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IGF2BP2-regulated alternative splicing of NFIC causes excessive granulosa cell proliferation in PCOS [IRIP-seq]

ABSTRACT: IGF2BP2-regulated alternative splicing of NFIC causes excessive granulosa cell proliferation in PCOS [IRIP-seq]

PROVIDER: PRJNA789393 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR17247072_1.fastq.gz	Fastqsanger.gz
	SRR17247072_2.fastq.gz	Fastqsanger.gz
	SRR17247073_1.fastq.gz	Fastqsanger.gz
	SRR17247073_2.fastq.gz	Fastqsanger.gz
	SRR17247074_1.fastq.gz	Fastqsanger.gz

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Similar Datasets

IGF2BP2-regulated alternative splicing of NFIC causes excessive granulosa cell proliferation in PCOS [IRIP-seq]

Project description:The expression of IGF2BP2 in GCs from PCOS patients was detected using RT-qPCR and western blot. We captured IGF2BP2-interacting transcripts, global transcriptome together with alternative splicing by RNA immunoprecipitation sequencing (RIP-seq) and RNA sequencing (RNA-seq). KGN cells transfected with IGF2BP2 overexpressing plasmids and nuclear factor 1 C-type (NFIC) siRNAs, were applied to CCK-8, EdU and TUNEL assays. IGF2BP2 was highly expressed in GCs from PCOS patients. As a RBP, it preferentially bound to the 3’and 5’UTRs of mRNAs with GGAC motif and a newly found GAAG motif. The overexpression of IGF2BP2 changed the transcriptome profile of KGN cells. IGF2BP2 functioned to regulate alternative splicing events (ASEs) and promote cell proliferation through inhibiting exon skipping events of NFIC. In conclusion, we demonstrated that IGF2BP2 promotes granulosa cell proliferation via regulating alternative splicing of NFIC in PCOS. The findings help to better understand the roles of IGF2BP2 in the pathogenesis of PCOS.

2022-05-11 | GSE191023 | GEO

IGF2BP2-regulated alternative splicing of NFIC causes excessive granulosa cell proliferation in PCOS [RNA-seq]

2022-05-11 | GSE191022 | GEO

IGF2BP2-regulated alternative splicing of NFIC causes excessive granulosa cell proliferation in PCOS

Project description:IGF2BP2-regulated alternative splicing of NFIC causes excessive granulosa cell proliferation in PCOS

| PRJNA789474 | ENA

IGF2BP2-regulated alternative splicing of NFIC causes excessive granulosa cell proliferation in PCOS [RNA-seq]

Project description:IGF2BP2-regulated alternative splicing of NFIC causes excessive granulosa cell proliferation in PCOS [RNA-seq]

| PRJNA789394 | ENA

IGF2BP2-regulated alternative splicing of NFIC causes excessive granulosa cell proliferation in PCOS

Project description:This SuperSeries is composed of the SubSeries listed below.

2022-05-11 | GSE191031 | GEO

Analysis of differential gene expression related to steroid metabolism in the granulosa cell transcriptome of PCOS patients based on single-cell level

Project description:The development of granulosa cells has an impact on the development of pcos. We performed single-cell RNA-seq sequencing (scRNA-seq) of granulosa cells to analyse the heterogeneity of PCOS.

2024-01-11 | GSE240688 | GEO

Genome-wide methylation profiling in granulosa lutein cells of women with polycystic ovary syndrome (PCOS)

Project description:Our study is based on the hypothesis that PCOS can be explained by an integrated, epigenetic model, whereby environmental factors modify the effect of susceptibility genes and influence the clinical heterogeneity that is characteristic of the syndrome during adult life. With the aim to understand the molecular mechanisms underlying PCOS, we report results from a case-control, genome-wide methylation study using human DNA from granulosa lutein cells.

2019-03-01 | E-MTAB-6672 | biostudies-arrayexpress

Identification miRNA expression profiles of human granulosa cells obtained from PCOS patients and control individuals

Project description:The miRNA expression profiles of mural granulosa cells (MGCs) which were obtained from PCOS patients and control individuals were identified and compared.

2016-07-14 | GSE84376 | GEO

Long noncoding RNA expression profiles in granulosa cells from PCOS patients and women with normal ovarian reserve

Project description:LncRNAs and mRNAs profiling of gonadotropin-stimulated granulosa cells from PCOS patients and controls (women with normal ovarian reserve)

2020-03-05 | GSE95728 | GEO

To compare the transcriptome expression of cumulus granulosa cells between PCOS patients with insulin resistance and women undergoing assisted reproduction for fallopian tube reasons

Project description:Purpose polycystic ovary syndrome (PCOS) is the most common endocrine and metabolic disorder in women of childbearing age. It is characterized by follicular dysplasia and hyperandrogenemia. Insulin resistance plays an important role in the development of PCOS.However, the mechanism of regulation and interaction between insulin resistance and follicle development remains unclear.The aim of this study was to identify differential genes associated with follicle development in cumulus granulosa cells in PCOS patients with insulin resistance compared with controls. Methods In this study, RNA-seq, bioinformatics analysis and reverse transcription qPCR (RT-qPCR) were used to analyze the gene expression in cumulus granulosa cells.A total of seven cDNA libraries were constructed from three PCOS samples and four control samples.3 μg of RNA was used as starting material for each sample.Ribosomal RNA was removed using the Epicentre rigo-zero ™ Gold Kit (Epicentre, Illumina, Madison, WI, USA). Results Compared with the control group, there were 2233 DEGs in the PCOS group, including 1158 up-regulated genes and 1075 down-regulated genes. Some different expression patterns were observed in the two groups.The next series of experiments verified the effect of some genes on oocyte development. Conclusion Our study showed that the differential expression of transcriptome in cumulus granulosa cells could affect the growth, development and maturation of oocytes.Meanwhile, the results of RT-PCR and Elisa showed that the expression of renin angiotensin system was changed in PCOS patients with insulin resistance, and these changes could affect oocyte maturation and excretion through cumulus granulosa cells.

2023-10-01 | GSE216609 | GEO

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