British journal of haematology · 2016
ASH1L (a histone methyltransferase protein) is a novel candidate globin gene regulator revealed by genetic study of an English family with beta-thalassaemia unlinked to the beta-globin locus.
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Breton Amandine, Theodorou Andria, Aktuna Suleyman, Sonzogni Laura, Darling David, Chan Lucas, Menzel Stephan, van der Spek Peter J, Swagemakers Sigrid M A, Grosveld Frank, Philipsen Sjaak, Thein Swee Lay
Аннотация
In 1993, we described an English family with beta-thalassaemia that was not linked to the beta-globin locus. Whole genome sequence analyses revealed potential causative mutations in 15 different genes, of which 4 were consistently and uniquely associated with the phenotype in all 7 affected family members, also confirmed by genetic linkage analysis. Of the 4 genes, which are present in a centromeric region of chromosome 1, ASH1L was proposed as causative through functional mRNA knock-down and chromatin-immunoprecipitation studies in human erythroid progenitor cells. Our data suggest a putative role for ASH1L (Trithorax protein) in the regulation of globin genes.
Предметные рубрики MeSH
Cell LineChromosome MappingDNA-Binding ProteinsErythroid Precursor CellsGene Expression RegulationGene SilencingGenetic LinkageGenetic VariationGenome, HumanHigh-Throughput Nucleotide SequencingHistone-Lysine N-MethyltransferaseHistonesHumansPhenotypeRNA InterferenceTranscription Factorsbeta-Globinsbeta-Thalassemia