Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Rna-seq transcriptome data for Neurod1-homozygous null and Neurod1-heterozygous null murine E17 pancreatic endocrine cells

ABSTRACT: Rna-seq transcriptome data for Neurod1-homozygous null and Neurod1-heterozygous null murine E17 pancreatic endocrine cells

PROVIDER: PRJNA507176 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR8247830.fastq.gz	Fastqsanger.gz
	SRR8247831.fastq.gz	Fastqsanger.gz
	SRR8247832.fastq.gz	Fastqsanger.gz
	SRR8247833.fastq.gz	Fastqsanger.gz
	SRR8247826.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 8

Similar Datasets

Rna-seq transcriptome data for Neurod1-homozygous null and Neurod1-heterozygous null murine E17 pancreatic endocrine cells

Project description:The purpose of this study was to identify genes regulated by Neurod1 during murine pancreatic endocrine cell differentiation.

2018-11-28 | GSE122992 | GEO

NEUROD1 reinforces endocrine cell fate acquisition in pancreatic development

Project description:NEUROD1 is a transcription factor that helps maintain a mature phenotype of pancreatic β cells. Disruption of Neurod1 during pancreatic development causes severe neonatal diabetes; however, the exact role of NEUROD1 in the differentiation programs of endocrine cells is unknown. Here, we report a crucial role of the NEUROD1 regulatory network in endocrine lineage commitment and differentiation. Mechanistically, transcriptome and chromatin landscape analyses demonstrate that Neurod1 inactivation triggers a downregulation of endocrine differentiation transcription factors and upregulation of non-endocrine genes within the Neurod1-deficient endocrine cell population, disturbing endocrine identity acquisition. Neurod1 deficiency altered the H3K27me3 histone modification pattern in promoter regions of differentially expressed genes, which resulted in gene regulatory network changes in the differentiation pathway of endocrine cells, compromising endocrine cell potential, differentiation, and functional properties.

2023-08-17 | GSE236559 | GEO

Transcription profiling of mouse NeuroD1 knockout pineal glands vs 129 wild types at P0

Project description:This study determines pineal gland gene expression levels in the NeuroD1 knockout mouse at postnatal day zero. Comparison was performed against pineal gland gene expression levels in 129 wildtype mice also disected at P0. Experiment Overall Design: Wildype 129 mice served as the reference in comparing the levels of gene expression in the NeuroD1 transgenic animals. Experiment Overall Design: 3 pineal glands were disected at P0 during the daytime and pooled for each sample. Experiment Overall Design: 3 separate biological samplings were performed. Experiment Overall Design: Triplicate arrays were run for wildtype and the homozygous animals.

2008-06-14 | E-GEOD-6030 | biostudies-arrayexpress

The expression order determines the pioneer functions of Ngn3 and NeuroD1 in pancreatic endocrine differentiation

Project description:This study investigates the roles of Ngn3 and NeuroD1 in pancreatic endocrine differentiation. Using a new mouse model, we mapped NGN3 binding sites by CUT&RUN and demonstrated its pioneering role in making chromatin accessible by scATAC-seq. According to conditional knock-out and over-expression experiments and scRNA-seq, we domonstrated that NGN3's pioneering function was dose tolerance, with low doses sufficing, while NeuroD1, as a conventional TF, has no significant pioneer effects under normal phenomena. But when NGN3 was absent, NeuroD1 can alternatively acted as a pioneer factor, and sequential expression of NeuroD1 ahead of Ngn3 predominantly drives α-cell generation.

2025-02-15 | GSE270915 | GEO

Study 6- RNA-seq of female WIBJ2 hiPSC-derived cortical brain organoids and extra-embryonic lineages homozygous null for five different transcription factors

Project description:This study aimed to phenotype iPSC-derived cortical brain organoids that contain homozygous null alleles for transcription factor PAX6 and to phenotype iPSC-derived extra-embryonic cell lineages that contain homozygous null alleles for transcription factors PPARG, EPAS1, GCM1, and GRHL1. Null alleles were generated by the insertion of a premature termination codon with frameshift (PTC+1). This analysis provided insight into the impact of loss of function for these transcription factors in the respective cell lineages.

2025-02-03 | GSE288286 | GEO

Study 4- RNA-seq of male KOLF2.2J hiPSC-derived cortical brain organoids and extra-embryonic lineages homozygous null for six different transcription factors

Project description:This study aimed to phenotype iPSC-derived cortical brain organoids that contain homozygous null alleles for transcription factors DMRTA1 and TBR1 and to phenotype iPSC-derived extra-embryonic cell lineages that contain homozygous null alleles for transcription factors OVOL1, PITX1, LMO2, and ZBTB7C. Null alleles were generated by the insertion of a premature termination codon with frameshift (PTC+1). This analysis provided insight into the impact of loss of function for these transcription factors in the respective cell lineages.

2025-02-03 | GSE287843 | GEO

Study 3- RNA-seq of male KOLF2.2J hiPSC-derived cortical brain organoids homozygous null for six different transcription factors

Project description:This study aims to phenotype iPSC-derived cortical brain organoids that contain homozygous null alleles for transcription factors expressed in the early neuroectoderm. Null alleles were generated using three distinct genetic engineering approaches: full coding region deletion (KO), critical exon deletion (CE), and insertion of a premature termination codon with frameshift (PTC+1). RNA-seq data was generated at the indicated day post initiation of differentiation from hiPSCs. The study included the homozygous null alleles for the following transcription factors: LHX9, RFX4, PAX6, OTX1, LHX5, and FEZF2. This analysis provided insight into the differences between the various CRISPR-Cas9-based approaches and the impact of loss of function for these transcription factors in cortical brain organoid differentiation.

2025-02-03 | GSE287558 | GEO

Bulk RNA-seq study 9- RNA-seq of male KOLF2.2J hiPSC-derived cortical brain organoids homozygous null for eight different transcription factors.

Project description:This study aims to phenotype iPSC-derived cortical brain organoids that contain homozygous null alleles for transcription factors expressed in the early neuroectoderm. Null alleles were generated using insertion of a premature termination codon with frameshift (PTC+1). RNA-seq data was generated at the indicated day post initiation of differentiation from hiPSCs. The study included the homozygous null alleles for the following transcription factors: EMX2, FOXG1, POU3F2, SOX1, HES5, SOX21, POU3F1 and SP8. This analysis provided insight into the impact of loss of function for these transcription factors in cortical brain organoid differentiation.

2025-09-08 | GSE303918 | GEO

The expression order determines the pioneer functions of Ngn3 and NeuroD1 in pancreatic endocrine differentiation -2

2025-02-15 | GSE271546 | GEO