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Analysis of mRNA expression of livers from (PR)97 expressing mice

ABSTRACT: Analysis of mRNA expression of livers from (PR)97 expressing mice

PROVIDER: PRJNA998808 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR25432849.fastq.gz	Fastqsanger.gz
	SRR25432850.fastq.gz	Fastqsanger.gz
	SRR25432851.fastq.gz	Fastqsanger.gz
	SRR25432852.fastq.gz	Fastqsanger.gz

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Analysis of mRNA expression of livers from (PR)97 expressing mice

Project description:Nucleolar stress (NS) kills cells by p53-dependent and independent manners. To investigate the mechanisms of p53-indendendent toxicity, we here used (PR)n arginine-rich peptides as inducers of NS, which are found in patients of some neurodegenerative diseases. Although these peptides generate NS, how this translates to toxicity is poorly understood. We here reveal that whereas (PR)n expression leads to an overall decrease in protein abundance for the majority of the proteome, this occurs concomitant to an accumulation of free ribosomal proteins in the cytoplasm, which is a hallmark of ribosomopathies. Conversely, cells with acquired resistance to (PR)n peptides present a global downregulation of ribosomal proteins and low levels of mTOR signaling. In mice, systemic expression of (PR)97 drives widespread NS and accelerated ageing, associated to an increased expression of ribosomal proteins and mTOR hyperactivation. Furthermore, the progeroid phenotype of (PR)97-expressing mice is alleviated by rapamycin. Importantly, we show that the generalized accumulation of free ribosomal proteins is not restricted to (PR)n peptides, but is a common outcome in response to chemical or genetic perturbations that generate NS such as Actinomycin D, TIF-IA depletion or the expression or mutant HMGB1 forms recently associated to rare human diseases. Together, our study provides in vivo evidence for the role of NS as a driver of ageing in mammals, and describes a general model to understand the mechanisms behind p53-independent cell toxicity caused by NS.

2024-03-08 | GSE239319 | GEO

RNA-seq analysis of PR-expressing FTE cells (2D)

Project description:RNA-seq analysis of PR-expressing FTE cells (2D)

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Cardiac microarray changes in a transgenic mouse expressing a human mitochondrial progesterone receptor (PR-M).

Project description:A TET-On transgenic mouse model was develop for cardiac expression of a human mitochondrial progesterone receptor (PR-M). Expression was verified by immunohistochemistry and RT-PCR. Previous research with cell knockdown and overexpression has shown a ligand dependent increase in cellular respiration with this receptor. Mice expressing (N=3) or not expressing (N=3) PR-M were treated with progesterone for 19-21 days prior to sacrifice. Tissue from the apical cardiac ventrical was submitted for microarray.

2017-12-27 | GSE108551 | GEO

mRNA profiles of livers during postnatal development

Project description:mRNA profiles of livers during postnatal development

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Motor dysfunction and neurodegeneration in a C9orf72 mouse line expressing poly-PR

Project description:Motor dysfunction and neurodegeneration in a C9orf72 mouse line expressing poly-PR

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Chikungunya virus strain:PR-S4, PR-S5, PR-S6 (Puerto Rico)

Project description:Chikungunya virus strain:PR-S4, PR-S5, PR-S6 (Puerto Rico) Metagenomic assembly

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Title: Site specific O-GlcNAcylation of progesterone receptor (PR) supports PR attenuation of interferon stimulated genes (ISGs) and tumor growth in breast cancer

Project description:Hormone receptor (HR) positive breast cancer, defined by expression of estrogen (ER) and/or progesterone (PR) receptor expression, is the most commonly diagnosed type of breast cancer. PR alters the transcriptional landscape to support tumor growth in concert with or independent of ER. Understanding the mechanisms regulating PR function are critical to developing new strategies to treat HR+ breast cancer. O-GlcNAc is a post-translational modification responsible for nutrient sensing that fine tunes protein function. We have previously reported O-GlcNAcylation on PR. Although PR is heavily post translationally modified, primarily through phosphorylation, specific sites of O-GlcNAcylation on PR, and how they regulate PR action, have not been investigated. Using established PR-expressing breast cancer cell lines, we mapped the sites of O-GlcNAcylation on PR. RNA-sequencing revealed site-specific O-GlcNAcylation of PR is critical for ligand-independent suppression of interferon signaling, a regulatory function of PR previously studied in our lab. Furthermore, O-GlcNAcylation of PR enhances PR-driven tumor growth in vivo. We have delineated one mechanism regulating PR function in breast cancer that impacts tumor growth, and provided additional insight into the mechanism through which PR attenuates interferon signaling.

2024-06-17 | MSV000095057 | MassIVE

mRNA profiling of injured mouse livers with MycER activation

Project description:mRNA profiling of injured mouse livers with MycER activation

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Spontaneous development of hepatocellular carcinoma with cancer stem cell properties in PR-SET7 deficient livers.

Project description:PR-SET7-mediated histone-4 lysine-20 methylation has been implicated in mitotic condensation, DNA damage response and replication licencing. Here we show that PR-SET7 function in the liver is pivotal for maintaining genome integrity. Hepatocyte-specific deletion of PR-SET7 in mouse embryos resulted in G2 arrest followed by massive cell death and defect in liver organogenesis. Inactivation at postnatal stages caused cell duplication-dependent hepatocyte necrosis. Necrotic death was accompanied by inflammation, fibrosis and compensatory growth induction of neighboring hepatocytes and resident ductal progenitor cells. Prolonged necrotic-regenerative cycles coupled with oncogenic STAT3 activation replaced pre-existing hepatocytes with hepatocellular carcinoma derived entirely from cells with cancer stem cell characteristics. Hepatocellular carcinoma in these mice displays a cancer stem cell gene signature specified by the co-expression of ductal progenitor markers and oncofetal genes.

2014-12-01 | GSE61567 | GEO

Isolates of PR

Project description:Isolates of PR

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