Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Cell State Dependent Alteration of Melanoma Plasticity and Immunity by the Circadian Transcription Factor Bmal1 [scRNA-Seq]

ABSTRACT: Cell State Dependent Alteration of Melanoma Plasticity and Immunity by the Circadian Transcription Factor Bmal1 [scRNA-Seq]

PROVIDER: PRJNA835344 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR19094385.fastq.gz	Fastqsanger.gz
	SRR19094386.fastq.gz	Fastqsanger.gz
	SRR19094387.fastq.gz	Fastqsanger.gz
	SRR19094388.fastq.gz	Fastqsanger.gz
	SRR19094389.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 6

Similar Datasets

Cell State Dependent Alteration of Melanoma Plasticity and Immunity by the Circadian Transcription Factor Bmal1

Project description:Cell State Dependent Alteration of Melanoma Plasticity and Immunity by the Circadian Transcription Factor Bmal1

| PRJNA835337 | ENA

Cell State Dependent Alteration of Melanoma Plasticity and Immunity by the Circadian Transcription Factor Bmal1 [RNA-Seq]

Project description:The circadian transcription factor Bmal1 accelerates melanoma tumorigenesis through initial cell state dependent mechanisms in which Hif1??, Sox9 or Myh9, MRTF-SRF, AP-1 are involved and modulate tumor microenvironment to favor tumor growth

2023-05-04 | GSE202284 | GEO

Cell State Dependent Alteration of Melanoma Plasticity and Immunity by the Circadian Transcription Factor Bmal1 [ChIP-Seq]

2023-05-04 | GSE202288 | GEO

Cell State Dependent Alteration of Melanoma Plasticity and Immunity by the Circadian Transcription Factor Bmal1 [scRNA-Seq]

2023-05-04 | GSE202287 | GEO

Cell State Dependent Alteration of Melanoma Plasticity and Immunity by the Circadian Transcription Factor Bmal1 [ChIP-Seq II]

2023-05-04 | GSE214318 | GEO

Cell State Dependent Alteration of Melanoma Plasticity and Immunity by the Circadian Transcription Factor Bmal1 [ChIP-Seq]

Project description:Cell State Dependent Alteration of Melanoma Plasticity and Immunity by the Circadian Transcription Factor Bmal1 [ChIP-Seq]

| PRJNA835343 | ENA

Cell State Dependent Alteration of Melanoma Plasticity and Immunity by the Circadian Transcription Factor Bmal1 [RNA-Seq]

Project description:Cell State Dependent Alteration of Melanoma Plasticity and Immunity by the Circadian Transcription Factor Bmal1 [RNA-Seq]

| PRJNA835345 | ENA

Cell State Dependent Alteration of Melanoma Plasticity and Immunity by the Circadian Transcription Factor Bmal1 [ChIP-Seq II]

Project description:Cell State Dependent Alteration of Melanoma Plasticity and Immunity by the Circadian Transcription Factor Bmal1 [ChIP-Seq II]

| PRJNA884733 | ENA

Cell State Dependent Effects of Bmal1 on Melanoma Immunity and Tumorigenicity

Project description:The circadian clock regulator Bmal1 modulates tumorigenesis, but its reported effects are often inconsistent. Here, we show that Bmal1 has a context-dependent role in mouse melanoma tumor growth. Loss of Bmal1 in YUMM or B16 melanoma cells eliminated clock function, and diminished hypoxic gene expression signature and tumorigenesis, which could be rescued by ectopic expression of HIF-1a. By contrast, over-expressed wild-type or a dominant negative Bmal1 non-canonically sequestered myosin heavy chain 9 (Myh9) to increase MRTF-SRF activity and AP-1 transcriptional signature, and shift YUMM 2.1 cells from a Sox10high to a Sox9high immune resistant, mesenchymal cell state that is found in human melanomas. Our work uncovers a link between Bmal1, Myh9, mouse melanoma cell plasticity, and tumor immunity. This connection may underlie cancer therapeutic resistance and underpin the link between the circadian clock, MRTF-SRF and the cytoskeleton.

| MSV000090431 | MassIVE

The BMAL1/HIF2A heterodimer modulates circadian variations of myocardial injury

Project description:Cardiac injury following myocardial infarction exhibits a circadian pattern, yet the underlying mechanism remains unclear. To elucidate genes governing circadian variation of myocardial injury, we conducted transcriptomic profiling of left-ventricular tissues from mice or humans experiencing myocardial injury at different daytimes. Through comprehensive analyses, including transgenic mouse models and functional studies, we identified BMAL1 as a pivotal transcription factor modulating diurnal variation of myocardial injury. Remarkably, we discovered that BMAL1 regulates circadian-dependent cardiac injury by forming a transcriptionally active heterodimer with HIF2A. Substantiating this finding, we determined the cryo-EM structure of the BMAL1/HIF2F/DNA complex, revealing a previously unknown capacity for structural rearrangement within BMAL1. Furthermore, we confirmed amphiregulin (AREG) as a transcriptional target of the BMAL1/HIF2A heterodimer, critical for modulating circadian variation of myocardial injury. Finally, targeting the BMAL1/HIF2A-AREG pathway via timed AREG administration or enhancing circadian rhythm pharmacologically offered significant cardioprotection, implicating this pathway in treating ischemic heart disease.

2024-03-20 | GSE255307 | 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