The Sin3 histone deacetylase (HDAC) complex is a 1.2 MDa chromatin modifying complex that can repress transcription by binding to gene promoters and deacetylating histones. The Sin3/HDAC complex can affect cell cycle progression through multiple mechanisms and is among the targets of anticancer drugs, called HDAC inhibitors. We describe the identification of a new subunit of the Sin3 complex named family with sequence similarity 60 member A (FAM60A). We show that FAM60A/Sin3 complexes normally suppress the epithelial-to-mesenchymal transition (EMT) and cell migration. This occurs through transcriptional repression of genes that encode components of the TGF-beta signaling pathway. This work reveals that FAM60A and the Sin3 complex are upstream repressors of TGF-beta signaling, EMT and cell migration and extends the known biological roles of the Sin3 complex. This experiment investigates the role of FAM60A in gene expression by comparing A549 lung cancer cells treated with or without siRNA against FAM60A.
Human family with sequence similarity 60 member A (FAM60A) protein: a new subunit of the Sin3 deacetylase complex.
Specimen part, Cell line
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MicroRNA target prediction by expression analysis of host genes.
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View SamplesMutation of MTF in Arabidopsis increases Agrobacterium-mediated transformation susceptibility. Being a putative transcription factor, different genes controlling transformation may be regulated by MTF.
Cytokinins secreted by Agrobacterium promote transformation by repressing a plant myb transcription factor.
Specimen part
View SamplesTotal RNA samples from three biological replicates in which the hsa-mir-26b was overexpressed in HeLa cells were profiled by gene expression. As negative control, we used total RNA samples from HeLa cells transfected with cel-mir-67
MicroRNA target prediction by expression analysis of host genes.
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View SamplesTotal RNA samples from three biological replicates in which the hsa-mir-98 was overexpressed in HeLa cells were profiled by gene expression. As negative control, we used total RNA samples from HeLa cells transfected with cel-mir-67
MicroRNA target prediction by expression analysis of host genes.
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View SamplesWe used microarrays to detail the global programme of gene expression after 4 months of TFEB overexpression in the brain.
Selective clearance of aberrant tau proteins and rescue of neurotoxicity by transcription factor EB.
Specimen part, Treatment
View SamplesWe show that aneuploidy is common in wild isolates of yeast, which are inherently tolerant to chromosome amplification and down-regulate expression at 40% of amplified genes. To dissect the mechanism of this dosage response, we generated isogenic strain panels in which diploid cells carried either two, three, or four copies of the affected chromosomes. Using a mixture of linear regression (MLR) model to classify genes, we find that expression is actively down regulated in proportion to increased gene copy at up to 30% of genes. Genes subject to dosage control are under higher expression constraint – but show elevated rates of gene amplification – in wild populations, suggesting that dosage compensation buffers copy number variation (CNV) at toxic genes Overall design: RNA-seq and transcriptome analysis of S. cerevisiae natural isolates having aneuploidy. Technical triplicate was performed for isogenic diploid strains having 2, 3 and 4 copies of a given chromosome (strain panels), while technical duplicate or singulate was performed on all other aneuploids.
Dosage compensation can buffer copy-number variation in wild yeast.
Subject
View SamplesWe Report the genome-wide RNA expression levels in control and schizophrenia hiPSC dervied NPC treated with neuronal media for 2 days. In total about 15,000 gene expression were detected in all samples, of which 1349 were dysregualted. Overall design: Examination, identification and comparision of mRNA expression profliles in control and schizophrenia npc
Common developmental genome deprogramming in schizophrenia - Role of Integrative Nuclear FGFR1 Signaling (INFS).
Specimen part, Subject
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Retinoic acid is essential for Th1 cell lineage stability and prevents transition to a Th17 cell program.
Specimen part
View SamplesMouse Bcell, upon ectopic expression of the transcription factor Cebpa for 18h, can be reprogrammed to iPS with extremely high efficiency. To understand the molecular control of this phenomena we performed multiple high throughtput functionnal genomic analysis. Overall design: Transcriptomic by RNAseqencing (polyA+, non stranded) in Bcell, Bcell+Cebpa18h, Bcell+Cebpa18h+OKSM1d, Bcell+Cebpa18h+OKSM2d, ES cells
C/EBPα creates elite cells for iPSC reprogramming by upregulating Klf4 and increasing the levels of Lsd1 and Brd4.
No sample metadata fields
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