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Role of SWI/SNF-Related, Matrix Associated, Actin Dependent Regulator of Chromatin A4 (SMARCA4) core complex in epithelial innate response (RNA-seq)

ABSTRACT: We examine the epigenetic role of the SWI/SNF Related, Matrix Associated, Actin Dependent Regulator of Chromatin A4 (SMARCA4) in the epithelial response to RSV infection. Wild type and SMARCA4 silenced cells were subjected to short read illumina RNA Seq in the absence or presence of RSV infection. Cells were infected for 0, 16 h or 24 h prior to RNA seq.

ORGANISM(S): Homo sapiens

PROVIDER: GSE161846 | GEO | 2021/01/01

REPOSITORIES: GEO

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Role of SWI/SNF-Related, Matrix Associated, Actin Dependent Regulator of Chromatin A4 (SMARCA4) core complex in epithelial innate response (ATAC-seq)

Project description:We examine the epigenetic role of the SWI/SNF Related, Matrix Associated, Actin Dependent Regulator of Chromatin A4 (SMARCA4) in the epithelial response to RSV infection. Wild type and SMARCA4 silenced cells were subjected to ATAC-seq in the absence or presence of RSV infection. Cells were infected for 0 or 24 h prior to RNA seq.

2021-01-01 | GSE161847 | GEO

Role of SWI/SNF-Related, Matrix Associated, Actin Dependent Regulator of Chromatin A4 (SMARCA4) core complex in epithelial innate response

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

2021-01-01 | GSE161849 | GEO

Role of SWI/SNF-Related, Matrix Associated, Actin Dependent Regulator of Chromatin A4 (SMARCA4) core complex in epithelial innate response

Project description:Role of SWI/SNF-Related, Matrix Associated, Actin Dependent Regulator of Chromatin A4 (SMARCA4) core complex in epithelial innate response

| PRJNA679613 | ENA

SMARCA4 regulates BRD4 nuclear distribution in cellular plasticity

Project description:Inducible cell stress programs in basal epithelial cells shape repair and host defense pathways in mucosal surfaces. Previously, we discovered that expression of the core SWI/SNF complex ATPase, SMARCA4/Brg1, is required for genomic organization supporting a fully differentiated epithelial state, regulating cellular plasticity, paracrine mesenchymal signaling and anti-viral response. Here, we observe that SMARCA4 expression is intrinsically engaged with IFN response genes and dynamically engages the atypical histone acetyltransferase, BRD4, upon RSV infection, an association required for intrinsic immunity. To investigate the mechanisms how the SMARCA4 BRD4 complex functions in intrinsic immunity, we performed Cleavage Under Targets and Release Using Nuclease (CUT&RUN) of BRD4 binding in wild type (WT) and SMARCA4 knockdown (KD) small airway epithelial cells in mock- or RSV-infected states. In mock-infected cells, 4,017 high confidence BRD4 peaks are identified that localize to the gene bodies controlling motility programs. By contrast, RSV replication repositions BRD4 to 2,339 regions, upstream of transcription start sites in genes controlling inducible cytokine, cell adherence and anti-viral programs. RSV redistributes BRD4 into super enhancers regulating immune response-associated long noncoding RNAs. BRD4 binding is not affected by SMARCA4 KD in mock-infected cells, but BRD4 recruitment is reduced on 739 peaks after RSV infection, including superenhancers. These data extend the complex interrelationship between the SWI/SNF ATPases and that of the BRD4 bromodomain epithelial progenitors linking cell state and innate immunity.

2024-08-30 | GSE273399 | GEO

Role of SWI/SNF-Related, Matrix Associated, Actin Dependent Regulator of Chromatin A4 (SMARCA4) core complex in epithelial innate response (RNA-seq)

Project description:Role of SWI/SNF-Related, Matrix Associated, Actin Dependent Regulator of Chromatin A4 (SMARCA4) core complex in epithelial innate response (RNA-seq)

| PRJNA679615 | ENA

Role of SWI/SNF-Related, Matrix Associated, Actin Dependent Regulator of Chromatin A4 (SMARCA4) core complex in epithelial innate response (ATAC-seq)

Project description:Role of SWI/SNF-Related, Matrix Associated, Actin Dependent Regulator of Chromatin A4 (SMARCA4) core complex in epithelial innate response (ATAC-seq)

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SWI/SNF Subunits SMARCA4, SMARCD2 and DPF2 Collaborate in MLL-Rearranged Leukaemia Maintenance.

