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- Loughran, SJ, et al.
(författare)
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Mbd3/NuRD controls lymphoid cell fate and inhibits tumorigenesis by repressing a B cell transcriptional program
- 2017
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Ingår i: The Journal of experimental medicine. - : Rockefeller University Press. - 1540-9538 .- 0022-1007. ; 214:10, s. 3085-3104
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Tidskriftsartikel (refereegranskat)abstract
- Differentiation of lineage-committed cells from multipotent progenitors requires the establishment of accessible chromatin at lineage-specific transcriptional enhancers and promoters, which is mediated by pioneer transcription factors that recruit activating chromatin remodeling complexes. Here we show that the Mbd3/nucleosome remodeling and deacetylation (NuRD) chromatin remodeling complex opposes this transcriptional pioneering during B cell programming of multipotent lymphoid progenitors by restricting chromatin accessibility at B cell enhancers and promoters. Mbd3/NuRD-deficient lymphoid progenitors therefore prematurely activate a B cell transcriptional program and are biased toward overproduction of pro–B cells at the expense of T cell progenitors. The striking reduction in early thymic T cell progenitors results in compensatory hyperproliferation of immature thymocytes and development of T cell lymphoma. Our results reveal that Mbd3/NuRD can regulate multilineage differentiation by constraining the activation of dormant lineage-specific enhancers and promoters. In this way, Mbd3/NuRD protects the multipotency of lymphoid progenitors, preventing B cell–programming transcription factors from prematurely enacting lineage commitment. Mbd3/NuRD therefore controls the fate of lymphoid progenitors, ensuring appropriate production of lineage-committed progeny and suppressing tumor formation.
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- Oláh, János, et al.
(författare)
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Revision of the European Rhyacophila fasciata species complex by fine phenomics of the paramere (Trichoptera, Rhyacophilidae)
- 2020
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Ingår i: Opuscula Zoologica Instituti Zoosystematici et Oecologici Universitatis Budapestinensis. - 0237-5419 .- 2063-1588. ; 51:1, s. 21-54
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Tidskriftsartikel (refereegranskat)abstract
- The poorly known, so called widely distributed and highly varying species of the European Rhyacophila fasciata species complex are revised by fine phenomics of the paramere organisation. In this species complex paramere is the most diverse organ. It is the speciation trait integrating the initial split of speciation by its stimulatory and titillating function involved in the early processes of reproductive isolation. Based on paramere organisation and on the character state of distribution three lineages have been delineated in the Rhyacophila fasciata species complex: the European R. fasciata lineage, the Caucasian R. aliena lineage and the R. mysica lineage distributed from Albania to Pakistan. In the R. fasciata lineage we have distinguished three clades of species: R. fasciata with five species, R. matrensis with seven species, and R. denticulata with seven species. We have re-diagnosed three known species: R. fasciata Hagen, 1859, R. denticulataMcLachlan, 1879, R. sociata Navas, 1916 and described 15 species new to science: R. biharensis Oláh sp. nov., R. bulgarica Oláh sp. nov., R. coppai Oláh sp. nov., R. csornahorensis Oláh & Szczęsny sp. nov., R. ferda Oláh sp. nov., R. kopasa Oláh & Coppa sp. nov., R. matrensis Oláh, & Szczęsny sp. nov., R. retezatensis Oláh sp. nov., R. rova Oláh & Coppa sp. nov. R. ruda Oláh & Johanson sp. nov., R. salfa Oláh sp. nov., R. soreda Coppa & Oláh sp. nov. R. suna Oláh sp. nov., R. tuhega Oláh sp. nov., R. zemplenensis Oláh sp. nov. The species status of Rhyacophila gemella Navas, 1923 was reinstated.
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- van Es, Michael A, et al.
(författare)
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Genome-wide association study identifies 19p13.3 (UNC13A) and 9p21.2 as susceptibility loci for sporadic amyotrophic lateral sclerosis
- 2009
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Ingår i: Nature genetics. - : Springer Science and Business Media LLC. - 1546-1718 .- 1061-4036. ; 41:10, s. 1083-1087
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Tidskriftsartikel (refereegranskat)abstract
- We conducted a genome-wide association study among 2,323 individuals with sporadic amyotrophic lateral sclerosis (ALS) and 9,013 control subjects and evaluated all SNPs with P < 1.0 x 10(-4) in a second, independent cohort of 2,532 affected individuals and 5,940 controls. Analysis of the genome-wide data revealed genome-wide significance for one SNP, rs12608932, with P = 1.30 x 10(-9). This SNP showed robust replication in the second cohort (P = 1.86 x 10(-6)), and a combined analysis over the two stages yielded P = 2.53 x 10(-14). The rs12608932 SNP is located at 19p13.3 and maps to a haplotype block within the boundaries of UNC13A, which regulates the release of neurotransmitters such as glutamate at neuromuscular synapses. Follow-up of additional SNPs showed genome-wide significance for two further SNPs (rs2814707, with P = 7.45 x 10(-9), and rs3849942, with P = 1.01 x 10(-8)) in the combined analysis of both stages. These SNPs are located at chromosome 9p21.2, in a linkage region for familial ALS with frontotemporal dementia found previously in several large pedigrees.
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