Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

RNAseq in Acly wild-type or conditional KO mouse T-ALLs

ABSTRACT: RNAseq in Acly wild-type or conditional KO mouse T-ALLs

PROVIDER: PRJNA945381 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR23878300_1.fastq.gz	Fastqsanger.gz
	SRR23878300_2.fastq.gz	Fastqsanger.gz
	SRR23878301_1.fastq.gz	Fastqsanger.gz
	SRR23878301_2.fastq.gz	Fastqsanger.gz
	SRR23878302_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 36

Similar Datasets

RNAseq in Acly wild-type or conditional KO mouse T-ALLs

Project description:RNAseq in Acly wild-type or conditional KO mouse T-ALLs

| PRJNA1127506 | ENA

ChIPseq in Acly wild-type or conditional KO mouse T-ALLs

Project description:ChIPseq in Acly wild-type or conditional KO mouse T-ALLs

| PRJNA1127521 | ENA

RNAseq in Acly wild-type or conditional KO mouse T-ALLs

Project description:C57BL6 mice harboring Acly conditional knockout NOTCH1-ΔE-induced leukemias were treated with vehicle (control) or tamoxifen to induce isogenic deletion of Acly. Here we report the gene expression profile of leukemic blasts obtained from the spleen from control- or tamoxifen-treated leukemic mice, either in an acute setting or in long-term survival setting

2025-03-15 | GSE227492 | GEO

RNAseq in Acly wild-type or conditional KO mouse T-ALLs

2025-02-11 | GSE270579 | GEO

ChIPseq in Acly wild-type or conditional KO mouse T-ALLs

Project description:C57BL6 mice harboring Acly conditional knockout NOTCH1-ΔE-induced leukemias were treated with vehicle (control) or tamoxifen to induce isogenic deletion of Acly.

2025-02-25 | GSE270580 | GEO

RNAseq in Sirt1 wild-type or conditional KO mouse T-ALLs

Project description:RNAseq in Sirt1 wild-type or conditional KO mouse T-ALLs

| PRJNA839727 | ENA

RNAseq in Sirt1 wild-type or conditional KO mouse T-ALLs

Project description:C57BL6 mice harboring Sirt1 conditional knockout NOTCH1-DE-induced leukemias were treated with vehicle (control) or tamoxifen to induce isogenic deletion of Sirt1. Here we report the gene expression profile of leukemic blasts obtained from the spleen from control- or tamoxifen-treated leukemic mice.

2022-12-08 | GSE203387 | GEO

Expression data by ACLY knockdown

Project description:De novo lipogenesis is activated in most cancers. Several lipogenic enzymes are implicated in oncogenesis and represent potential cancer therapeutic targets. RNA interference-mediated depletion of ATP citrate lyase (ACLY), the enzyme that catalyzes the first step of de novo lipogenesis, leads to growth suppression in a subset of human cancer cells. Here we demonstrate the molecular basis and potential biomarkers for ACLY-targeting therapy. First, suppression of cancer cell growth by ACLY depletion involves down-regulation of fatty acid elongase ELOVL6 at the transcriptional level. Lipid profiling revealed that ACLY depletion alters fatty acid composition in triglyceride; increased palmitate and decreased longer fatty acids, in accordance with ELOVL6 down-regulation. Second, ACLY depletion increases reactive oxygen species (ROS), whereas addition of antioxidant reduces ROS and attenuates the growth suppression. Third, ACLY depletion or ROS stimulation induce phosphorylation of AMP-activated protein kinase (AMPK), a sensor of energy and lipid metabolism. Analysis of various cancer cell lines revealed that the levels of AMPK phosphorylation (p-AMPK) correlate with the basal ROS levels, and that cancer cells with low basal p-AMPK (i.e., low basal ROS) levels are highly susceptible to ACLY depletion-mediated growth suppression. Finally, in clinical colon cancer tissues, p-AMPK levels are significantly decreased in aggressive tumors and correlate with the levels of 8-hydroxydeoxyguanosine, a hallmark of ROS stimulation. Together, these data suggest that ACLY inhibition suppresses cancer growth via palmitate-mediated lipotoxicity, and p-AMPK could be a predictive biomarker for its therapeutic outcome. Two cell lines are treated with ACLY siRNA. The samples include controls of each cell line.

2014-04-13 | E-GEOD-37243 | biostudies-arrayexpress

Inhibition of ACLY enhances tumor immunogenicity and resolves MASH-driven HCC

Project description:Immunosuppressive tumor microenvironments are common in cancers such as metabolic dysfunction-associated steatohepatitis (MASH)-driven hepatocellular carcinoma. To further investigate tumor–immune interactions, we performed spatial transcriptomics on livers from MASH-driven HCC mouse models (WD-DEN, WT or Acly KO mice and from WD-CCL4, Vehicle, or EVT0185 (100mg/kg) treated mice). GO enrichment analysis of spatially resolved tumor cells showed increased fatty acid and lipid metabolism in both Acly KO and EVT0185-treated mice Spatial analysis also revealed a selective increase in B cells, but not T cells, macrophages, or NKT cells, in tumors from Acly KO and EVT0185-treated mice.

2025-06-30 | GSE297081 | GEO