Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Microarray analysis of Wild-type vs. Brpf1-deficient P4 mouse brain

ABSTRACT: RNA was isolated from three pairs of wild-type and Brpf1-deficient mouse brains (the dorsal cortex part) at postnatal day 4 for microarray analysis.

ORGANISM(S): Mus musculus

PROVIDER: GSE63909 | GEO | 2015/04/08

SECONDARY ACCESSION(S): PRJNA269383

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Microarray analysis of Wild-type vs. Brpf1-deficient P4 mouse brain

Project description:RNA was isolated from three pairs of wild-type and Brpf1-deficient mouse brains (the dorsal cortex part) at postnatal day 4 for microarray analysis. The cDNA samples were then labeled and mixed for hybridization with one array. The data from three arrays were obtained and used for bioinformatic analysis.

2015-04-08 | E-GEOD-63909 | biostudies-arrayexpress

Microarray analysis of Wild-type vs. Brpf1-deficient E8.75 mouse embryo

Project description:RNA was isolated from three pairs of wild-type and Brpf1-deficient E8.75 mouse embryos for microarray analysis.

2015-05-15 | GSE63908 | GEO

Microarray analysis of Wild-type vs. Brpf1-deficient E8.75 mouse embryo

Project description:RNA was isolated from three pairs of wild-type and Brpf1-deficient E8.75 mouse embryos for microarray analysis. The cDNA samples were then labeled and mixed for hybridization with one array. The data from three arrays were obtained and used for bioinformatic analysis.

2015-05-15 | E-GEOD-63908 | biostudies-arrayexpress

RNA-Seq analysis of wild-type and Brpf1-null fetal liver LSK cells

Project description:To compare the impact of hematopoietic-specific Brpf1 gene inactivation, LSK (Lin-Sca1+cKit1+) cells were sorted from wild-type and Brpf1-null fetal liver cells for RNA-Seq. Four E14.5 embryos were used to pool sufficient LSK cells for total RNA isolation and subsequent sequencing on HiSq2500. Two independent pairs of wild-type and mutant RNA samples (each of which contained LSK cells pooled from four embryos) were used for oligo-dT primed RNA Seq.

2016-08-10 | E-GEOD-83483 | biostudies-arrayexpress

RNA-Seq analysis of wild-type and Brpf1-null fetal liver LSK cells

Project description:To compare the impact of hematopoietic-specific Brpf1 gene inactivation, LSK (Lin-Sca1+cKit1+) cells were sorted from wild-type and Brpf1-null fetal liver cells for RNA-Seq.

2016-08-10 | GSE83483 | GEO

brpf1 knockdown reduces inhibitory neurotransmission and regulates gene expression of GABAergic interneurons derived from MGE

Project description:Our research is to investigate the role of Brpf1 in the development and function of GABAergic interneurons. To test this, we used mouse primary in vitro cultured GABAergic interneurons derived from medial ganglionic eminence (MGE) and utilized AAV-shBrpf1 virus to knockdown Brpf1. We performed mRNA-seq on the total RNA extracted from the infected neurons .We found that most of the up-regulated genes after Brpf1 knockdown were involved in processes such as protein binding, gene negative transcription, ubiquitination, and inflammation by mRNA-seq. We found that many genes related to neuronal calcium, potassium ion transport and neurotransmitter release changed after Brpf1 was knockdown.Our results demonstrate the key role of Brpf1 in related gene expression of GABAergic interneurons, and provide new lights on the underlying neurobiological mechanisms of BRPF1 mutations that cause mental retardation in children or adolescents.

2021-02-23 | GSE157903 | GEO

Deficiency of intellectual disability-related gene Brpf1 attenuated hippocampal excitatory neurotransmission and impaired learning and memory behavior

Project description:We hypothesized that mouse Brpf1 plays critical roles in the morphology and function of hippocampal neurons, and its deficiency leads to learning and memory deficits. To test this, we performed immunofluorescence, whole-cell patch clamp, mRNA-Seq on shBrpf1 infected primary cultured hippocampal neurons to study the effect of Brpf1 knockdown on neuronal morphology, electrophysiological characteristics and gene regulation. In addition, we performed stereotactic injection into adult mouse hippocampus to knockdown Brpf1 in vivo and examined the learning and memory ability by Morris Water Maze. We found that mild knockdown of Brpf1 reduced mEPSC frequency of cultured hippocampal neurons, before any significant changes of dendritic morphology showed. We also found that hippocampal knockdown of Brpf1 reduced the learning and memory ability of mice to some extent. Finally, mRNA-Seq analyses showed that genes related to learning, memory, movement and synaptic transmission (such as C1ql1, Gpr17, Htr1d, Glra1, Cxcl10, Grin2a) were dysregulated upon Brpf1 knockdown. Our results showed that Brpf1 mild knockdown attenuated hippocampal excitatory neurotransmission and reduced learning and memory ability, which helps explain the symptoms of patients with BRPF1 mutations.

2021-05-19 | GSE174600 | GEO

BRPF1 co-occupies with H3K4me3 and H3K23ac in human ESCs essential to pluripotency [RNA-Seq]

Project description:Post-translational modifications (PTMs) on histones play essential roles in cell fate decisions during development. However, how these PTMs are recognized and coordinated remains to be fully illuminated. Here, we show that BRPF1, a multi-histone binding module protein, is essential to maintain pluripotency in human embryonic stem cells (ESCs). BRPF1, H3K4me3 and H3K23ac substantially co-occupy the active and stemness genes in hESCs. BRPF1 deletion impairs H3K23ac and leads to pluripotency exit and closed chromatin accessibility on stemness genes. Deletion of the N terminal or PHD-zinc knuckle-PHD (PZP) modules completely impairs BRPF1 to maintain hESC pluripotency while PWWP module deletion only partially impact its functions. Together, we reveal that the multi-histone binding module protein, BRPF1 co-ordinates the crosstalk between different histone modifications to maintain the pluripotency in hESCs.

2022-12-21 | GSE213694 | GEO