Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

A total RNA-Seq screen reveals that the splicing inhibitor Isoginkgetin blocks transcription elongation

ABSTRACT: Pharmacological perturbation is a powerful tool for understanding gene expression, but identification of the specific steps of this multi-step process targeted by small molecules remains challenging. Here we apply total RNA-Seq to distinguish specific pharmacological effects on transcription and pre-mRNA processing, revealing unexpectedly that the splicing inhibitor isoginkgetin blocks transcription elongation.An RNA-Seq screen reveals that the compounds TBBz and CYT387 mimic the transcriptional effects of isoginkgetin and are inhibitors of CSNK2A2, suggesting that isoginkgetin blocks transcription elongation via inhibition of CSNK2A2. Our results reveal RNA-Seq screening as a tool for disentangling complex pharmacological effects on gene expression.

ORGANISM(S): Homo sapiens

PROVIDER: GSE86857 | GEO | 2016/09/17

SECONDARY ACCESSION(S): PRJNA343235

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Isoginkgetin induces autophagic cell death in hepatocellular carcinoma [RNA-Seq]

Project description:Purpose: Our previous studies have identified Isoginkgetin as an inducer of autophagic cell death in hepatocellular carcinoma. We set out to analyze how isoginkgetin regulates gene expression in HepG2 cells. Methods: RNA-seq was performed with two repetitions in HepG2 followed by treatment with DMSO and 20 μM Isoginkgetin for 24 h. Conclusions: Isoginkgetin treatment reduces the expression of glucose transporters in HepG2 cells.

2023-03-22 | GSE188533 | GEO

Isoginkgetin induces autophagic cell death in hepatocellular carcinoma [ChIP-Seq]

Project description:Purpose: Our previous studies have identified isoginkgetin as an inducer of autophagic cell death in hepatocellular carcinoma. We set out to analyze how isoginkgetin regulates the genome-wide enhancer activity in HepG2 cells. Methods: ChIP-seq for H3K27ac was performed in HepG2 followed by treatment with 20 μM isoginkgetin for 24 h. Conclusions: Isoginkgetin treatment reduces the expression of glucose transporters and inhibts SLC2A1 enhancer activity in HepG2 cells.

2023-03-22 | GSE188534 | GEO

Isoginkgetin induces autophagic cell death in hepatocellular carcinoma [ChIP-seq 2]

Project description:Purpose: Our previous studies have identified isoginkgetin as an inducer of autophagic cell death in hepatocellular carcinoma. We set out to analyze how isoginkgetin regulates the genome-wide enhancer activity in HepG2 cells. Methods: ChIP-seqs for H3K4me, H4K8ac, H3K27me3 and H3K9ac were performed in HepG2 followed by treatment with 20 μM isoginkgetin for 24 h. Conclusions: Isoginkgetin treatment reduces the expression of glucose transporters and inhibts SLC2A1 enhancer activity in HepG2 cells.

2023-03-22 | GSE202612 | GEO

Microarray analysis of isoginkgetin-treated HCT116 and HCT116p53-/- cells

Project description:Isoginkgetin (IGG) is a small molecule inhibitor of the spliceosome although the direct target remains elusive. Widespread failure to accurately remove introns poses a risk to cells and organisms through the potential production of aberrant mRNAs and proteins. The cellular responses to accumulation of these intermediates and/or the direct interference of spliceosome assembly itself may constitute a splicing stress but this is not well defined yet. We used oligonucleotide microarrays to assess genome wide changes in gene expression associated with exposure to IGG in HCT116 cells and an isogenic subline lacking the p53 tumor suppressor that responds to a variety of transcriptional stresses (Oncogene 18 (3), 583-592). Two of the 3 enriched pathways identified using PANTHER analysis of differentially expressed transcripts are linked to the ATF4 transcription factor and these effects are p53-independent.

2021-07-23 | GSE180623 | GEO

Pharmacological Activation of STING blocks SARS-CoV-2 infection

Project description:Pharmacological Activation of STING blocks SARS-CoV-2 infection

| PRJNA699591 | ENA

Homo sapiens

Project description:A total RNA-Seq screen reveals that the splicing inhibitor Isoginkgetin blocks transcription elongation

| PRJNA343235 | ENA

Liver gene expression analysis of male ApoE-/- mice treated with Isoginkgetin

Project description:Isoginkgetin (ISOGK) is a biflavone derived from Ginkgo Biloba that inhibits RNA splicing. ISOGK has been reported to have various protective effects, including anti-inflammatory, antioxidant, and anti-tumorigenic properties. The study aimed to investigate the impact of ISOGK treatment on atherosclerosis induced by a Western diet in ApoE-/- mice. After seven weeks of a high-fat diet, ISOGK was administered intraperitoneally for eight weeks. At the endpoint, mice were euthanized for sample collection, and a series of indicators were tested. The study results indicate that the ISOGK treatment group significantly reduced the area of aortic plaques, aortic sinus plaques, and the necrotic core area. Additionally, ISOGK significantly lowered the levels of total cholesterol in the serum. These findings suggest that ISOGK is effective in treating atherosclerosis and reducing blood lipid levels.

2024-05-15 | GSE261858 | GEO

Microarray analysis of isoginkgetin-treated HCT116 and HCT116p53-/- cells

Project description:Microarray analysis of isoginkgetin-treated HCT116 and HCT116p53-/- cells

| PRJNA748989 | ENA

RNA sequencing analysis of isoginkgetin and thapsigargin treated HCT116 and HCT116 ATF4 deficient cells

Project description:Activating transcription factor 4 (ATF4) is activated during cellular stress through a pathway called the integrated stress response (ISR). We had previously reported that the splicing inhibitor isoginkgetin (IGG) activates ATF4 and ATF4-dependent transcripts. To determine the role of ATF4 in the transcriptional response to IGG, we used tandem CRISPR cas9 gene editing to create an ATF4 deficient HCT116 (colon cancer) cell line. We completed RNA sequencing on HCT116 parental and HCT116 ATF4 deficient cells treated with IGG, and thapsigargin (Tg), a positive control for ATF4 activation. We found that IGG led to the differential expression of 76 transcripts, and 58 of these were dependent on ATF4. Tg led to a far more robust transcriptional response, which appeared to be less ATF4 dependent.

2024-10-09 | GSE249009 | GEO

CTCF blocks anti-sense transcription initiation at divergent gene promoters [ChIP-Seq]

Project description:CTCF blocks anti-sense transcription initiation at divergent gene promoters [ChIP-Seq]

| PRJNA725535 | ENA