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YTHDF3 modulates the stability of Cbln1 mRNA by recruiting BTG2 and is implicated in the impaired cognition of prenatal hypoxia offspring

ABSTRACT: YTHDF3 modulates the stability of Cbln1 mRNA by recruiting BTG2 and is implicated in the impaired cognition of prenatal hypoxia offspring

PROVIDER: PRJNA1047547 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR27109806_1.fastq.gz	Fastqsanger.gz
	SRR27109806_2.fastq.gz	Fastqsanger.gz
	SRR27109807_1.fastq.gz	Fastqsanger.gz
	SRR27109807_2.fastq.gz	Fastqsanger.gz
	SRR27109808_1.fastq.gz	Fastqsanger.gz

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YTHDF3 modulates the stability of Cbln1 mRNA by recruiting BTG2 and is implicated in the impaired cognition of prenatal hypoxia offspring

Project description:The “Fetal Origins of Adult Disease (FOAD)” hypothesis holds that adverse factors during pregnancy can increase the risk of chronic diseases in offspring. Here, we investigated the effects of prenatal hypoxia (PH) on brain structure and function in adult offspring and explored the role of the N6-methyladenosine (m6A) pathway. The results suggest that abnormal cognition in PH offspring may be related to dysregulation of the m6A pathway, specifically increased levels of YTHDF3 in the hippocampus. YTHDF3 interacts with BTG2 and is involved in the decay of Cbln1 mRNA, leading to the down-regulation of Cbln1 expression. Deficiency of Cbln1 may contribute to abnormal synaptic function, which in turn causes cognitive impairment in PH offspring. This study provides new scientific clues for understanding the mechanisms of impaired cognition in PH offspring and provides a theoretical basis for the treatment of cognitive impairment in offspring exposed to PH.

2024-01-17 | GSE249147 | GEO

Transcriptome analyses of trophoblast upon YTHDF3 knockdown

Project description:YTHDF3 play important role in regulation of trophoblast activity, we examined the downstream genes of YTHDF3 via transcriptome sequencing

2020-03-24 | GSE135407 | GEO

BTG1 and BTG2 Regulate B Linege Commitment by Modulation of EBF1 Activity

Project description:The human BTG1 and BTG2 genes are targeted by genetic alterations in hematological malignancies. In this study we examined the unique and overlapping functions of Btg1 and Btg2 in mouse B cell development. Mice deficient for Btg1 and Btg2 displayed the strongest phenotype with a decrease in B cell numbers in bone marrow due to impaired B cell commitment and immature B cell differentiation. To determine the underlying mechanism, microarray expression analyis was performed on early (B220+ CD43+) and late (B220+ CD43-) B cells of WT and Btg1;Btg2 dKO mice. Total RNA obtained from sorted B220+ CD43+ ( Hardy fractions ABC) and B220+ CD43- (Hardy fractions DEF) BM cells of WT and Btg1-/-;Btg2-/- mice. In total 4 samples were analyzed and no replicates were included.

2014-03-19 | E-GEOD-55997 | biostudies-arrayexpress

BTG1 and BTG2 Regulate B Linege Commitment by Modulation of EBF1 Activity

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Gene expression signatures in Ythdf3-/- and WT hematopoietic stem cells

Project description:Analysis of Ythdf3-/- and WT hematopoietic stem cell (lineage-, c-kit+ Sca-1+ CD150+, CD34-). The hematopoietic stem cell (HSC) were purified from the bone marrow of WT and Ythdf3-/- mice.

2024-06-09 | GSE176458 | GEO

YTHDF3 improves translation initiation of mRNAs with N6-methyladenosine methylation at 5’ untranslated region by facilitating eIF2AK2 recruitment in oxaliplatin-resistant colorectal cancer - RIP-seq dataset

Project description:Oxaliplatin as a first-line drug frequently causes the chemo-resistance on colorectal cancer (CRC). N6-methyladenosine (m6A) methylation has been largely acknowledged in multiple biological functions. However, the molecular mechanisms underlying the m6A methylation in modulating anticancer drug resistance in CRC are still obscure. In present study, RIP-seq was conducted to investigate the occupancy of N6-methyladenosine RNA binding protein 3 (YTHDF3) served as “readers” that can recognize m6A modification site in HCT116 cells with oxaliplatin resistance (HCT116R). Then, YTHDF3 was knockdown by siRNA in HCT116 cells with oxaliplatin resistance, and RIP-seq was further conducted to investigate m6A methylation of HCT116, HCT116R and HCT116R cells with YTHDF3 knockdown.

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iCLIP-Seq analyses of YTHDF3-bound RNAs

Project description:We found that YTHDF3 work as m1A reader,but the potential substrate RNA remain elusive.

2020-03-24 | GSE135642 | GEO

RNAseq of cultured neonatal rat ventricular cardiomyocytes treated with siRNA for Btg1 and Btg2 knockdown.

Project description:Total RNA was isolated from n=3 culture wells per siRNA treatment group, from 6 independent primary neonatal rat cardiomyocyte isolations. RNA was pooled to obtain n=3 independent samples per siRNA treatment group for sequencing. The siRNA treatment groups were= siScr (Scramble control), siBtg12 (Btg1/Btg2 double knockdown), siBtg1 (Btg1 single knockdown), siBtg2 (Btg2 single knockdown).

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YTHDF3 Induces the Translation of m6A-enriched Metastasis-associated Gene Transcripts to Promote Breast Cancer Brain Metastasis [m6A-seq]

Project description:Brain metastasis is a major cause of cancer mortality, but its molecular mechanisms are severely understudied. We found that YTHDF3 overexpression clinically correlates with brain metastases in breast cancer patients and is required for brain metastasis. Silencing YTHDF3 suppressed the brain metastasis of breast cancer cells in vitro and in vivo. Integrated transcriptome and m6A-seq analysis revealed alter expression of selected YTHDF3 target genes, including ST6GALNAC5, GJA1, and EGFR by promoting m6A-dependent translation of these target transcripts. Our work uncovers an essential role of YTHDF3 in controlling the interaction between cancer cells and brain microenvironment, thereby gaining brain metastatic competence.

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YTHDF3 Induces the Translation of m6A-enriched Metastasis-associated Gene Transcripts to Promote Breast Cancer Brain Metastasis [RIP-Seq]

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