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Transcriptome profiling of RBM3 overexpression in A431 cells

ABSTRACT: Transcriptome profiling of RBM3 overexpression in A431 cells

PROVIDER: PRJNA1103222 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR28775010_1.fastq.gz	Fastqsanger.gz
	SRR28775010_2.fastq.gz	Fastqsanger.gz
	SRR28775011_1.fastq.gz	Fastqsanger.gz
	SRR28775011_2.fastq.gz	Fastqsanger.gz
	SRR28775012_1.fastq.gz	Fastqsanger.gz

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Transcriptome profiling of RBM3 overexpression in A431 cells

Project description:This study aims to investigate the transcriptional changes induced by overexpression of RNA-binding protein RBM3 in A431 human epidermoid carcinoma cells. Lentiviral transduction was used to stably overexpress RBM3 in A431 cells. Total RNA was extracted from RBM3 overexpressing cells and control cells, followed by RNA-seq library preparation and sequencing on Illumina platform. Differential gene expression analysis will be performed to identify RBM3 targets and regulatory networks.

2025-05-01 | GSE264600 | GEO

human epidermoid carcinoma cell: Control (A431-P cells) vs. highly invasive subline (A431-III cells)

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human epidermoid carcinoma cell: Control (A431-P cells) vs. highly invasive subline (A431-III cells)

Project description:Transcriptional profiling of human epidermoid carcinoma cell comparing control A431-P cells with highly invasive subline A431-III cells No treatmentt, A431-P cells vs. A431-III cells. A431-P cells are used as a reference to invstigate A431-III cells.

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RNA-binding protein RBM3 negatively regulates innate lymphoid cells (ILCs) and lung inflammation

Project description:Innate lymphoid cells (ILCs) promote lung inflammation in diseases such as asthma through cytokine production. RNA-binding proteins (RBPs) are critical post-transcriptional regulators of cellular function though the role of RBPs in innate lymphoid cells is unknown. Here, we demonstrate that RNA-binding motif 3 protein (RBM3) is one of the most highly expressed RBPs in Thy1.2+ lung ILCs after fungal allergen challenge and is further induced by epithelial cytokines TSLP and IL-33 in both human and mouse ILCs. Single (rbm3-/-) and double (rbm3-/-rag2-/-) knockout mice exposed via the airway to the asthma-associated fungal allergen Alternaria alternata displayed increases in eosinophilic lung inflammation and ILC activation compared to control mice. In addition to increased Th2 cytokine production, rbm3-/- ILCs produced elevated IL-17A. The negative regulation by RBM3 in ILC responses was direct as purified rbm3-/- ILCs were hyperinflammatory in vitro and in vivo after stimulation with IL-33. Transcriptomic analysis by RNA-sequencing of rbm3-/- lung ILCs showed increased type 2 and 17 cytokines as well as global expression differences in critical cytokines, receptors, transcription factors, and survival transcripts compared with WT ILCs. Importantly, these transcript changes were independent of the numbers of AU-rich elements (AREs) which RBM3 is known to bind. Thus, regulation of ILC responses by RNA-binding proteins offers novel mechanistic insight into lung ILC biology and ILC-driven inflammatory diseases.

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