Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Altered BAF53A (ACTL6A) Stoichiometry Drives Human Squamous Cell Carcinoma [CnR]

ABSTRACT: Altered BAF53A (ACTL6A) Stoichiometry Drives Human Squamous Cell Carcinoma [CnR]

PROVIDER: PRJNA659023 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR12508510_1.fastq.gz	Fastqsanger.gz
	SRR12508510_2.fastq.gz	Fastqsanger.gz
	SRR12508511_1.fastq.gz	Fastqsanger.gz
	SRR12508511_2.fastq.gz	Fastqsanger.gz
	SRR12508512_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 88

Similar Datasets

Altered BAF53A (ACTL6A) Stoichiometry Drives Human Squamous Cell Carcinoma [RNA-seq]

Project description:Altered BAF53A (ACTL6A) Stoichiometry Drives Human Squamous Cell Carcinoma [RNA-seq]

| PRJNA659021 | ENA

Altered BAF53A (ACTL6A) Stoichiometry Drives Human Squamous Cell Carcinoma [ATAC-seq]

Project description:Altered BAF53A (ACTL6A) Stoichiometry Drives Human Squamous Cell Carcinoma [ATAC-seq]

| PRJNA659022 | ENA

Altered BAF53A (ACTL6A) Stoichiometry Drives Human Squamous Cell Carcinoma [CnR]

Project description:To determine whether the chromatin accessibility for YAP/TEADs in squamous cell carcinoma cells is directly regulated by BAF53A within BAF complexes, we performed CUT&RUN to profile the distribution of YAP, TEAD1, and BAF155 (a DNA binding subunit of BAF complexes) across the genome.

2021-10-29 | GSE156787 | GEO

Altered BAF53A (ACTL6A) Stoichiometry Drives Human Squamous Cell Carcinoma [RNA-seq]

Project description:To identify genes regulated by BAF53A, we carried out RNA-seq analysis in three SCC cell lines after BAF53A knockdown by siRNA and in normal keratinocytes with BAF53A overexpression.

2021-10-29 | GSE156785 | GEO

Altered BAF53A (ACTL6A) Stoichiometry Drives Human Squamous Cell Carcinoma [ATAC-seq]

Project description:To identify accessible chromatin regions regulated BAF53A in squamous cell carcinomas (SCCs), we performed ATAC-seq in FaDu SCC cell lines after BAF53A knockdown by siRNA and in normal keratinocytes with BAF53A overexpression.

2021-10-29 | GSE156786 | GEO

ACTL6a Enforces the Epidermal Progenitor State by Suppressing SWI/SNF-Dependent Induction of KLF4

Project description:Somatic progenitors suppress differentiation to maintain tissue self-renewal. While epigenetic regulators of DNA and histone modifications can support such repression, a role for nuclear actin-like proteins is unclear. In epidermis, ACTL6a/BAF53A was found enriched in progenitors and down-regulated during differentiation. Conditional ACTL6a deletion abolished epidermal self-renewal and induced terminal differentiation, whereas ectopically expressed ACTL6a suppressed differentiation. Among known activators of epidermal differentiation, KLF4 was found to control 227 genes also regulated by ACTL6a. ACTL6a loss upregulated KLF4 and its target genes, effects that were blocked by KLF4 depletion. Among multiple ACTL6a-interacting epigenetic regulators, the SWI/SNF complex was required for KLF4 activation and differentiation. In progenitors, ACTL6a loss led to enhanced SWI/SNF binding to the promoters of KLF4 and other differentiation genes. ACTL6a thus maintains the undifferentiated progenitor state, in part by suppressing SWI/SNF complex-enabled induction of KLF4. Gene expression analysis: To identify the gene set controlled by ACTL6a in human keratinocyte. Total RNA was isolated in biologic duplicate from cells with ACTL6a loss as compared to controls, and hybridized to Affymetrix HG-U133 2.0 Plus arrays.

2012-11-30 | E-GEOD-36222 | biostudies-arrayexpress

ACTL6a Enforces the Epidermal Progenitor State by Suppressing SWI/SNF-Dependent Induction of KLF4

2012-11-30 | GSE36222 | GEO

Antarctica Stoichiometry

Project description:Antarctica Stoichiometry Targeted loci

| PRJNA476992 | ENA

ACTL6a knockout peripheral nerve RNA seq at postnatal day 3

Project description:Cells need to integrate chemical and physical signals into transcriptional programs. In the peripheral nerves, axonal caliber selection by specialized Schwann cells, is critical for developmental myelination. However, only mechanisms through which Schwann cells sense chemical signals are well characterized. We identify ACtin-Like protein 6a (ACTL6a), a component of the SWI/SNF chromatin remodeling complex, as critical for axonal caliber recognition and developmental myelination. ACTL6a is expressed in the developing nerve and, when activated by contact with axons or nanofibers of specific caliber, it promotes the eviction of repressive histone marks thereby enhancing the transcriptional program of myelination. Mutant mice with Schwann cells lacking ACTL6a display aberrant recognition of axonal caliber, resulting in defective radial sorting and lower levels of transcripts regulating myelination of developing nerves. We suggest that developing peripheral nerves require an ACTL6a-dependent integration of physical and chemical signals in Schwann cells to release of repressive histone modifications and promote myelination.

2022-03-08 | GSE179340 | GEO

Microarray Samples for shACTL6A in HNSCC Cells to Investigate How ACTL6A and p63 Activate Hippo-YAP in SCC

Project description:Loss-of-function mutations in SWI/SNF chromatin remodeling subunit genes are observed in many cancers, but an oncogenic role for SWI/SNF is not well established. Here we reveal that ACTL6A, encoding a SWI/SNF subunit linked to stem and progenitor cell function, is frequently co-amplified and highly expressed together with the p53 family member p63 in head and neck squamous cell carcinoma (HNSCC). ACTL6A and p63 physically interact and cooperatively control a transcriptional program that promotes proliferation and suppresses differentiation, in part through activation of the Hippo-YAP pathway via regulators including WWC1. Consequently, loss of ACTL6A or p63 in tumor cells induces YAP phosphorylation and inactivation, associated with growth arrest and terminal differentiation, all phenocopied by WWC1 overexpression. In vivo, ectopic ACTLC6A/p63 expression promotes tumorigenesis, while ACTL6A expression and YAP activation are highly correlated in primary HNSCC and predict poor patient survival. Thus, ACTL6A and p63 collaborate as oncogenic drivers in HNSCC. Gene expression profiling of HNSCC cells with and without ablated endogenous ACTL6A via lentiviral shRNA.

2016-11-18 | GSE88831 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data