Search results for "BLOOD Commentary"

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Cohesin-dependent regulation of gene expression during differentiation is lost in cohesin-mutated myeloid malignancies.

2019

Cohesin complex disruption alters gene expression, and cohesin mutations are common in myeloid neoplasia, suggesting a critical role in hematopoiesis. Here, we explore cohesin dynamics and regulation of hematopoietic stem cell homeostasis and differentiation. Cohesin binding increases at active regulatory elements only during erythroid differentiation. Prior binding of the repressive Ets transcription factor Etv6 predicts cohesin binding at these elements and Etv6 interacts with cohesin at chromatin. Depletion of cohesin severely impairs erythroid differentiation, particularly at Etv6-prebound loci, but augments self-renewal programs. Together with corroborative findings in acute myeloid le…

0301 basic medicineMaleCohesin complexChromosomal Proteins Non-HistoneImmunologyGene DosageCell Cycle ProteinsBiologyRegulatory Sequences Nucleic AcidBiochemistryHistones03 medical and health sciences0302 clinical medicineNeoplasmshemic and lymphatic diseasesCell Line TumorBiomarkers TumorHumansTranscription factorRegulation of gene expressionHematopoietic stem cell homeostasisMyeloid NeoplasiaMyeloproliferative DisordersCohesinProto-Oncogene Proteins c-etsGene Expression Regulation LeukemicETS transcription factor familyMyeloid leukemiafood and beveragesCell BiologyHematologyHematopoietic Stem CellsCell biologyChromatinHematopoiesisRepressor Proteins030104 developmental biologyGene Expression Regulation030220 oncology & carcinogenesisMutationFemalesense organsbiological phenomena cell phenomena and immunityNeoplasm GradingBLOOD CommentaryProtein BindingBlood
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Dynamics of complement activation in aHUS and how to monitor eculizumab therapy.

2014

Atypical hemolytic-uremic syndrome (aHUS) is associated with genetic complement abnormalities/anti–complement factor H antibodies, which paved the way to treatment with eculizumab. We studied 44 aHUS patients and their relatives to (1) test new assays of complement activation, (2) verify whether such abnormality occurs also in unaffected mutation carriers, and (3) search for a tool for eculizumab titration. An abnormal circulating complement profile (low C3, high C5a, or SC5b-9) was found in 47% to 64% of patients, irrespective of disease phase. Acute aHUS serum, but not serum from remission, caused wider C3 and C5b-9 deposits than control serum on unstimulated human microvascular endotheli…

MaleTime FactorsClinical Trials and ObservationsComplement Membrane Attack Complexurologic and male genital diseasesBiochemistryGlomerulonephritisInside BLOOD Commentaryhemic and lymphatic diseasesMembranoproliferative glomerulonephritisMonoclonalHumanizedComplement ActivationAtypical Hemolytic Uremic SyndromeEndothelial CellHematologyRemission Inductionfood and beveragesHematologyComplement C3Eculizumabmedicine.anatomical_structureFactor HFemalecomplementaHUS eculizumabmedicine.drugMembranoproliferativeHumanmedicine.medical_specialtyEndotheliumMonitoringTime FactorGlomerulonephritis MembranoproliferativeImmunologyBiologyAntibodies Monoclonal HumanizedAntibodiesInternal medicineAtypical hemolytic uremic syndromemedicineHumansPhysiologicMonitoring PhysiologicAdenosine Diphosphate RiboseEndothelial CellsCell Biologymedicine.diseaseComplement systemImmunologyAdenosine Diphosphate Ribose; Antibodies Monoclonal Humanized; Atypical Hemolytic Uremic Syndrome; Complement Activation; Complement C3; Complement Membrane Attack Complex; Endothelial Cells; Female; Glomerulonephritis Membranoproliferative; Hemolytic-Uremic Syndrome; Humans; Male; Remission Induction; Time Factors; Monitoring Physiologic; Hematology; Biochemistry; Cell Biology; ImmunologyHemolytic-Uremic SyndromeComplement membrane attack complexBlood
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