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Chromatin IP sequencing of the nuclear factor HMGB1 in livers from mice after a metabolic stress either induced by a 12-week high fat diet consumption or a fasting (6hours)-refeeding (8hours) challenge.

ABSTRACT: Chromatin IP sequencing of the nuclear factor HMGB1 in livers from mice after a metabolic stress either induced by a 12-week high fat diet consumption or a fasting (6hours)-refeeding (8hours) challenge.

PROVIDER: PRJEB51677 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	ERR9286570.fastq.gz	Fastqsanger.gz
	ERR9286562.fastq.gz	Fastqsanger.gz
	ERR9286563.fastq.gz	Fastqsanger.gz
	ERR9286564.fastq.gz	Fastqsanger.gz
	ERR9286565.fastq.gz	Fastqsanger.gz

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Chromatin IP sequencing of the nuclear factor HMGB1 in livers from mice after a metabolic stress either induced by a 12-week high fat diet consumption or a fasting (6hours)-refeeding (8hours) challenge.

Project description:To unveil HMGB1 DNA occupancy in livers of mice after a metabolic stress either induced by a 12-week high fat diet consumption or a fasting (6hours)-refeeding (8hours) challenge. Challenges known to generate a robust activation of hepatic lipogenesis and liver steatosis.

2022-03-31 | E-MTAB-11543 | biostudies-arrayexpress

Gene expression profiling using cDNA microarray of HMGB1fl/fl and HMGB1ΔHep liver samples from mice subjected to a 12 week-HFD regimen or a Fasting/Refeeding challenge

Project description:To unveil any gene expression difference induced by hepatocyte specific-Hmgb1 gene deletion in mice after a metabolic stress either induced by a 12-week high fat diet consumption or a fasting (6hours)-refeeding (8hours) challenge. Challenges known to generate a robust activation of hepatic lipogenesis and liver steatosis.

2022-03-31 | E-MTAB-11541 | biostudies-arrayexpress

ATAC-sequencing to evaluate the global chromatin dynamics in the absence of hepatic-HMGB1 in livers from mice on fed with chow diet or after a metabolic stress induced by a fasting (6hours)-refeeding (8hours) challenge.

Project description:Hepatocyte nuclei were purified from liver samples harvested from HMGB1fl/fl (n=2) and HMGB1ΔHep (n=2) mice upon chow diet feeding or after fasting-refeeding.

2022-03-31 | E-MTAB-11542 | biostudies-arrayexpress

Gene expression profile showing novel insight for fasting–refeeding response in zebrafish muscle.

Project description:Gene expression profile was investigated using zebrafish muscle unger fasting-refeeding conditions. This study revealed fasting-refeeding responsive genes in zebrafish muscle.

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Fasting/fed/refeeding RNAseq experiment conducted on mice with xenografted human livers.

Project description:Human hepatic gene regulations by fasting and refeeding in a mouse model with humanized liver generated from a single donor were reported.

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HMGB1 interactome in prostate and ovarian cancer cells

Project description:This study reports the interactome of HMGB1 in prostate and ovarian cancer cells, which includes a variety of proteins involved in diverse cellular processes. Subcellular fractionation is used to map the distribution of interacting proteins. In the nucleus, HMGB1 interacts directly with NuRD complex subunit RBBP7, as confirmed by yeast two-hybrid. Amongst HMGB1 interacting proteins are also subunits of the THOC complex and the septin complex. THOC5 IP-MS experiments confirmed that THOC proteins interact with septins and also with RAB11.

2022-02-17 | PXD026258 | Pride

Prolonged fasting/refeeding modifies proteome profile and parvalbumin expression in the fast-twitch muscle of pacu (Piaractus mesopotamicus)

