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Transcriptome analysis of human lung andenocarcinoma cell line A549, in which ARAF was depleted and reconstituted with an empty vector control, ARAF wildtype, or a dimer deficient and kinase inactive mutant.

ABSTRACT: Transcriptome analysis of human lung andenocarcinoma cell line A549, in which ARAF was depleted and reconstituted with an empty vector control, ARAF wildtype, or a dimer deficient and kinase inactive mutant.

PROVIDER: PRJNA629473 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR11650300.fastq.gz	Fastqsanger.gz
	SRR11650301.fastq.gz	Fastqsanger.gz
	SRR11650296.fastq.gz	Fastqsanger.gz
	SRR11650297.fastq.gz	Fastqsanger.gz
	SRR11650298.fastq.gz	Fastqsanger.gz

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Transcriptome analysis of human lung andenocarcinoma cell line A549, in which ARAF was depleted and reconstituted with an empty vector control, ARAF wildtype, or a dimer deficient and kinase inactive mutant.

Project description:RNA sequencing analysis of A549 cells that were depleted for ARAF (shARAF) and reconstituted with either empty vector control (+EV) or ARAF wildtype (+ARAF) or dimer deficient ARAF kinase (+R362H) respectively to identify factors that are differentially regulated by ARAF and its kinase activity. In particular, we discovered that ARAF regulates genes that are involved in proliferation and malignant growth by surpressing gene expression of members of the ERBB3/ AKT signaling pathway. At the same time, a functional interpretation of the differentially expressed (DE) genes with topGO indicated an important role of ARAF in regulation of genes involved in, among others, cell adhesion, cell motility, epithelial cell migration.

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