHROPOIETIC PORPHYRIA | GENE | TRANSFERRIN | INEFFECTIVE ERYTHROPOIESIS | MOUSE MODEL | LIVER | BETA-THALASSEMIA | IDENTIFICATION | HEMATOLOGY | EXPRESSION | DEFICIENCY | Erythropoiesis | Hepcidins - metabolism | Heme - metabolism | Humans | Stress, Physiological | Anemia, Hemolytic - genetics | Hepatocytes - metabolism | Macrophages | Iron Overload - etiology | Biological Transport | Iron Overload - metabolism | Anemia, Hemolytic - complications | Anemia, Hemolytic - metabolism | Disease Models, Animal | Gene Expression | Iron - urine | Hepcidins - blood | Mice, Transgenic | Iron - metabolism | Mice, Knockout | Animals | Erythrocytes - metabolism | Biomarkers | Hepcidins - genetics | Mice | Spleen - physiology | Anemia, Hemolytic - blood | Apoptosis
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