Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Transcriptome of Knockdown Pspc1 in the MS1 pancreatic islet endothelial cell line

ABSTRACT: Specific knockout Pspc1 in mouse endothelial cells cause neonatal death with multiple defects related to vascular development. The transcriptome of Pspc1 knockdown in MS1 cells corresponded to the findings from in-vivo model and reveal dampened signaling pathways.

ORGANISM(S): Mus musculus

PROVIDER: GSE205995 | GEO | 2022/06/16

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Transcriptome of Knockdown Pspc1 in the MS1 pancreatic islet endothelial cell line

Project description:Transcriptome of Knockdown Pspc1 in the MS1 pancreatic islet endothelial cell line

| PRJNA848769 | ENA

RNA sequencing (RNA-SEQ) of PSPC1 knockdown by shRNA in A549 cells

Project description:We show that PSPC1 is required for cancer cell motilities and stemness properties in vitro and lung metastasis in vivo. We used high throughput sequencing to analyze the PSPC1 regulated gene expression. Loss of PSPC1 results in significant gene expression level changes in thousands of individual transcripts in key regulators of the EMT, CSCs and TGFb signaling.

2018-02-02 | GSE65523 | GEO

RNA sequencing results of cell migration and adhesion induced by modulated expression of paraspeckle protein PSPC1

Project description:We found that PSPC1 potent facilitates HCC cells motility, adhesion, cytoskeleton assembling as well as cell spreading. To elucidate underlying mechanisms regulation by PSPC1, we performed the RNA-seq analysis of overexpression of PSPC1 in SK-Hep1 cell line and knockdown od PSPC1 in Hep3B cell line to evaluate its effects on gene expression.

2020-04-14 | GSE148551 | GEO

RNA sequencing (RNA-SEQ) of PSPC1 Knockout in A549 cells with TGFb1 stimulation

2018-04-10 | GSE103293 | GEO

RNA sequencing results of EMT and CSC phenotypes induced by modulated expression of wild-type and mutated PSPC1 and PTK6

Project description:We found that PSPC1 is the master activator for transcription factors of EMT and stemness and accompanies c-Myc activation to facilitate tumour growth. To elucidate mechanisms that the underlying post-translational modification of PSPC1, we performed the RNA-seq analysis of overexpression of PSPC1, alone and with PTK6, and PSPC1 tyrosine residue mutation in SK-Hep1 cells. We performed c-terminal of PSPC1 and its mutated nuclear localization site (NLS) in Mahlavu cells to evaluate its inhibitory effects on gene expression. Moreover, we further treated with HGF in Huh-7 cells to examineThe role of downstream signaling pathways of the PSPC1 and PTK6 regulation in microenviroment.

2019-05-22 | GSE114856 | GEO

A TET1-PSPC1-Neat1 molecular axis modulates PRC2 functions in controlling stem cell bivalency [ChIP-seq]

Project description:The mammalian Ten-eleven translocation (TET) family proteins regulate the epigenome through catalytic activity (CA)-dependent and -independent functions. While catalytic activity of TETs has been intensely studied as DNA demethylation enzymes, little is known about their CA-independent function in early embryo development. Here we defined the CA-independent function of TET1 in naïve-to-formative pluripotent states transition. Using a proteomics method, we mapped the TET1 interactome and identified Paraspeckle component 1 (PSPC1) as a partner of TET1 for transcriptional repression at the bivalent genes in early development. Genome-wide location analysis revealed that PSPC1-bound regions largely overlap with TET1 and Polycomb repressive complex 2 (PRC2) subunits. Functional studies with genetic methods indicated that PSPC1 and TET1 repress, while lncRNA Neat1 activates the bivalent genes during their transcriptional activation. In embryonic stem cell (ESC) state, Neat1 tethers TET1, PSPC1, and PRC2 at promoters. During the ESCs to formative Epiblast like stem cells (EpiLCs) differentiation, PSPC1 and TET1 repress the PRC2 affinity to nascent mRNA transcripts of bivalent genes, while Neat1 facilitates PRC2 binding to those transcripts. Our study reveals a molecular mechanism by which proteins TET1 and PSPC1, and lncRNA Neat1 dynamically regulate gene transcription by modulating the PRC2 activity in pluripotent states transition.

2022-06-07 | GSE182442 | GEO

A TET1-PSPC1-Neat1 molecular axis modulates PRC2 functions in controlling stem cell bivalency [RNA-seq]

2022-06-07 | GSE182441 | GEO