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Translatome profiling of warm temperature (35°C -> 38.5°C) treated mouse embryonic fibroblast cells in the presense or absence of PI3K inhibitor, 17β-hydroxy wortmannin

ABSTRACT: Translatome profiling of warm temperature (35°C -> 38.5°C) treated mouse embryonic fibroblast cells in the presense or absence of PI3K inhibitor, 17β-hydroxy wortmannin

PROVIDER: PRJNA870739 | ENA |

REPOSITORIES: ENA

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Translatome profiling of warm temperature (35°C -> 38.5°C) treated mouse embryonic fibroblast cells in the presense or absence of PI3K inhibitor, 17β-hydroxy wortmannin

Project description:To see a possible effect of PI3K inhibition on a physiological warm temperature shift (WTS, 35°C to 38.5°C)-induced ribosomal accumulation on the Per2 minimal uORF, we performed Ribo-seq using dexamethasone-synchronized WTS-treated mouse embryonic fibroblast cells with or without 17β-hydroxy wortmannin (wortm) treatment at a circadain rising phase of Per2.

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Transcriptome and translatome profiling of warm temperature (35°C -> 38.5°C) treated mouse embryonic fibroblast cells

Project description:To see a possible effect of a physiological warm temperature shift (WTS, 35°C to 38.5°C) on Per2 transcription and translation in mammalian cells, we performed RNA-seq and Ribo-seq using dexamethasone-synchronized mouse embryonic fibroblast cells with or without WTS treatment at a circadain rising phase of Per2.

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Transcriptome and translatome profiling of warm temperature (35°C -> 38.5°C) treated mouse embryonic fibroblast cells

Project description:Transcriptome and translatome profiling of warm temperature (35°C -> 38.5°C) treated mouse embryonic fibroblast cells

| PRJNA779283 | ENA

Expression data from the study of the oestrognic activity of glabridin in Ishikawa cells in comparison to 17β-oestradiol (17β-E2)

Project description:The general objective of this study was to investigate the effects of glabridin in Ishikawa cells in comparison to 17β-oestradiol by studying its mechanism of action via Affymetrix GeneChip® PrimeViewTM array The treatments were the unctreated control, 10µM glabridin, 100nM glabridin, 1nM 17β-E2 and the combination treatment of 1nM 17β-E2 with 100nM glabridin. The cells were treated for 72 hours and the RNA were extracted for microarray and RT-qPCR study.

2015-04-29 | E-GEOD-68333 | biostudies-arrayexpress

Targeting phosphorylation of 17β-hydroxysteroid dehydrogenase 13 at serine 33 to treat nonalcoholic steatohepatitis

Project description:17β-hydroxysteroid dehydrogenase-13 (17β-HSD13) is a liver-rich lipid droplet associated protein, encoding by gene HSD17B13, that acted as an important regulator of hepatic lipid metabolism. Increased expression of 17β-HSD13 promotes hepatic lipid accumulation in rodents, and a common loss-of-function variant of HSD17B13 (rs72613567: TA) is related to better outcome in patients with various chronic liver diseases. To understand the role of 17β-HSD13 in liver lipid metabolism under normal and high-fat feeding conditions, we characterized the effect of protein phosphorylation of 17β-HSD13 on hepatic lipid homeostasis. We identify Ser33 as an important protein kinase A (PKA)-mediated phosphorylation site of 17β-HSD13 that physically interact with ATGL and facilitates its translocation to lipid droplets to enhance lipolysis. Mutation of Ser33 to Ala (S33A) in 17β-HSD13 reduces ATGL-dependent lipolysis and increases lipid droplet size in cultured hepatocytes by reducing CGI-58-mediated ATGL activation. Consistently, a transgenic knock-in mouse strain carrying HSD17B13 S33A mutation (HSD17B1333A/A) spontaneously develops liver steatosis with reduced lipolysis. Moreover, HSD17B1333A/A mice are more prone to high fat-induced hepatic steatosis and inflammation. Finally, we found Reproterol, a potential HSD17B13 modulator and FDA-approved drug, confers a protection against liver steatosis possibly through phosphorylation of 17β-HSD13 at Ser33 in a PKA-dependent manner. In summary, we demonstrate a critical role and the underlying mechanism of hepatic 17β-HSD13 phosphorylation in the pathogenesis of NAFLD. Our findings highlight the potential of targeting 17β-HSD13 phosphorylation as a novel therapeutic approach for NAFLD.

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Identification of warm-sensitive neuron markers using PhosphoTRAP

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TET1-mediated DNA hydroxy-methylation regulates adult remyelination

Project description:Adult myelination is essential for brain function and response to injury, but the molecular mechanisms remain elusive. Here we identify DNA hydroxy-methylation, an epigenetic mark catalyzed by Ten-Eleven translocation (TET) enzymes, as necessary for adult myelin repair. While DNA hydroxy-methylation and high levels of TET1 were detected in young adult mice during myelin regeneration after demyelination, this process was defective in old mice. Constitutive or inducible lineage-specific ablation of Tet1 (but not of Tet2) recapitulated the age-related decline of DNA hydroxy-methylation and inefficient remyelination. Genome-wide hydroxy-methylation and transcriptomic analysis identified solute carrier gene families as TET1 targets. Lower transcripts for these genes in Tet1 mutants and old mice were associated with swelling at the neuroglial interface, a phenotype detected also in zebrafish Slc12a2b mutants. We conclude that TET1-mediated DNA hydroxy-methylation is necessary for adult myelination after injury, by modulating the levels of the solute carrier SLC12A2 at the axo-myelin interface.

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Project description:This experiment performed RNA-seq of transcriptome and translatome (translating mRNA) of Caco-2 cells We extracted transcriptome and translatome from Caco-2 cells and deep sequenced them

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3β-Hydroxy-friedelan-17β-carboxylic acid.

Project description:The title compound, C(30)H(50)O(3), which was isolated from a marine endophytic fungus, is a new friedelan derivative. The mol-ecule contains five six-membered rings, which exhibit boat (ring A), distorted boat (ring B) and chair (rings C-E) conformations. The crystal structure is stabilized by inter-molecular O-H⋯O hydrogen bonds, which link neighbouring mol-ecules into 12-membered rings.

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MiRNA expression profile in human CD34+/CD105- cells derived from the renal artery subsequent to long warm ischemia compared short warm ischemia

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2015-04-29 | E-GEOD-68366 | biostudies-arrayexpress

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