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Role of ATF4 in regulation of kidney gene expressions, signaling pathways and functions [mouse]

ABSTRACT: Role of ATF4 in regulation of kidney gene expressions, signaling pathways and functions [mouse]

PROVIDER: PRJNA1231460 | ENA |

REPOSITORIES: ENA

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			Action	DRS
		Other
	SRR32566510_1.fastq.gz	Fastqsanger.gz
	SRR32566510_2.fastq.gz	Fastqsanger.gz
	SRR32566511_1.fastq.gz	Fastqsanger.gz
	SRR32566511_2.fastq.gz	Fastqsanger.gz

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Role of ATF4 in regulation of kidney gene expressions, signaling pathways and functions

Project description:Role of ATF4 in regulation of kidney gene expressions, signaling pathways and functions

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Role of ATF4 in regulation of kidney gene expressions, signaling pathways and functions [mouse]

Project description:Activating transcription factor 4 (ATF4) is a transcription factor that mediates the response to stress at the cellular, tissue, and organism level. We deleted the gene encoding ATF4 in the kidney proximal tubules of the wild type (WT) and TRACK (TRAnsgenic model of Cancer of the Kidney (TRACK)) mice by using a temporal and cell type-specific approach. We show that ATF4 plays a major role in regulating the transcriptome and proteome, which, in turn, influences the metabolome and kidney functions. ATF4 deletion changed transcripts of some transporters responsible for nutrient uptake and waste excretion. It modulates metabolisms of fatty acid and glucose in the mouse model of ccRCC. It also changes metabolism in RCC4 cells. These data indicate that ATF4 plays an important role in regulation of kidney functions.

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Role of ATF4 in regulation of kidney gene expressions, signaling pathways and functions [human RCC4]

Project description:Role of ATF4 in regulation of kidney gene expressions, signaling pathways and functions [human RCC4]

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Role of ATF4 in regulation of kidney gene expressions, signaling pathways and functions

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Translational activation of ATF4 through mitochondrial anaplerotic metabolic pathways is required for DLBCL growth and survival

Project description:Cancer cells frequently hijack adaptive stress response signals/pathways to protect themselves from metabolic or genetic vulnerabilities, pointing to candidate therapeutic targets. Among these SIRT3 was recently identified as a non-oncogene addiction mechanism in DLBCL through its role in glutamine metabolism. Here, we investigated downstream signaling pathways linked to SIRT3 function in lymphoma. We performed RNA-seq in DLBCL cells after SIRT3 knockdown and observed that ATF4 target genes were significantly downregulated in SIRT3 deficient cells. ATF4, a master regulator of cellular stress, was required to maintain proliferation and survival of DLBCL cells and its target genes were overexpressed in DLBCL patients as compared to normal germinal center B cells. Translation of ATF4 mRNA was inhibited in SIRT3 knockdown cells and expression of exogenous ATF4 partially rescued cell proliferation and viability inhibited by SIRT3 deficiency. Accordingly, ATF4 protein was expressed at relatively lower levels SIRT3 deficient murine lymphomas, whereas its higher expression was associated with more severe disease. We characterized mechanisms through which SIRT3 maintains ATF4 expression, downstream of its effects on glutamine entry into the TCA cycle and suppression of autophagy. Specifically, loss of SIRT3 disrupted amino acid metabolism in DLBCL cells, with subsequent impairment of ATF4 response to metabolic stressors such as glutamine depletion. Collectively, the data suggest a key SIRT3-ATF4 axis maintains survival of DLBCL cells enabling them to optimize amino acid metabolism and cope with metabolic vulnerabilities possibly associated with their high proliferative rate.

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lncRNA expressions of the kidney tissues of DKD patients and controls

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Effect of muscle-specific ATF4 gene knockout (ATF4 mKO) on skeletal muscle mRNA levels in aged mice.

Project description:For additional details see Ebert et al, Identification and Small Molecule Inhibition of an ATF4-dependent Pathway to Age-related Skeletal Muscle Weakness and Atrophy. Quadriceps femoris muscles were harvested from 22-month-old muscle-specfic ATF4 knockout (ATF4 mKO) mice and littermate controls. mRNA levels in ATF4 mKO muscles were normalized to levels in littermate control muscles.

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Global proteome analysis of ATF4 targets during ER stress.

Project description:Cancer cells exploit many of the cellular adaptive responses to support their survival needs. One such critical pathway in eukaryotic cells is the unfolded protein response (UPR) that is important in normal physiology as well as disease states, including cancer. Since UPR can serve as a lever between survival and death, regulated control of its activity is critical for tumor formation and growth although the underlying mechanisms are poorly understood. Here we show that one of the main transcriptional effectors of UPR, activating transcription factor 4 (ATF4), is essential for prostate cancer (PCa) growth and survival. To identify ATF4 target genes that mediate the ISR outcome and to get insight into its mechanism of action in PCa, we performed global proteomic expression profiling in parallel with transcriptomic expression profiling. These data show that ATF4 regulates important metabolic pathways in PCa cells.

2019-07-22 | PXD012858 | Pride

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