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RA-induced prominence-specific response resulted in distinctive regulation of Wnt and osteogenesis [miRNA-seq]

ABSTRACT: RA-induced prominence-specific response resulted in distinctive regulation of Wnt and osteogenesis [miRNA-seq]

PROVIDER: PRJNA997905 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR25396409_1.fastq.gz	Fastqsanger.gz
	SRR25396409_2.fastq.gz	Fastqsanger.gz
	SRR25396410_1.fastq.gz	Fastqsanger.gz
	SRR25396410_2.fastq.gz	Fastqsanger.gz
	SRR25396411_1.fastq.gz	Fastqsanger.gz

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RA-induced prominence-specific response resulted in distinctive regulation of Wnt and osteogenesis

Project description:RA-induced prominence-specific response resulted in distinctive regulation of Wnt and osteogenesis

| PRJNA997895 | ENA

RA-induced prominence-specific response resulted in distinctive regulation of Wnt and osteogenesis [mRNA-seq]

Project description:RA-induced prominence-specific response resulted in distinctive regulation of Wnt and osteogenesis [mRNA-seq]

| PRJNA997904 | ENA

RA-induced prominence-specific response resulted in distinctive regulation of Wnt and osteogenesis.

Project description:Proper retinoic acid (RA) signaling is essential for normal craniofacial development. Both excessive RA and RA deficiency in early embryonic stage may lead to a variety of craniofacial malformations, for example, cleft palate, which have been investigated extensively. Dysregulated Wnt and Shh signaling were shown to underlie the pathogenesis of RA-induced craniofacial defects. In our present study, we showed a spatiotemporal-specific effect of RA signaling in regulating early development of facial prominences. Although inhibited Wnt activities was observed in E12.5/E13.5 mouse palatal shelves, early exposure of excessive RA induced Wnt signaling and Wnt-related gene expression in E11.5/E12.5 mouse embryonic frontonasal/maxillary processes. A conserved regulatory network of miR-484-Fzd5 was identified to play critical roles in RA-regulated craniofacial development using RNA-seq. In addition, subsequent osteogenic/chondrogenic differentiation were differentially regulated in discrete mouse embryonic facial prominences in response to early RA induction, demonstrated using both in vitro and in vivo analyses.

| S-EPMC10403638 | biostudies-literature

RA-induced prominence-specific response resulted in distinctive regulation of Wnt and osteogenesis [mRNA-seq]

Project description:Proper retinoic acid (RA) signaling is essential for normal craniofacial development. Both excessive RA and RA deficiency in early embryonic stage led to a variety of craniofacial malformations, e.g., cleft palate, which have been investigated extensively. Dysregulated Wnt and Shh signaling were shown to underlie the pathogenesis of RA-induced craniofacial defects. In our present study, we showed a spatiotemporal-specific effect of RA signaling in regulating early development of facial prominences. While inhibited the Wnt activities in E12.5/E13.5 mouse palatal shelves, early exposure of excessive RA induced Wnt signaling and Wnt-related gene expression in mouse embryonic Frontonasal/Maxillary processes. A conserved regulatory network of miR-484-Fzd5 was identified to play critical roles in RA regulated craniofacial development using RNA-seq.

2023-07-29 | GSE238062 | GEO

RA-induced prominence-specific response resulted in distinctive regulation of Wnt and osteogenesis [miRNA-seq]

2023-07-29 | GSE238063 | GEO

RA-induced prominence-specific response resulted in distinctive regulation of Wnt and osteogenesis

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

2023-07-29 | GSE238064 | GEO

Rhodothermaceae bacterium RA strain:RA

Project description:Rhodothermaceae bacterium RA strain:RA Genome sequencing

| PRJNA308615 | ENA

Osteogenesis Chip-Seq

Project description:Osteogenesis Chip-Seq

| PRJEB4494 | ENA

Osteogenesis RNA-Seq

Project description:Osteogenesis RNA-Seq

| PRJEB4496 | ENA

Phosphoproteome of RA-responsive and RA-resistant breast cancer cell lines

Project description:Retinoic acid (RA), the main active vitamin A metabolite, controls multiple biological processes such as cell proliferation and differentiation through genomic programs and kinase cascades activation. Due to these properties, RA has proven anti-cancer capacity. Several breast cancer cells respond to the antiproliferative effects of RA, while others are RA-resistant. However, the overall signaling and transcriptional pathways that are altered in such cells have not been elucidated. Here, in a large-scale analysis of the phosphoproteins and in a genome-wide analysis of the RA-regulated genes, we compared two human breast cancer cell lines, a RA-responsive one, the MCF7 cell line, and a RA-resistant one, the BT474 cell line, which depicts several alterations of the "kinome".

2020-10-15 | PXD005911 | Pride

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