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Obesity Disrupts the Pituitary-Hepatic UPR Communication Leading to NAFLD Progression (liver bulk RNA seq)

ABSTRACT: Obesity Disrupts the Pituitary-Hepatic UPR Communication Leading to NAFLD Progression (liver bulk RNA seq)

PROVIDER: PRJNA1096108 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR28551823_1.fastq.gz	Fastqsanger.gz
	SRR28551823_2.fastq.gz	Fastqsanger.gz
	SRR28551824_1.fastq.gz	Fastqsanger.gz
	SRR28551824_2.fastq.gz	Fastqsanger.gz
	SRR28551825_1.fastq.gz	Fastqsanger.gz

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Obesity Disrupts the Pituitary-Hepatic UPR Communication Leading to NAFLD Progression (pituitary scRNA seq)

Project description:Obesity alters circulating levels of pituitary hormones that govern hepatic immune-metabolic homeostasis, and dysregulation of which leads to NAFLD. Here, using diet induced obese and IRE1PKO mice, we uncovered an blunted unfolded protein response (UPR) but elevated inflammatory signatures in pituitary glands of obese mice. Mechanistically, we demonstrated that the pituitary IRE1alpha-XBP1 UPR branch is essential for protecting against pituitary endocrine defects and NAFLD progression in obesity.

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Project description:Obesity alters circulating levels of pituitary hormones that govern hepatic immune-metabolic homeostasis, and dysregulation of which leads to NAFLD. Here, using diet induced obese mouse, we uncovered an blunted unfolded protein response (UPR) but elevated inflammatory signatures in pituitary glands of obese mice. Mechanistically, we demonstrated that the pituitary IRE1alpha-XBP1 UPR branch is essential for protecting against pituitary endocrine defects and NAFLD progression in obesity.

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Obesity Disrupts the Pituitary-Hepatic UPR Communication Leading to NAFLD Progression (pituitary scRNA seq)

Project description:Obesity Disrupts the Pituitary-Hepatic UPR Communication Leading to NAFLD Progression (pituitary scRNA seq)

| PRJNA1096109 | ENA

Obesity Disrupts the Pituitary-Hepatic UPR Communication Leading to NAFLD Progression (pituitary bulk RNA seq)

Project description:Obesity Disrupts the Pituitary-Hepatic UPR Communication Leading to NAFLD Progression (pituitary bulk RNA seq)

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Obesity Disrupts the Pituitary-Hepatic UPR Communication Leading to NAFLD Progression (liver bulk RNA seq)

Project description:Obesity alters circulating levels of pituitary hormones that govern hepatic immune-metabolic homeostasis, and dysregulation of which leads to NAFLD. Here, using diet induced obese mouse and IRE1PKO mice, we uncovered an blunted unfolded protein response (UPR) but elevated inflammatory signatures in pituitary glands of obese mice. Mechanistically, we demonstrated that the pituitary IRE1alpha-XBP1 UPR branch is essential for protecting against pituitary endocrine defects and NAFLD progression in obesity.

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Project description:Germline mutations in BRAF and other components of the Mitogen-Activated Protein Kinase (MAPK) pathway are associated with the congenital syndromes collectively known as RASopathies. Here, we report the association of Septo-Optic Dysplasia (SOD) including hypopituitarism and Cardio-Facio-Cutaneous (CFC) syndrome in patients harboring mutations in BRAF. Phosphoproteomic analyses demonstrate that these genetic variants are gain-of-function mutations leading to activation of the MAPK pathway. Activation of the MAPK pathway by conditional expression of the BrafV600E/+ allele, or the knock-in BrafQ241R/+ allele (corresponding to the most frequent human CFC-causing mutation, BRAFp.Q257R), leads to abnormal cell lineage determination and terminal differentiation of hormone-producing cells, causing hypopituitarism. Expression of the BrafV600E/+ allele in embryonic pituitary progenitors leads to an increased expression in cell cycle inhibitors, cell growth arrest and apoptosis but not tumour formation. Our findings show a critical role for BRAF in hypothalamo-pituitary-axis development both in mouse and human and implicate mutations found in RASopathies as a cause of endocrine deficiencies in humans

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