Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

ATF3 COORDINATES SERINE AND NUCLEOTIDE METABOLISM TO DRIVE CELL CYCLE PROGRESSION IN ACUTE MYELOID LEUKEMIA

ABSTRACT: ATF3 COORDINATES SERINE AND NUCLEOTIDE METABOLISM TO DRIVE CELL CYCLE PROGRESSION IN ACUTE MYELOID LEUKEMIA

PROVIDER: PRJNA723331 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR14288660.fastq.gz	Fastqsanger.gz
	SRR14288661.fastq.gz	Fastqsanger.gz
	SRR14288662.fastq.gz	Fastqsanger.gz
	SRR14288663.fastq.gz	Fastqsanger.gz
	SRR14288664.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 6

Similar Datasets

ATF3 COORDINATES SERINE AND NUCLEOTIDE METABOLISM TO DRIVE CELL CYCLE PROGRESSION IN ACUTE MYELOID LEUKEMIA

Project description:Murine cells with KMT2A-rearrangements, MLL-AF9; ATF3 initiates transcriptional programs associated with serine and nucleotide metabolism

2021-07-20 | GSE172453 | GEO

Gene Regulation by ATF3 in response to serine deprivation

Project description:The goal of this study is to identify genes that are regulated by activiating transcription factor (ATF3) in the cellular response to serine deprivation. Serine biosynthesis is crucial for cancer cells to proliferate and survival under serine-limiting conditions. We found that ATF3 expression induced by serine deprivation supports cancer cell growth. This RNA-seq study is thus designed to understand how ATF3 regulates serine biosynthesis in cells. The results indicate that ATF3 regulates the genes involved in the serine synthesis pathway.

2021-11-09 | GSE164850 | GEO

ATF3 coordinates serine and nucleotide metabolism to drive cell cycle progression in acute myeloid leukemia.

Project description:Metabolic reprogramming is a common feature of many human cancers, including acute myeloid leukemia (AML). However, the upstream regulators that promote AML metabolic reprogramming and the benefits conferred to leukemia cells by these metabolic changes remain largely unknown. We report that the transcription factor ATF3 coordinates serine and nucleotide metabolism to maintain cell cycling, survival, and the differentiation blockade in AML. Analysis of mouse and human AML models demonstrate that ATF3 directly activates the transcription of genes encoding key enzymatic regulators of serine synthesis, one-carbon metabolism, and de novo purine and pyrimidine synthesis. Total steady-state polar metabolite and heavy isotope tracing analyses show that ATF3 inhibition reduces de novo serine synthesis, impedes the incorporation of serine-derived carbons into newly synthesized purines, and disrupts pyrimidine metabolism. Importantly, exogenous nucleotide supplementation mitigates the anti-leukemia effects of ATF3 inhibition. Together, these findings reveal the dependence of AML on ATF3-regulated serine and nucleotide metabolism.

| S-EPMC8452149 | biostudies-literature

Gene Regulation by ATF3 in response to serine deprivation

Project description:Gene Regulation by ATF3 in response to serine deprivation

| PRJNA692204 | ENA

Activating transcription factors Atf3/Atf4 drive early molecular events preceding neural stem cell differentiation and control neuron formation [Short]

Project description:The generation of new neurons from neural stem cells is tightly controlled by transcriptional programs. To induce cell fate switches that establish neuronal identities, differentiating neural precursor cells (NPCs) must undergo rapid and dynamic gene expression changes. However, the neuronal fate-determining molecular events that precede NPC differentiation are incompletely understood. Using high temporal resolution transcriptional profiling of adult hippocampal NPC differentiation, we here identified the activating transcription factors Atf3 and Atf4 as early switch regulators that drive NPC fate and control neuron formation. We found that Atf3/4 are rapidly upregulated in NPCs upon induction of differentiation and drive dynamic gene expression changes associated with neurogenesis. Pharmacological and genetic perturbation of Atf4 demonstrated its importance for neuron formation. Sustained overexpression of Atf3 hampered neurogenesis by repressing long non-coding RNA Miat. Our results demonstrate the critical role of an Atf3/Atf4-controlled transcriptional network in driving early molecular events during neurogenesis.

