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Phosphatase MAP4K4 regulates neutrophil development through the apoptosis pathway

ABSTRACT: Phosphatase MAP4K4 regulates neutrophil development through the apoptosis pathway

PROVIDER: PRJNA1157446 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR30562495_1.fastq.gz	Fastqsanger.gz
	SRR30562495_2.fastq.gz	Fastqsanger.gz
	SRR30562496_1.fastq.gz	Fastqsanger.gz
	SRR30562496_2.fastq.gz	Fastqsanger.gz

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Phosphatase MAP4K4 regulates neutrophil development through the apoptosis pathway

Project description:The role of MAP4K4 in the development of neutrophils remains largely unexplored. We utilized single cell sequencing (scRNA-seq) technology to elucidate the impact of Map4k4 deficiency on neutrophil maturation within mouse bone marrow. Through the application of scRNA-seq, we characterized the transcriptional changes across various stages of neutrophil development in both Map4k4-deficient (Map4k4-cKO) and control mice.

2025-02-12 | GSE276482 | GEO

POPX2 phosphatase regulates apoptosis through the TAK1-IKK-NF-κB pathway.

Project description:Chemoresistance is one of the leading causes that contributes to tumor relapse and poor patient outcome after several rounds of drug therapy. The causes of chemoresistance are multi-factorial. Ultimately, it is the balance of pro- and anti-apoptotic activities in the cells. We have previously reported links between POPX2 serine/threonine phosphatase with cell motility and invasiveness of breast cancer cells. Here, we show that POPX2 plays a role in the regulation of apoptosis. The effect of POPX2 on apoptosis centers on the inactivation of TGF-β activated kinase (TAK1). TAK1 is essential for several important biological functions including innate immunity, development and cell survival. We find that POPX2 interacts directly with TAK1 and is able to dephosphorylate TAK1. Cells with lower levels of POPX2 exhibit higher TAK1 activity in response to etoposide (VP-16) treatment. This subsequently leads to increased translocation of NF-κB from the cytosol to the nucleus. Consequently, NF-κB-mediated transcription of anti-apoptotic proteins is upregulated to promote cell survival. On the other hand, cells with higher levels of POPX2 are more vulnerable to apoptosis induced by etoposide. Our data demonstrate that POPX2 is a negative regulator of TAK1 signaling pathway and modulates apoptosis through the regulation of TAK1 activity. As inhibition of TAK1 has been proposed to reduce chemoresistance and increase sensitivity to chemotherapy in certain types of cancer, modulation of POPX2 levels may provide an additional avenue and consideration in fine-tuning therapeutic response.

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Posttranscriptional control of the neutrophil transcriptome by tristetraprolin promotes neutrophil apoptosis and compromises host antimicrobial defense

Project description:Posttranscriptional regulation of mRNA levels in neutrophils and its consequences for immune responses are unexplored. By employing profiling of the neutrophil transcriptome we show that the mRNA-destabilizing protein tristetraprolin (TTP) limits the expression of hundreds of genes, including genes negatively regulating apoptosis. Elicited TTP-deficient neutrophils exhibited reduced apoptosis and were increased in numbers. The anti-apoptotic protein Mcl-1 was elevated in TTP-deficient neutrophils and Mcl1 mRNA was bound and destabilized by TTP. Ablation of TTP in macrophages and neutrophils resulted in an improved defense and survival of mice during invasive infection with Streptococcus pyogenes. Mice lacking myeloid TTP prevented dissemination of bacteria and efficiently blunted systemic disease by massive but controlled neutrophil deployment. These data identify posttranscriptional control by TTP to restrict neutrophils and antimicrobial defense.

2017-05-05 | GSE77801 | GEO

Phosphatase, Mg2+/Mn2+ Dependent 1B (Ppm1b) regulates the self-renewal of HSCs through the Wnt/β-catenin pathway [scRNA-Seq]

Project description:Hematopoietic stem cells (HSCs) have unique abilities to renew themselves and generate differentiated progenies of all blood cell lineages; however, how HSCs maintain the balance of self-renewal and lineage differentiation remains largely unknown. Herein, we showed that in mice the hematologic system deletion of Phosphatase, Mg2+/Mn2+ Dependent 1B (Ppm1b), a protein serine or threonine phosphatase highly expressed in HSCs, induces the suppression of phenotypic HSC expansion due to the blockage of cell cycle. Loss of Ppm1b impairs HSC self-renewal and hematopoietic reconstitution which were revealed by limiting dilution and BM transplantation assays. Through transcriptomic analysis, we observed that the Wnt/β-catenin pathway is downregulated in Ppm1b-deficient mice. Mechanistically, we provided evidence that Ppm1b interacted with β-catenin by performing a proximity ligation assay. Moreover, using an HN252 as a small molecule probe, we further found that Ppm1b inhibition suppressed the self-renewal of HSC and led to a decrease in common lymphoid progenitor cells, resulting in a reduction of B cells in the bone marrow and peripheral blood in turn. In the study we characterized an indispensable role of Ppm1b in regulating HSC self-renewal and B cell development via Wnt/β-catenin pathway.

2024-07-31 | GSE237746 | GEO

Phosphatase, Mg2+/Mn2+ Dependent 1B (Ppm1b) regulates the self-renewal of HSCs through the Wnt/β-catenin pathway [bulk RNA-Seq]

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NAA enhances cell yields by inhibiting apoptosis pathway

Project description:NAA enhances cell yields by inhibiting apoptosis pathway

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Phosphatase, Mg2+/Mn2+ Dependent 1B (Ppm1b) regulates the self-renewal of HSCs through the Wnt/β-catenin pathway

Project description:Phosphatase, Mg2+/Mn2+ Dependent 1B (Ppm1b) regulates the self-renewal of HSCs through the Wnt/β-catenin pathway

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2023-03-31 | GSE225139 | GEO

METTL3 mediated m6A mRNA methylation regulates neutrophil activation through targeting TLR4 signaling (Ribosome-Seq)

Project description:To investigate the effect of METTL3 function in the regulation of neutrophil activation, we established neutrophil METTL3 knock out mice by crossing METTL3flox/flox mice with Lyzm-cre mice. We then performed gene expression profiling analysis using data obtained from Ribosome-seq of isolated neutrophil from METTL3f/f and METTL3f/f Lyzm-Cre mice .

2023-03-31 | GSE225140 | GEO

METTL3 mediated m6A mRNA methylation regulates neutrophil activation through targeting TLR4 signaling (RNA-Seq)

Project description:To investigate the effect of METTL3 function in the regulation of neutrophil activation, we established neutrophil METTL3 knock out mice by crossing METTL3flox/flox mice with Lyzm-cre mice. We then performed gene expression profiling analysis using data obtained from RNA-seq of isolated neutrophil from METTL3f/f and METTL3f/f Lyzm-Cre mice with or without intraperitoneal injection of lipopolysaccharide (LPS) treatment.

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