Homo sapiens
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA827594 | ENA |
REPOSITORIES: ENA
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Project description: Not available
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Project description:RNA extracted at 240min. Samples are rRNA depleted. Expression measurement of Homo sapiens genes.
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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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Project description:SPO11-promoted DNA double-strand breaks (DSBs) formation is a crucial step for meiotic recombination, and it is indispensable to detect the broken DNA ends accurately for dissecting the molecular mechanisms behind. Here, we report a novel technique, named DEtail-seq (DNA End tailing followed by sequencing), that can directly and quantitatively capture the meiotic DSB 3’ overhang hotspots at single-nucleotide resolution.
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Project description:The impairment of the intestinal barrier will lead to the accumulation of fat and harmful substances in the liver, inducing hepatic steatosis or steatohepatitis. Zhang et al. identified NSD2 in the intestine as a novel and essential regulator of hepatic steatosis. NSD2 directly regulates transcriptional activation of ERN1 through the modification of H3 dimethylated on lysine 36 (H3K4me36), thereby activating the ERN1-JNK axis to induce inflammatory response, intestinal barrier impairment, and hepatic steatosis. This functional mechanism of NSD2 provides a potential therapeutic target for this disease.
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Project description:The impairment of the intestinal barrier will lead to the accumulation of fat and harmful substances in the liver, inducing hepatic steatosis or steatohepatitis. Zhang et al. identified NSD2 in the intestine as a novel and essential regulator of hepatic steatosis. NSD2 directly regulates transcriptional activation of ERN1 through the modification of H3 dimethylated on lysine 36 (H3K4me36), thereby activating the ERN1-JNK axis to induce inflammatory response, intestinal barrier impairment, and hepatic steatosis. This functional mechanism of NSD2 provides a potential therapeutic target for this disease.
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Project description:Identify factors associated with preserved hepatic insulin sensitivity despite of hepatic steatosis.
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