Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

RNA-seq analysis of PRMT5 targeted genes in Tu686 cells

ABSTRACT: RNA-seq analysis of PRMT5 targeted genes in Tu686 cells

PROVIDER: PRJNA646318 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR12223772_1.fastq.gz	Fastqsanger.gz
	SRR12223772_2.fastq.gz	Fastqsanger.gz
	SRR12223773_1.fastq.gz	Fastqsanger.gz
	SRR12223773_2.fastq.gz	Fastqsanger.gz
	SRR12223774_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 8

Similar Datasets

RNA-seq analysis of PRMT5 targeted genes in Tu212 cells

Project description:RNA-seq analysis of PRMT5 targeted genes in Tu212 cells

| PRJNA655917 | ENA

RNA-seq analysis of PRMT5 targeted genes in Tu212 cells

Project description:RNA-sequencing was performed to identify the possible underlying signaling pathway of PRMT5 overexpressing in Tu212 cells. Cells were treated with pEZ-PRMT5 or pEZ-Vector.

2020-08-08 | GSE155879 | GEO

RNA-seq analysis of PRMT5 targeted genes in Tu686 cells

Project description:RNA-seq was performed to identify transcriptional targets of PRMT5 in Tu686 cells treated with shPRMT5 or shNC.PRMT5 was abnormally upregulated in high-grade laryngeal carcinoma tissues. The expression of PRMT5 was positively correlated with tumor stages, lymphatic metastasis and poor outcome.. Western blotting and immunofluorescence analyses observed that PRMT5 expression significantly downregulation of E-cadherin and upregulationg of N-cadherin, Snail and MMP9 in laryngeal carcinoma cells. All these changes were further confirmed by RNA-seq analysis of biological process and cellular component.

2020-07-16 | GSE154449 | GEO

RNA-seq analysis of PRMT5-regulated genes in irradiated/non-irradiated LNCaP cells

Project description:DNA Double-strand break (DSB) repair is critical for cell survival and genome integrity. Upon recognition of DSBs, repair proteins are transiently upregulated to facilitate repair through homologous recombination (HR) or non-homologous end joining (NHEJ). We present evidence that PRMT5 cooperates with pICln to function as a master epigenetic activator of DNA damage response (DDR) genes involved in HR, NHEJ, and G2 arrest (including RAD51, BRCA1, and BRCA2) to upregulate gene expression upon DNA damage. Contrary to the predominant role of PRMT5 as an epigenetic repressor, our results demonstrate that PRMT5 and pICln can activate gene expression, potentially independent of PRMT5’s obligate cofactor MEP50. Targeting PRMT5 or pICln hinders repair of DSBs in multiple cancer cell lines, and both PRMT5 and pICln expression positively correlates with DDR genes across 32 clinical cancer data sets. Thus, targeting PRMT5 or pICln may be explored in combination with radiation or chemotherapy for cancer treatment.

2019-12-05 | GSE111620 | GEO

RNA deep sequencing to compare genome-wide differences between PRMT5/knockdown and control AML cells

Project description:We report the pro-leukemic activities of PRMT5 in AML partly via modulating the transcription of key genes. The goal of this experiment is to confirm the changes observed in expression of genes targeted by PRMT5 activities. RNA Deep sequencing was employed to validate and reproduce the changes measured by quantitative reverse transcription polymerase chain reaction (qRTâPCR) techniques. Total RNA samples from MV4-11 cell line (FLT3-ITD AML) following PRMT5 knockdown using specific short hairpin RNA (shRNA) was used to compare gene expression pattern between PRMT5/Knockdown and control (control: MV4-11 cells transduced with scramble control).

