Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Identification of Transcription Factor MIZ1 Binding Sites in Human B Cell Lines [ChIP-seq]

ABSTRACT: Identification of Transcription Factor MIZ1 Binding Sites in Human B Cell Lines [ChIP-seq]

PROVIDER: PRJNA981123 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR24865674.fastq.gz	Fastqsanger.gz
	SRR24865675.fastq.gz	Fastqsanger.gz
	SRR24865676.fastq.gz	Fastqsanger.gz
	SRR24865677.fastq.gz	Fastqsanger.gz
	SRR24865678.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 8

Similar Datasets

Identification of Transcription Factor MIZ1 Binding Sites in Human B Cell Lines [ChIP-seq]

Project description:A previous study has successfully identified the binding sites of Transcription Factor MIZ1 in murine B cells. In order to shed light on the potential relevance between mouse and human, this experiment aimed to identify MIZ1's binding sites in human B cell lines. By uncovering these binding sites, we can gain insights into the conservation and potential functional significance of MIZ1 in B cell biology across species.

2025-06-07 | GSE234360 | GEO

Analysis of MIZ1, MYC-ER and MYC-ERVD binding sites in MCF10A cells

Project description:Oncogenic levels of Myc expression sensitize cells to multiple apoptotic stimuli and this protects long-lived organisms from cancer development. How cells discriminate physiological from supra-physiological levels of Myc is largely unknown. Here we show that induction of apoptosis by Myc in breast epithelial cells requires association of Myc with Miz1. Gene expression and ChIP-sequencing experiments show that oncogenic levels of Myc, but not of MycV394D, a point mutant that does not bind Miz1, recruit Miz1 to core promoters and enable binding of Myc/Miz1 complexes to low-affinity target sites, correlating with repression of a specific set of target genes. Repressed genes encode proteins involved in cell adhesion, migration and wound healing; their promoters are enriched for binding sites of the serum response (SRF) factor. Restoring SRF activity attenuates Myc-induced apoptosis in response to glutamine starvation, exposure to Trail and to DNA damage. We propose that supra-physiological levels of Myc engage Miz1 in repressive DNA binding complexes and suppress transcriptional progress.

2015-07-10 | GSE59146 | GEO

Analysis of MIZ1, MYC-ER and MYC-ERVD binding sites in MCF10A cells

2015-07-10 | E-GEOD-59146 | biostudies-arrayexpress

Identification of Transcription Factor Binding Sites using ATAC-seq

Project description:Identification of Transcription Factor Binding Sites using ATAC-seq

| PRJNA484892 | ENA

In vitro, genomic context identification of transcription factor binding sites

Project description:In vitro, genomic context identification of transcription factor binding sites

| PRJNA257554 | ENA

Widespread perturbation of ETS factor binding sites in cancer

Project description:Widespread perturbation of ETS factor binding sites in cancer

| PRJNA903909 | ENA

Widespread perturbation of ETS factor binding sites in cancer

Project description:Widespread perturbation of ETS factor binding sites in cancer

| PRJNA922088 | ENA

STARR-seq based mutagenesis of transcription factor binding sites

Project description:STARR-seq based mutagenesis of transcription factor binding sites

| PRJNA597469 | ENA

Analysis of MYC and MIZ1 binding and MIZ1-dependent gene expression changes in MCF10A cells

Project description:Analysis of MYC and MIZ1 binding and MIZ1-dependent gene expression changes in MCF10A cells

| PRJNA254495 | ENA

Miz1 is required to maintain autophagic flux

Project description:Miz1 is a zinc finger protein that regulates expression of cell cycle inhibitors as part of a complex with Myc. Cell cycle-independent functions of Miz1 are poorly understood. Here, we use a Nestin-Cre transgene to delete an essential domain of Miz1 in the central nervous system (Miz1ΔPOZNes). Miz1ΔPOZNes mice display cerebellar neurodegeneration characterized by the progressive loss of Purkinje cells. Chromatin immunoprecipitation sequencing and biochemical analyses show that Miz1 activates transcription upon binding to a non-palindromic sequence present in core promoters. Target genes of Miz1 encode regulators of autophagy and proteins involved in vesicular transport that are required for autophagy. Miz1ΔPOZ neuronal progenitors and fibroblasts show reduced autophagic flux. Consistently, polyubiquitinated proteins and p62/Sqtm1 accumulate in the cerebella of Miz1ΔPOZNes mice, characteristic features of defective autophagy. Our data suggest that Miz1 may link cell growth and ribosome biogenesis to the transcriptional regulation of vesicular transport and autophagy.

2013-09-27 | GSE48602 | 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