Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

M229-Par and M229-Res cells

ABSTRACT: M229-Par and M229-Res cells

PROVIDER: PRJNA834748 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR19052804_1.fastq.gz	Fastqsanger.gz
	SRR19052804_2.fastq.gz	Fastqsanger.gz
	SRR19052805_1.fastq.gz	Fastqsanger.gz
	SRR19052805_2.fastq.gz	Fastqsanger.gz
	SRR19052806_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 24

Similar Datasets

Analysis of open chromatin structures in M229-Par and M229-Res cells by ATAC seq analysis .

Project description:Briefly, Melanoma M229-Par and M229-Res were analysed for open chromatin structures using ATAC seq Analysis.

2022-07-07 | GSE202117 | GEO

Analysis of M229-Par and M229-Res cells by Illumina HiSeq instrument (4000 or equivalent) seq analysis .

Project description:Briefly, Melanoma M229-Par and M229-Res were analysed for transcriptional changes using RNA seq Analysis.

2022-07-07 | GSE202118 | GEO

Analysis of open chromatin structures in M229-Par and M229-Res cells by ATAC seq analysis .

Project description:Analysis of open chromatin structures in M229-Par and M229-Res cells by ATAC seq analysis .

| PRJNA834744 | ENA

Analysis of M229-Par and M229-Res cells by Illumina HiSeq instrument (4000 or equivalent) seq analysis .

Project description:Analysis of M229-Par and M229-Res cells by Illumina HiSeq instrument (4000 or equivalent) seq analysis .

| PRJNA834743 | ENA

Acinetobacter baumannii strain:RES-1687 | isolate:RES-1687

Project description:Acinetobacter baumannii strain:RES-1687 | isolate:RES-1687 Genome sequencing and assembly

| PRJNA907294 | ENA

M229-Par and M229-Res cells

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

2022-07-07 | GSE202122 | GEO

PAR-TERRA RNA directs homologous sex chromosome pairing

Project description:In mammals, homologous chromosomes rarely pair outside meiosis. One exception is the X chromosome, which transiently pairs during X-chromosome inactivation (XCI). How two chromosomes find each other in 3D space is not known. Here, we reveal a required interaction between the X-inactivation center (Xic) and the telomere in mouse embryonic stem (ES) cells. The subtelomeric, pseudoautosomal regions (PARs) of the two sex chromosomes (X and Y) also undergo pairing in both female and male cells. PARs transcribe a class of telomeric RNA, dubbed PAR-TERRA, which accounts for a vast majority of all TERRA transcripts. PAR-TERRA binds throughout the genome, including to the PAR and Xic. During X-chromosome pairing, PAR-TERRA anchors the Xic to the PAR, creating a ‘tetrad’ of pairwise homologous interactions (Xic–Xic, PAR–PAR, and Xic–PAR). Xic pairing occurs within the tetrad. Depleting PAR-TERRA abrogates pairing and blocks initiation of XCI, whereas autosomal PAR-TERRA induces ectopic pairing. We propose a ‘constrained diffusion model’ in which PAR-TERRA creates an interaction hub to guide Xic homology searching during XCI.

2017-07-10 | GSE69887 | GEO

Chromatin Immunoprecipation Sequencing in 3T3-L1 preadipocytes using Par-4 antibody

Project description:Prostate apoptosis response-4 (Par-4) is a tumor suppressor protein that is extensively investigated in cancer. The objective of this study is to determine the physiological function of Par-4 in normal cells. Our findings indicated that genetic loss of Par-4 in mice primarily results in adipocyte hypertrophy and obesity, and secondary leads to hepatic steatosis and insulin resistance. Moreover, we noted that Par-4 is downregulated in human subjects who are likely to become obese in the future, thereby serving as a predictor of obesity. Importantly, ChIP-Seq indicated that MDM2 is a target of Par-4 protein, which is known to function as a transcriptional coregulator. We show that Par-4 loss upregulates MDM2 target protein p53, and that p53 further induces complement factor C3 and its proteolytic fragment acylation stimulating protein (ASP), an adipokine that is known to be causally associated with obesity. These studies led to the identification of the Par-4-MDM2-p53-C3/ASP axis in regulation of obesity by Par-4.

2022-03-25 | GSE159147 | GEO

Tumor suppressor Par-4 activates autophagy-dependent ferroptosis

Project description:Ferroptosis is a unique iron-dependent form of non-apoptotic cell death characterized by devastating lipid peroxidation. Whilst growing evidence suggests that ferroptosis is a type of autophagy-dependent cell death, the underlying molecular mechanisms regulating ferroptosis are largely unknown. In this study, through an unbiased RNA-sequencing screening, we demonstrate the activation of a multi-faceted tumor-suppressor protein Par-4/PAWR during ferroptosis. Functional studies reveal that genetic depletion of Par-4 effectively blocks ferroptosis, whereas Par-4 overexpression sensitizes cells to undergo ferroptosis. More importantly, we have determined that Par-4-triggered ferroptosis is mechanistically driven by the autophagic machinery. Upregulation of Par-4 promotes activation of ferritinophagy (autophagic degradation of ferritin) via the nuclear receptor co-activator 4 (NCOA4), resulting in excessive release of free labile iron and, hence, enhanced lipid peroxidation and ferroptosis. Inhibition of Par-4 dramatically suppresses the NCOA4-mediated ferritinophagy signaling axis. Our results also establish that Par-4 activation positively correlates with reactive oxygen species (ROS) production, which is critical for ferritinophagy-mediated ferroptosis. Furthermore, Par-4 knockdown effectively blocked ferroptosis-mediated tumor suppression in the mouse xenograft models. Collectively, these findings reveal that Par-4 has a crucial role in ferroptosis, which could be further exploited for cancer therapy.

2024-05-24 | GSE267823 | GEO

Escherichia coli strain:PAR

Project description:Escherichia coli PAR genome

| PRJNA292046 | ENA