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Daidzein activates Akt pathway to promote the proliferation of female germline stem cells through upregulating Clec11a

ABSTRACT: Daidzein activates Akt pathway to promote the proliferation of female germline stem cells through upregulating Clec11a

PROVIDER: PRJNA818540 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR18429488_1.fastq.gz	Fastqsanger.gz
	SRR18429488_2.fastq.gz	Fastqsanger.gz
	SRR18429489_1.fastq.gz	Fastqsanger.gz
	SRR18429489_2.fastq.gz	Fastqsanger.gz
	SRR18429490_1.fastq.gz	Fastqsanger.gz

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Daidzein activates Akt pathway to promote the proliferation of female germline stem cells through upregulating Clec11a

Project description:Female germline stem cells (FGSCs) have been successfully isolated from postnatal mammalian and human ovarian tissues. However, the effects and mechanisms of action of natural small-molecule compounds on FGSCs are largely unknown. Here, we determined the effects of daidzein, a phytoestrogen present in soybean , on cell viability and proliferation using Cell Counting Kit-8 (CCK8) and 5-ethynyl-2-deoxyuridine (EdU). We found that daidzein promoted the viability and proliferation of FGSCs in a concentration-dependent manner. To elucidate the mechanism underlying this, we performed RNA-Seq in daidzein-treated FGSCs and controls. The results showed that there were 153 upregulated and 156 downregulated genes after daidzein treatment. We confirmed the expression of some genes related to cell proliferation in the sequencing results by RT-PCR, such as Type C lectin domain family 11 member a (Clec11a), Mucin1 (Muc1), Glutathione peroxidase 3 (Gpx3), and Tet methylcytosine dioxygenase 1(Tet1). The high expression of Clec11a at the protein level after daidzein treatment was also confirmed by western blotting. Furthermore, recombinant mouse Clec11a (rmClec11a) protein was shown to promote the viability and proliferation of FGSCs. However, knockdown of Clec11a inhibited the viability and proliferation of FGSCs, which could not be rescued by the administration of daidzein. These results indicate that daidzein promoted the viability and proliferation of FGSCs through Clec11a. In addition, both daidzein and rmClec11a activated the Akt signaling pathway in FGSCs. However, Clec11a knockdown inhibited this pathway, which could not be rescued by daidzein administration. Taken together, our findings revealed that daidzein activates the Akt signaling pathway to promote cell viability and proliferation through upregulating Clec11a. This study should deepen our understanding of the developmental mechanism of FGSCs and female infertility.

2025-03-20 | GSE199120 | GEO

STING Signaling Contributes to Celastrol-induced Pyroptosis of Female Germline Stem Cells by Upregulating NLRP3

Project description:STING Signaling Contributes to Celastrol-induced Pyroptosis of Female Germline Stem Cells by Upregulating NLRP3

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Metformin promotes female germline stem cell proliferation by upregulating Gata-binding protein 2 with histone β-hydroxybutyrylation.

Project description:Metformin promotes female germline stem cell proliferation by upregulating Gata-binding protein 2 with histone β-hydroxybutyrylation.

| PRJNA900536 | ENA

Metformin promotes female germline stem cell proliferation by upregulating Gata-binding protein 2 with histone β-hydroxybutyrylation [ChIP-seq]

Project description:We use ChIP-seq to report the most comprehensive survey to date of chromatin organization in female germline stem cells

2023-04-26 | GSE217782 | GEO

Metformin promotes female germline stem cell proliferation by upregulating Gata-binding protein 2 with histone β-hydroxybutyrylation [ChIP-seq]

Project description:Metformin promotes female germline stem cell proliferation by upregulating Gata-binding protein 2 with histone β-hydroxybutyrylation [ChIP-seq]

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Metformin promotes female germline stem cell proliferation by upregulating Gata-binding protein 2 with histone β-hydroxybutyrylation [RNA-seq]

Project description:Metformin promotes female germline stem cell proliferation by upregulating Gata-binding protein 2 with histone β-hydroxybutyrylation [RNA-seq]

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DUX4 activates germline genes, retroelements and immune-mediators: Implications for facioscapulohumeral dystrophy

Project description:Facioscapulohumeral dystrophy (FSHD) is one of the most common inherited muscular dystrophies. The causative gene remains controversial and the mechanism of pathophysiology unknown. Here we identify genes associated with germline and early stem cell development as targets of the DUX4 transcription factor, a leading candidate gene for FSHD. The genes regulated by DUX4 are reliably detected in FSHD muscle but not in controls, providing direct support for the model that misexpression of DUX4 is a causal factor for FSHD. Additionally, we show that DUX4 binds and activates LTR elements from a class of MaLR endogenous primate retrotransposons and suppresses the innate immune response to viral infection, at least in part through the activation of DEFB103, a human defensin that can inhibit muscle differentiation. These findings suggest specific mechanisms of FSHD pathology and identify candidate biomarkers for disease diagnosis and progression. Examine Dux4 full isoform binding sites in human fibroblast.

2012-01-03 | E-GEOD-33838 | biostudies-arrayexpress

CDK5 activates Hippo signaling to confer resistance to radiotherapy via upregulating TAZ in lung cancer

Project description:CDK5 activates Hippo signaling to confer resistance to radiotherapy via upregulating TAZ in lung cancer

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LncRNA-LPE binding to TCP1 activates the PI3K/AKT signaling pathway in preeclampsia

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PRMT5-mediated arginine methylation activates AKT kinase to govern tumorigenesis

Project description:AKT is involved in a number of key cellular processes including cell proliferation, apoptosis and metabolism. Hyperactivation of AKT is associated with many pathological conditions, particularly cancers. Emerging evidence indicates that arginine methylation is involved in modulating AKT signaling pathway. However, whether and how arginine methylation directly regulates AKT kinase activity remain unknown. Here we report that protein arginine methyltransferase 5 (PRMT5), but not other PRMTs, promotes AKT activation by catalyzing symmetric dimethylation of AKT1 at arginine 391 (R391). Mechanistically, AKT1-R391 methylation cooperates with phosphatidylinositol 3,4,5 trisphosphate (PIP3) to relieve the pleckstrin homology (PH)-in conformation, leading to AKT1 membrane translocation and subsequent activation by phosphoinositide-dependent kinase-1 (PDK1) and the mechanistic target of rapamycin complex 2 (mTORC2). As a result, deficiency in AKT1-R391 methylation significantly suppresses AKT1 kinase activity and tumorigenesis. Lastly, we show that PRMT5 inhibitor synergizes with AKT inhibitor or chemotherapeutic drugs to enhance cell death. Altogether, our study suggests that R391 methylation is an important step for AKT activation and its oncogenic function.

2022-02-17 | PXD026071 | Pride

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