Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR28804326_1.fastq.gz | Fastqsanger.gz | |||
| SRR28804326_2.fastq.gz | Fastqsanger.gz | |||
| SRR28804327_1.fastq.gz | Fastqsanger.gz | |||
| SRR28804327_2.fastq.gz | Fastqsanger.gz | |||
| SRR28804328_1.fastq.gz | Fastqsanger.gz |
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Project description:This experiment was conducted to identify novel XBP-1 targets involved in liver metabolism. The following abstract from the submitted manuscript describes the major findings of this work. The IRE1a-XBP1s axis regulates the COPII-mediated secretory program in response to nutrient availability. Lin Liu, Jie Cai, Xijun Liang, Qian Zhou, Huimin Wang, Chenyun Ding, Yuangang Zhu, Liwei Xiao, Tingting Fu, Zhisheng Xu, Jing Liu, Yujing Yin, Lei Fang, Bin Xue, Yan Wang, Aibin He, Yong Liu, Xiao-Wei Chen, and Zhenji Gan The cytoplasmic coat protein complex-II (COPII) is an evolutionarily conserved machinery that is essential for efficient trafficking of protein and lipid cargos. How the COPII machinery is regulated to meet the metabolic demand in response to alterations of nutritional state remains largely unexplored, however. Here, we show that dynamic changes of COPII-mediated secretion parallel the activation of XBP1s, the critical transcription factor in handling cellular ER stress, in both live cells and mouse liver upon physiological fluctuations of nutrient availability. Using live-cell imaging approaches, we demonstrate that XBP1s is sufficient to promote COPII-dependent secretion, mediating the nutrient stimulatory effects. ChIP-seq and RNA-seq analyses reveal that nutritional signals induce dynamic XBP1s occupancy of promoters of COPII secretion-related genes, thereby driving COPII-directed secretory process. Liver-specific disruption of the IRE1a-XBP1s signaling branch results in diminished COPII-mediated secretion. Reactivation of XBP1s in mice lacking hepatic IRE1a restores COPII-mediated lipoprotein secretion, and reverses the fatty liver and hypolipidemia phenotypes. Thus, our results demonstrate a previously unappreciated mechanism in the metabolic control of liver protein and lipid secretion: the IRE1a-XBP1s axis functions as a nutrient-sensing regulatory nexus that integrates nutritional states and the COPII secretory program.
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Project description:To investigate the role of PFKP in laryngea cancer, we established a LIU-LSC-1 cell line with PFKP knocked down by lentivirus technique. We then performed gene expression profiling targeting the RNA-seq data of the control and PFKP knockdown groups.
2024-08-08 | GSE248242 | GEO
Project description:transcriptional profiling of L. monocytogenes ctsR mutant under pressure treatment SUBMITTER_CITATION: Liu, Y., Huang, L., Joerger, R.D., Gunther, N.W. 2012. Genes that are involved in high hydrostatic pressure treatments in a Listeria monocytogenes Scott A ctsR deletion mutant. Journal of Microbial and Biochemical Technology. 4:050-056.
2013-02-14 | GSE32172 | GEO
Project description:This experiment was conducted to identify mRNA transcripts alteration in muscle from skeletal muscle-sepcific Fundc1-knockout mice. The following abstract from the submitted manuscript describes the major findings of this work. Mitophagy directs muscle-adipose crosstalk to alleviate dietary obesity. Tingting Fu, Zhisheng Xu, Lin Liu, Qiqi Guo, Hao Wu, Xijun Liang, Danxia Zhou, Liwei Xiao, Lei Liu, Yong Liu, Min-Sheng Zhu, Quan Chen and Zhenji Gan. The quality of mitochondria in skeletal muscle is essential for maintaining metabolic homeostasis during adaptive stress responses. However, the precise control mechanism of muscle mitochondrial quality and its physiological impacts remain unclear. Here, we demonstrate that FUNDC1, a mediator of mitophagy, plays a critical role in controlling muscle mitochondrial quality as well as metabolic homeostasis. Skeletal muscle-specific ablation of FUNDC1 in mice resulted in LC3-mediated mitophagy defect, leading to impaired mitochondrial energetics. This caused decreased muscle fat utilization and endurance capacity during exercise. Interestingly, mice lacking muscle FUNDC1 were protected against high-fat diet-induced obesity with improved systemic insulin sensitivity and glucose tolerance despite reduced muscle mitochondrial energetics. Mechanistically, FUNDC1 deficiency elicited a retrograde response in muscle that upregulated FGF21 expression, thereby promoting the thermogenic remodeling of adipose tissue. Thus, these findings reveal a pivotal role of FUNDC1-dependent mitochondrial quality-control in mediating the muscle-adipose dialogue to regulate systemic metabolism.
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Project description:The lysine 23 of histone H3 (H3K23me2) positively correlates with H3K9me3 and H3K27me3, marks enriched in heterochromatic regions (Ho, J.W. et al., 2014; Garrigues, J.M. et al., 2015; Liu, T. et al., 2015), and negatively correlates with H3K36me2/3 and H3K23/27ac, modifications enriched in actively transcribed regions. Similarly to the reported distribution of H3K9me3 (Ho, J.W. et al., 2014; Garrigues, J.M. et al., 2015), H3K23me2 is enriched on autosomal arms and is depleted from the central regions of the autosomes and from most of the lenght of the X chromosome.
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Project description:Lacticaseibacillus paracasei strain:KL1-Liu Genome sequencing and assembly
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Project description:Chromatin immunoprecipitation of FOXK2 (tagged with Flag and His tags) in U2OS cells detected by SOLiD sequencing. ***Correction March 2014: The sample “FOXK2_Dox_treated” has been renamed, it was originally named “FOXK2_rep2”. A new sample “FOXK2_rep2” has been added, with new files. It has come to our attention that one of the FOXK2 ChIP-seq replicates 'FOXK2_rep2' that we used in our paper recent paper (Ji, Z., Donaldson, I.J., Liu, J., Hayes, A., Zeef, L.A.H. and Sharrocks, A.D. (2012) The forkhead transcription factor FOXK2 promotes AP-1-mediated transcriptional regulation. Mol. Cell. Biol. 32, 385-398. doi:10.1128/MCB.05504-11) was incorrect. The replicate was actually treated with doxorubicin prior to ChIP-seq analysis resulting in the loss of many FOXK2 binding events.***
2011-01-20 | E-MTAB-565 | biostudies-arrayexpress