2024-01-18 | GSE253532 | GEO

Activating transcription factors Atf3/Atf4 drive early molecular events preceding neural stem cell differentiation and control neuron formation [Long]

2024-01-18 | GSE253304 | GEO

Activating transcription factors Atf3/4 drive early molecular events during neural stem cell differentiation and control neuron formation [RNA-seq]

2024-01-18 | GSE253374 | GEO

ATF3 regulation of serine metabolism

Project description:ATF3 is a common stress sensor, and its expression can be induced by serine deprivation. The goal of this project is to determine whether ATF3 regulates serine biosynthesis. ATF3-wildtype and –knockout cells are cultured in complete or serine-free medium supplemented with 13C-6-glucose for 24 h for stable isotope tracing. The results show that ATF3 appears to promote serine biosynthesis.

2021-08-11 | ST001909 | MetabolomicsWorkbench

ATF3 coordinates the survival/proliferation of cardiac macrophages to protect against ischemia-reperfusion injury

Project description:Cardiac resident MerTK+ macrophages exert multiple protective roles post-ischemic injury, however, the mechanisms regulating their fate are not fully understood. Here we show that GAS6-inducible transcription factor ATF3 prevents apoptosis of MerTK+ macrophages after ischemia-reperfusion (IR) injury, by repressing the transcription of multiple genes involved in type I interferon expression (Ifih1 and Infb1) and apoptosis (Apaf1). Mice lacking ATF3 in cardiac macrophages or myeloid cells showed excessive loss of MerTK+ cardiac macrophages, poor angiogenesis, and worse heart dysfunction post-IR, which were rescued by the transfer of MerTK+ cardiac macrophages. GAS6 administration improved cardiac repair in an ATF3-dependent manner. Finally, we showed a negative association of GAS6 and ATF3 expression with the risk of major adverse cardiac events in patients with ischemic heart disease. These results indicate that the GAS6-ATF3 axis has a protective role against IR injury by regulating MerTK+ cardiac macrophage survival/proliferation.

2023-11-07 | GSE247139 | GEO

ATF3 is a novel regulator of mouse neutrophil migration.

Project description:Expression of the activating transcription factor 3 (ATF3) gene is induced by Toll-like receptor (TLR) signaling. In turn, ATF3 protein inhibits the expression of various TLR-driven pro-inflammatory genes. Given its counter-regulatory role in diverse innate immune responses, we defined the effects of ATF3 on neutrophilic airway inflammation in mice. ATF3 deletion was associated with increased lipopolysaccharide (LPS)-driven airway epithelia production of CXCL1, but not CXCL2, findings concordant with a consensus ATF3-binding site identified solely in the Cxcl1 promoter. Unexpectedly, ATF3-deficient mice did not exhibit increased airway neutrophilia after LPS challenge. Bone marrow chimeras revealed a specific reduction in ATF3-/- neutrophil recruitment to wild type lungs. In vitro, ATF3-/- neutrophils exhibited a profound chemotaxis defect. Global gene expression analysis identified ablated Tiam2 expression in ATF3-/- neutrophils. TIAM2 regulates cellular motility by activating Rac1-mediated focal adhesion disassembly. Notably, ATF3-/- and ATF3-sufficient TIAM2 knockdown neutrophils, both lacking TIAM2, exhibited increased focal complex area, along with excessive CD11b-mediated F-actin polymerization. Together, our data describe a dichotomous role for ATF3-mediated regulation of neutrophilic responses: inhibition of neutrophil chemokine production, but promotion of neutrophil chemotaxis. Ly6G+ neutrophils were purified by magnetic beads from WT or ATF3 KO bone marrow and RNA was immediately isolated for global gene expression using microarrays.

2014-04-05 | E-GEOD-53973 | biostudies-arrayexpress

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