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Leukemia risk factor ARID5B Coordinates HDAC-Mediated Transcriptional Repression [RNA-Seq]

ABSTRACT: We employed a combination of proteomics, genomics and transcriptomics to describe the molecular mechanisms of ARID5B. We identify that ARID5B interacts with MIER1, C16ORF87, HDAC1 and HDAC2 forming a repressor complex. The former localizes to active regions of the genome, tethering HDAC1 and HDAC2 to enhancers and promoters. Genes actively repressed by the ARID5B repressor complex are involved in B cell-specific signaling.

ORGANISM(S): Homo sapiens

PROVIDER: GSE297397 | GEO | 2026/05/19

REPOSITORIES: GEO

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Leukemia risk factor ARID5B Coordinates HDAC-Mediated Transcriptional Repression [CUT&Run]

Project description:We employed a combination of proteomics, genomics and transcriptomics to describe the molecular mechanisms of ARID5B. We identify that ARID5B interacts with MIER1, C16ORF87, HDAC1 and HDAC2 forming a repressor complex. The former localizes to active regions of the genome, tethering HDAC1 and HDAC2 to enhancers and promoters. Genes actively repressed by the ARID5B repressor complex are involved in B cell-specific signaling.

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Effect of Arid5b overexpression on the B cell development

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Inhibition of class I histone deacetylases 1 and 2 promotes urothelial carcinoma cell death by various mechanisms (HDAC inhibitor treatments)

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Comparative genomic hybridisation of gDNA from HDAC1-/-; HDAC2+/- diseased mouse thymocytes and sample matched wild-type tail

Project description:Histone deacetylase 1 and 2 (HDAC1/2) regulate chromatin structure as the catalytic core of the Sin3A, NuRD and CoREST co-repressor complexes. To better understand the key pathways regulated by HDAC1/2 in the adaptive immune system and inform their exploitation as drug targets, we have generated mice with a T cell specific deletion and performed comparative genomic hybridisation using genomic DNA from HDAC1-/-; HDAC2+/- diseased thymocytes and sample-matched, wild-type tail. A data set from a related transcription-profiling study comparing HDAC1-/-; HDAC2+/- mouse thymus tissue against thymus tissues from wild-type counterparts has also been deposited at ArrayExpress under accession E-MTAB-1432: http://www.ebi.ac.uk/arrayexpress/experiments/E-MTAB-1432

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Molecular mechanisms of ARID5B-mediated genetic susceptibility to acute lymphoblastic leukemia

Project description:There is growing evidence for the inherited basis of susceptibility to childhood acute lymphoblastic leukemia (ALL). Genome-wide association studies have identified non-coding ALL risk variants at the ARID5B gene locus, but their exact functional effects and the molecular mechanism linking ARID5B to B-ALL leukemogenesis remain largely unknown. In this study, by targeted sequencing in germline DNA of 5,008 children with ALL, we identified 31 common variants in ARID5B significantly associated with leukemia risk, all of which were non-coding. Six cis-regulatory elements at the ARID5B locus were discovered using CRISPR-based high-throughput enhancer screening. Strikingly, the top ALL risk variant (rs7090445, P=1.82×10-10) is located precisely within the strongest enhancer element, which is also distally tethered to the ARID5B promoter. The rs7090445 variant allele disrupts the MEF2C binding motif sequence, resulting in reduced MEF2C affinity and decreased local chromosome accessibility. MEF2C influences ARID5B expression in ALL, likely via a transcription factor complex with RUNX1. Using the UK Biobank dataset (n=349,861), we showed that rs7090445 was also associated with lymphocyte percentage and count in the general population (P=8.6×10-22 and 2.1×10-18, respectively). Taken together, our results indicate that ALL risk variants in ARID5B function by modulating cis-regulatory elements at this locus.

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Leukemia risk factor ARID5B Coordinates HDAC-Mediated Transcriptional Repression

Project description:This SuperSeries is composed of the SubSeries listed below.

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Expression data from primary MEF lacking either HDAC1, HDAC2 or both

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2010-07-30 | E-GEOD-20100 | biostudies-arrayexpress

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2019-11-14 | PXD011869 | Pride

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