Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

GSTM1 binding RNA RIP-seq

ABSTRACT: GSTM1 binding RNAs were analyzed by imprinting RNA-sequencing of specific antibody-retrieved complexes from peritoneal macrophage cells lysis.

ORGANISM(S): Mus musculus

PROVIDER: GSE134024 | GEO | 2020/12/21

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

GOT2 binding RNA RIP-seq

Project description:Flag-taged GOT2 binding RNAs were analyzed by imprinting RNA-sequencing of Flag antibody-retrieved complexes from MEF cells lysis.

2017-12-14 | GSE100229 | GEO

Ribosome binding RNA from mouse macrophage cells

Project description:Ribosome binding RNAs were analyzed by imprinting RNA-sequencing of ribosome-retrieved complexes from mouse macrophage cells lysis.

2017-12-14 | GSE100739 | GEO

GSTM1 binding RNA RIP-seq

Project description:GSTM1 binding RNA RIP-seq

| PRJNA553509 | ENA

IRF3-binding RNA RIP-seq

Project description:Flag-taged IRF3-binding RNAs were analyzed by imprinting RNA-sequencing of anti-flag antibody-retrieved complexes from macrophages lysate.

2021-11-09 | GSE138699 | GEO

Ac4c modifications down-regulation in macrophages promotes suppressive tumor microenvironment in HCC (RIP-Seq)

Project description:Ac4C-binding RNAs were analyzed by imprinting RNA-sequencing of anti-Ac4C antibody-retrieved complexes from macrophages lysate. We then performed gene expression profiling analysis using data obtained from RIP-seq of peritoneal macrophages incubated with IFN-G

2024-01-31 | GSE227526 | GEO

Effects of GSTM1 knockdown on astrocyte transcriptional responses to TNF-alpha stimulation

Project description:To investigate the role of GSTM1, we knocked down GSTM1 expression in primary mouse astrocytes using lenvirtus vector expressing Gstm1 shRNAmir and then exposed them to TNF-alpha. Non-silencing shRNAmir and non-stimulation served as shRNA and treatment controls, respectively.

2023-01-25 | GSE217052 | GEO

GSTM1 null genotype underpins recurrence of NF2 meningiomas

Project description:Introduction: Meningiomas are the most common primary central nervous system (CNS) tumor in adults, comprising one-third of all primary adult CNS tumors. Although several recent publications have identified molecular alterations in meningioma including characteristic mutations, copy number alterations, and gene expression signatures, our understanding of the drivers of meningioma recurrence is limited. Objective: To identify gene expression signatures of 1p-22q-NF2- meningioma recurrence, with concurrent biallelic inactivation of NF2 and loss of chr1p that are heterogenous but enriched for recurrent meningiomas. Methods: Transcriptomic alterations present in recurrent versus primary 1p-22q-NF2- meningiomas were identified using RNA sequencing (RNA-seq) data in a clinically annotated cohort. Results: Recurrent 1p-22q-NF2- meningiomas were enriched for a newly identified GSTM1 null genotype compared to primary meningiomas that showed variable GSTM1 expression and independent external validation was performed. Conclusions: The GSTM1 null genotype is a novel biomarker of 1p-22q-NF2- meningioma recurrence that resolves heterogeneity in existing meningioma subtypes and may be used to guide future clinical management decisions on extent of treatment to improve patient outcomes.

2024-12-09 | GSE283616 | GEO

PRDM16 restricts cellular senescence by upregulating GSTM1

Project description:Cellular senescence is a hallmark of aging, and the accumulation of senescent cells (SnCs) accelerates the aging process and contributes to aging-related organ disorders. The PRDMs exhibit robust transcriptional regulatory activity and govern a wide range of biological processes. However, the role of PRDMs in cellular senescence and aging remain unclear. Here, we have demonstrated that PRDM16, among PRDMs, is decreased significantly in multiple organs of aged mice compared to young mice. Global Prdm16 deletion contributes to cellular senescence in various organs, including the kidney, heart, lung, brain hippocampus, stomach, and gut; subsequently leading to accelerated aging-related organ injury. Furthermore, tubular specific Prdm16 deletion aggravates irradiation induced kidney aging, and aging-related kidney disease subjected to ischemia reperfusion surgery. Exogenous PRDM16 gene delivery by lentivirus effectively attenuates cellular senescence in vitro and in vivo. Mechanistically, PRDM16 improves glutathione metabolism and inhibits oxidative DNA damage, the driving force of senescence. Especially, PRDM16 increases glutathione-S-transferase activity by upregulating the transcription of GSTM1. Transfection of GSTM1 restored cellular senescence and kidney aging caused by PRDM16 deficiency. Taken together, we provide a potential target for investigating the anti-aging therapy.

2025-08-25 | GSE275768 | GEO

PRDM16 restricts cellular senescence by upregulating GSTM1

Project description:PRDM16 restricts cellular senescence by upregulating GSTM1

| PRJNA1152955 | ENA

PRDM16 reduces cellular senescence by upregulating GSTM1

Project description:PRDM16 reduces cellular senescence by upregulating GSTM1

| PRJNA1314125 | ENA