2016-05-19 | E-GEOD-75215 | biostudies-arrayexpress

ChIP-on-chip from MDA-MB-231 cells with PHF1, CUL4B and PRMT5

Project description:It has been reported that PHF1, CUL4B and PRMT5 all play important roles in epigenetic regulation. We reported that PHF1, CRL4B and PRMT5 may act as a complex in transcriptional regulation and have a vital effect in breast cancer progression. So we performed ChIP-on-chip assays to find unique promoters co-targeted by PHF1, CUL4B and PRMT5. PHF1, CUL4B and PRMT5 have a predominant cooperation, at least in MDA-MB-231 cells. comparison of PHF1, CUL4B and PRMT5 target genes

2016-07-07 | E-GEOD-84071 | biostudies-arrayexpress

RNA-seq analysis of 22Rv1 cells with PRMT5, MEP50, pICln knockdown

Project description:PRMT5 is a methyltransferase that catalyzes symmetric dimethylation of arginine residues in histones (H4R3, H3R8, H3R2, and H2AR3) to regulate transcription of target genes. While PRMT5 is generally considered an epigenetic repressor, recent evidence from our lab and others demonstrate that PRMT5 also functions as an epigenetic activator. Although in vitro biochemical studies suggest that the PRMT5 interacting proteins methylosome protein 50 (MEP50) and methylosome subunit pICln enhance PRMT5 enzymatic activity, how these interacting proteins cooperate with PRMT5 to regulate gene transcription in vivo remains to be elucidated. Here we perform RNA-seq analysis of prostate cancer cells 22Rv1 with knockdown of PRMT5, MEP50, and pICln, in order to elucidate how these proteins control transcriptome.

2022-05-05 | GSE154951 | GEO

Resistance to PRMT5-targeted therapy in mantle cell lymphoma

Project description:Mantle cell lymphoma (MCL) is an incurable B-cell non-Hodgkin lymphoma, and patients who relapse on targeted therapies have poor prognosis. Protein arginine methyltransferase 5 (PRMT5), an enzyme essential for B-cell transformation, drives multiple oncogenic pathways and is overexpressed in MCL. Despite the antitumor activity of PRMT5 inhibition (PRT-382/PRT-808), drug resistance was observed in a patient-derived xenograft (PDX) MCL model. Decreased survival of mice engrafted with these PRMT5 inhibitor-resistant cells vs treatment-naive cells was observed (P = .005). MCL cell lines showed variable sensitivity to PRMT5 inhibition. Using PRT-382, cell lines were classified as sensitive (n = 4; 50% inhibitory concentration [IC50], 20-140 nM) or primary resistant (n = 4; 340-1650 nM). Prolonged culture of sensitive MCL lines with drug escalation produced PRMT5 inhibitor-resistant cell lines (n = 4; 200-500 nM). This resistant phenotype persisted after prolonged culture in the absence of drug and was observed with PRT-808. In the resistant PDX and cell line models, symmetric dimethylarginine reduction was achieved at the original PRMT5 inhibitor IC50, suggesting activation of alternative resistance pathways. Bulk RNA sequencing of resistant cell lines and PDX relative to sensitive or short-term-treated cells, respectively, highlighted shared upregulation of multiple pathways including mechanistic target of rapamycin kinase [mTOR] signaling (P < 10-5 and z score > 0.3 or < 0.3). Single-cell RNA sequencing analysis demonstrated a strong shift in global gene expression, with upregulation of mTOR signaling in resistant PDX MCL samples. Targeted blockade of mTORC1 with temsirolimus overcame the PRMT5 inhibitor-resistant phenotype, displayed therapeutic synergy in resistant MCL cell lines, and improved survival of a resistant PDX.

2024-04-09 | GSE229517 | GEO

Resistance to PRMT5 Inhibitor Targeted Therapy in MCL [RNA-seq]

Project description:Resistance to PRMT5 Inhibitor Targeted Therapy in MCL [RNA-seq]

| PRJNA1004222 | ENA

Resistance to PRMT5 Inhibitor Targeted Therapy in MCL [RNA-seq]

Project description:To identify the transcriptomic changes underlying acquired PRMT5 inhibitor resistance in MCL cell lines (n=3/group) and MCL PDX

2023-12-30 | GSE240555 | 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