Project description:Skeletal muscle in fish presents a high plasticity controlled by a dynamic balance between anabolic and catabolic signaling pathways. Decreased food availability can inhibit muscle growth and trigger muscle catabolism pathways, thu promoting muscle atrophy. In contrast, anabolism may be favored during restoration of food supply, promoting the muscle growth. Considering this, we analyzed fast-twitch muscle of juvenile Piaractus mesopotamicus (pacu) submitted to a prolonged fasting (30 days) and refeeding (up to 30 days) using shotgun proteomics and gene expression analysis. The relative rate of weight and length increase, as well as the expression of mafbx and igf -1 genes, suggest that prolonged fasting caused muscle atrophy and that 30 days of refeeding led to partial compensatory growth. Shotgun proteomics analysis identified 99 proteins after fasting and 71 proteins after refeeding periods, of which 23 and 17 were differentially expressed after fasting and after 30 days of refeeding, respectively. Most of these differentially expressed proteins were related to cytoskeleton, muscle contraction and muscle metabolism. Among these, parvalbumin (PVALB), a calcium-binding protein and food allergen, was selected for further RT-qPCR analysis, which showed that pvalb mRNA was not changed after 30 days of fasting and 30 days of refeeding, but it was downregulated after 6h and 24h of refeeding. This suggests a post-transcriptional regulation of PVALB in fish muscle. In conclusion, our results suggest that muscle atrophy and partial compensatory growth caused by prolonged fasting and refeeding affected the muscle proteome and PVALB expression. Our results can contribute to the understanding of muscle anabolic and catabolic pathways in response to changes in food availability.

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Characterization of chromatin and gene expression changes during fasting and refeeding in mouse liver [RNA-Seq]

Project description:The discovery of FoxO1 as an effector of insulin action on gene expression filled a gap in our knowledge of insulin signaling. The metabolic impact of hepatic FoxO1 has been demonstrated in genetic mouse models showing that FoxO1 inhibition can reverse diabetes. However, the gamut of FoxO1 targets is unknown, due to the lack of robust genome-wide chromatin occupancy data. To elucidate the genomic architecture of the FoxO1 effect on liver metabolism, we integrated genome-wide ChIP-seq and RNA-seq. During the physiological transition from fasting to refeeding, hepatic FoxO1 translocated from the nucleus to the cytoplasm. At the same time points, cistrome analysis demonstrated that 60% of FoxO1 target sites were cleared by refeeding. RNA-seq from mice following acute liver-specific FoxO1 ablation allowed us to integrate the data in a comprehensive FoxO1 regulome. We identified four distinct classes of FoxO1 targets. Class I targets are enriched in genes regulating cell homeostasis, have FoxO1 sites clustered in promoters and do not show regulation with fasting/refeeding. Class II is comprised of canonical FoxO1 metabolic targets coordinately regulated with other fasting-inducible TFs, such as PPARA, CREB, and GR through promoters. Class III is enriched in glucose metabolic genes regulated through active enhancers, as detected by H3K4me1 and H3K27ac histone marks. Class IV is comprised of triglyceride (TG) and lipoprotein metabolism genes, regulated through intron sites, and characterized by an uneven response to fasting/refeeding regulation.

2022-05-24 | GSE151545 | GEO

Characterization of chromatin and gene expression changes during fasting and refeeding in mouse liver [ChIP-Seq]

2022-05-24 | GSE151544 | GEO

Liver X receptor controls a bifurcated transcriptional program where lipogenesis genes overshoot upon refeeding while cholesterol biosynthesis genes return to pre-fasting levels [lxr_chip]

Project description:Transitions from a fed to a fasted state are common in mammals. The liver orchestrates adaptive responses to feeding/fasting by transcriptionally regulating metabolic pathways of energy usage and storage. Transcriptional and enhancer dynamics following cessation of fasting (refeeding) were never explored. We aimed to inspect the transcriptional and chromatin events occurring upon refeeding, their kinetic behavior and their molecular drivers. We found that the refeeding response is temporally-organized with an early response focused on ramping up protein translation while later stages of refeeding drive a bifurcated lipid synthesis program. While both lipid synthesis pathways were inhibited during fasting, cholesterol biosynthesis genes returned to their basal levels upon refeeding while lipogenesis genes significantly overshoot above pre-fasting levels. Lipogenic gene overshoot is dictated by Liver X Receptor alpha (LXRα) which directly binds and activates lipogenic enhancers. These findings unravel the mechanism behind the long-known phenomenon of refeeding fat overshoot.

2024-07-10 | GSE243051 | GEO

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