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CD93 negatively regulates astrogenesis in response to MMRN2 through transcription repressor ZFP503 in the developing brain

ABSTRACT: CD93 negatively regulates astrogenesis in response to MMRN2 through transcription repressor ZFP503 in the developing brain

PROVIDER: PRJNA555993 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR9729125_1.fastq.gz	Fastqsanger.gz
	SRR9729125_2.fastq.gz	Fastqsanger.gz
	SRR9729126_1.fastq.gz	Fastqsanger.gz
	SRR9729126_2.fastq.gz	Fastqsanger.gz
	SRR9729127_1.fastq.gz	Fastqsanger.gz

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Similar Datasets

CD93 negatively regulates astrogenesis in response to MMRN2 through transcription repressor ZFP503 in the developing brain

Project description:Astrogenesis is repressed in the early embryonic period, and occurs in the late embryonic period. A variety of external and internal signals contribute to the sequential differentiation of neural stem cell. Here, we discover that the immune-related CD93 plays a critical role in the onset of astrogenesis in mouse. CD93 expression is detected in neural stem cell and neuron but bot in astrocyte, and declines as differentiation proceeds. CD93 knockout increases astrogenesis at the expense of neuron production during the late embryonic period. CD93 responds to the ECM protein MMRN2 to trigger the repression of astrogenesis. In mechanism, CD93 delivers the signal through a series of phosphorylation cascade to β-Catenin, then β-Catenin transfers to nucleus to activate Zfp503 transcription. The transcription repressor ZFP503 inhibits Gfap transcription by binding to the Gfap promoter with the help of Grg5. Furthermore, the abnormal differentiation in astrogenesis and neurogenesis caused by CD93 knockout results in autism-like behaviors. Taken together, our study reveals that CD93 is a negative regulator in controlling the proper time of astrogenesis, and provides a new sight in therapy for psychiatric disorders.

2019-07-26 | GSE134642 | GEO

CD93 negatively regulates astrogenesis in response to MMRN2 through the transcriptional repressor ZFP503 in the developing brain.

Project description:Astrogenesis is repressed in the early embryonic period and occurs in the late embryonic period. A variety of external and internal signals contribute to the sequential differentiation of neural stem cells. Here, we discovered that immune-related CD93 plays a critical negative role in the regulation of astrogenesis in the mouse cerebral cortex. We show that CD93 expression is detected in neural stem cells and neurons but not in astrocytes and declines as differentiation proceeds. Cd93 knockout increases astrogenesis at the expense of neuron production during the late embryonic period. CD93 responds to the extracellular matrix protein Multimerin 2 (MMRN2) to trigger the repression of astrogenesis. Mechanistically, CD93 delivers signals to β-Catenin through a series of phosphorylation cascades, and then β-Catenin transduces these signals to the nucleus to activate Zfp503 transcription. The transcriptional repressor ZFP503 inhibits the transcription of glial fibrillary acidic protein (Gfap) by binding to the Gfap promoter with the assistance of Grg5. Furthermore, Cd93 knockout mice exhibit autism-like behaviors. Taken together, our results reveal that CD93 is a negative regulator of the onset of astrogenesis and provide insight into therapy for psychiatric disorders.

| S-EPMC7196765 | biostudies-literature

CD93+ and CD93- HSCs comparison

Project description:CD93+ and CD93- HSCs comparison

| PRJNA701025 | ENA

CD93+ and CD93- HSCs comparison [RNA-Seq]

Project description:CD93+ and CD93- HSCs comparison [RNA-Seq]

| PRJNA701026 | ENA

CD93+ and CD93- HSCs comparison [ATAC-Seq]

Project description:CD93+ and CD93- HSCs comparison [ATAC-Seq]

| PRJNA701027 | ENA

Targeting CD93 on Monocytes revitalizes Anti-Tumor Immunity by Enhancing the Function and Infiltration of CD8+ T Cells

Project description:In this study, we found that monocytes in the peritumoral tissues of HCC significantly increased levels of CD93 expression, and these CD93+ monocytes collocated with CD8+ T cells, whose density was much higher in peri-tumor than intra-tumor areas. In vitro experiments showed that glycolytic switch mediated tumor-induced CD93 up-regulation in monocytes via the Erk signaling pathway. CD93 on the one hand could enhance PD-L1 expression through the AKT-GSK3β axis, while on the other hand induce monocytes to produce versican, a type of matrix component which interacted with hyaluronan and collagens to inhibit CD8+ T cell migration. Consistently, levels of CD93+ monocytes positively correlated with the density of peritumoral CD8+ T cells while negatively correlated with that of intratumoral CD8+ T cells. Targeting CD93 on monocytes not only increased the infiltration and activation of CD8+ T cells, but also enhanced tumor sensitivity to anti-PD-1 treatment in mice in vivo.

2024-10-30 | GSE276062 | GEO

Gene expression analysis of genes differentially expressed between CD93-ko mice and wild-type mice in post ischemic mice brain tissue

Project description:To further decipher CD93-dependent pathways, we compared global expression profiles of ischemic (ipsilateral) hemispheres of CD93-deficient mice (CD93-ko) with expression profiles of wild-type mice. Total RNA obtained from CD93-ko and WT mice at different time points after cerebral ischemia and from untreated brain tissue

2010-03-23 | E-GEOD-21002 | biostudies-arrayexpress

Gene expression analysis of genes differentially expressed between CD93-ko mice and wild-type mice in post ischemic mice brain tissue

2010-03-23 | GSE21002 | GEO

Comparison of transcriptional profiles of (1) intestinal ILC3s isolated from WT and IL-17D-deficient mice; (2) CD93+ILC3s and CD93-ILC3s from WT mice

Project description:IL-17D/CD93 axis was essential for ILC3s hemostasis. In order to further understand how IL-17D-CD93 axis regulate ILC3s function, we conducted RNA-seq analysis of ILC3s.

2021-05-20 | GSE165788 | GEO

JA-INDUCIBLE MYC2-LIKE1 acts as a repressor and negatively regulates jasmonate signaling in Arabidopsis

Project description:Jasmonate (JA) is a plant hormone that controls trade-offs between plant growth and responses to biotic and abiotic stresses. Although recent studies uncover core mechanism for JA-induced responses in Arabidopsis thaliana, it remains elusive how plants attenuate those responses. We report here that a basic-helix-loop-helix type transcription factor named JA-INDUCIBLE MYC2-LIKE1 (JAM1) acts as a transcriptional repressor and negatively regulates JA signaling. Arabidopsis plants expressing the chimeric repressor for JAM1 exhibited a substantial reduction of JA responses, including JA-induced inhibition of root growth, accumulation of anthocyanin, and male fertility. These plants were also compromised in resistance to attack by Spodoptera exigua. Conversely, jam1-4 loss-of-function mutants showed enhanced JA responsiveness, including increased resistance to the insect attack. Competitive binding of JAM1 and MYC2 to the target sequence of MYC2 suggested negative regulation of JA signaling by JAM1 and suppression of MYC2 function. These results indicate that JAM1 plays a pivotal role in fine-tuning of JA-mediated stress responses and plant growth by negatively regulating JA signaling. Transcriptomes of ProJAM1:JAM1-SRDX, ProMYC2:MYC2-SRDX and wild-type Arabidopsis seedlings with or without jasmonic acid were compared.

2013-07-03 | E-GEOD-42552 | biostudies-arrayexpress

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