Project description:Alterations in chromatin structure caused by deregulated epigenetic mechanisms collaborate with underlying genetic lesions to promote cancer. SMARCA4/BRG1, a core component of the SWI/SNF ATP-dependent chromatin-remodelling complex, has been implicated by its mutational spectrum as exerting a tumour-suppressor function in many solid tumours; recently however, it has been reported to sustain leukaemogenic transformation in MLL-rearranged leukaemia in mice. Here we further explore the role of SMARCA4 and the two SWI/SNF subunits SMARCD2/BAF60B and DPF2/BAF45D in leukaemia. We observed the selective requirement for these proteins for leukaemic cell expansion and self-renewal in-vitro as well as in leukaemia. Gene expression profiling in human cells of each of these three factors suggests that they have overlapping functions in leukaemia. The gene expression changes induced by loss of the three proteins demonstrate that they are required for the expression of haematopoietic stem cell associated genes but in contrast to previous results obtained in mouse cells, the three proteins are not required for the expression of c-MYC regulated genes.

| S-EPMC4646637 | biostudies-literature

siRNA Knockdown of SWI/SNF complex proteins in prostate cancer cell lines

Project description:Here we performed transcriptional profiling of the prostate cancer cell lines LNCaP and 22Rv1 comparing non-targeting siRNA treatment versus siRNAs targeting SWI/SNF complex proteins (SMARCA2, SMARCA4, and SMARCB1). Goal was to determine the effect of SWI/SNF knockdown on gene expression in prostate cancer. Two-condition experiment: non-targeting siRNA versus SWI/SNF-siRNA treated cells. Three SWI/SNF proteins were targeted: SMARCA2, SMARCA4, and SMARB1. Biological replicates: 1 control replicate, 2 treatment replicates per SWI/SNF protein. Technical replicates: 1 replicate per SWI/SNF protein. Cell lines: 22Rv1 and LNCaP.

2013-07-20 | E-GEOD-40384 | biostudies-arrayexpress

Structure of an actin-related subcomplex of the SWI/SNF chromatin remodeler.

Project description:The packaging of DNA into nucleosomal structures limits access for templated processes such as transcription and DNA repair. The repositioning or ejection of nucleosomes is therefore critically important for regulated events, including gene expression. This activity is provided by chromatin remodeling complexes, or remodelers, which are typically large, multisubunit complexes that use an ATPase subunit to translocate the DNA. Many remodelers contain pairs or multimers of actin-related proteins (ARPs) that contact the helicase-SANT-associated (HSA) domain within the catalytic ATPase subunit and are thought to regulate ATPase activity. Here, we determined the structure of a four-protein subcomplex within the SWI/SNF remodeler that comprises the Snf2 HSA domain, Arp7, Arp9, and repressor of Ty1 transposition, gene 102 (Rtt102). Surprisingly, unlike characterized actin-actin associations, the two ARPs pack like spoons and straddle the HSA domain, which forms a 92-Å-long helix. The ARP-HSA interactions are reminiscent of contacts between actin and many binding partners and are quite different from those in the Arp2/3 complex. Rtt102 wraps around one side of the complex in a highly extended conformation that contacts both ARPs and therefore stabilizes the complex, yet functions to reduce by ?2.4-fold the remodeling and ATPase activity of complexes containing the Snf2 ATPase domain. Thus, our structure provides a foundation for developing models of remodeler function, including mechanisms of coupling between ARPs and the ATPase translocation activity.

| S-EPMC3587198 | biostudies-literature

Exploring TCR-like CAR-Engineered Lymphocyte Cytotoxicity against MAGE-A4

Project description:In this work, we compared the expression profiles of Anti-MAGE-A4- transduced T-cells with Anti-MAGE-A4- transduced T-cells co-cultured with SK-Mel-37.

2023-07-31 | GSE238191 | GEO

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