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Time course hepatic RNA-Seq in the SRC-3 WT versus KO mice

ABSTRACT: We report the hepatic total gene expression (starting at ZT0 and proceeding every four hours for two complete 12-hour cycles) in the liver of SRC-3 WT and KO mice.

ORGANISM(S): Mus musculus

PROVIDER: GSE175560 | GEO | 2021/12/31

REPOSITORIES: GEO

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Time course SRC-3 ChIP-Seq and XBP1s ChIP-Seq in the C57BJ/L6 WT, SRC-3 WT versus KO, and Xbp1 WT versus LKO mice under chow and fasting conditions

Project description:We report the hepatic SRC-3 and XBP1s cistrome at 4-hour interval timecourse zeitgeber times (ZTs) in the liver of the C57BJ/L6 WT mice under chow and fasting conditions; we also chose liver samples at CT24, ZT0 and ZT8 for comprehensive SRC-3 and XBP1s ChIP-Seq to interrogate the genomic binding profiles of hepatic SRC-3 and XBP1s in vivo.

2021-12-31 | GSE175559 | GEO

Time course Total RNA-Seq in Xbp1 flx/flx (WT, wild-type) mice and AlbCre;Xbp1 flx/flx (XBP1 LKO, liver-specific knockout) mice

Project description:We reported the hepatic total gene expression (starting at CT0 and proceeding every two hours for four complete 12-hour cycles) in the liver of wild-type mice and XBP1 liver-specific knockout mice.

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Time course XBP1s ChIP-Seq in Xbp1 flx/flx (WT, wild-type) mice and AlbCre;Xbp1 flx/flx (XBP1 LKO, liver-specific knockout) mice

Project description:We reported the hepatic XBP1s cistrome (starting at CT0 and proceeding every four hours for three complete 12-hour cycles) in the liver of wild-type mice and XBP1 liver-specific knockout mice; we also chose liver samples at CT0 and CT8 (four hours before the dusk 12-hour rhythmic peak) for comprehensive XBP1s ChIP-Seq to interrogate the genomic binding profiles of hepatic XBP1s in vivo.

2020-05-24 | GSE150889 | GEO

Time course hepatic RNA-Seq in the SRC-3 WT versus KO mice

Project description:Time course hepatic RNA-Seq in the SRC-3 WT versus KO mice

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Individual SRC-2 and SRC-3 knock-down in MCF-7 cells

Project description:Experimental aim: identification of SRC-2 and SRC-3-related genes in MCF-7 breast cancer cells. Experimental workflow: 1. shRNA transduction. MCF-7 cells were transduced with a mix of lentiviral particles containing five individual lentiviral pLKO.1-puro short hairpin (sh) RNA plasmids targeting different sequences on SRC-2 or SRC-3 mRNA and a pLKO.1-puro empty vector control. The puromycin selections were maintained for three weeks to obtain cells containing stably integrated shRNA. 2. Sample preparation. RNA was extracted from eight independent replicates expressing the pLKO.1-puro empty shRNA vector (shKTR), from eight replicates of SRC-2 shRNA expressing cells (shSRC-2), and from seven replicates of SRC-3 shRNA expressing cells (shSRC-3). 300 ng of total RNA from each cell sample was biotin-labelled and amplified.

2019-07-01 | E-MTAB-7018 | biostudies-arrayexpress

Defining the mammalian coactivation of hepatic 12-hour clock and lipid metabolism

Project description:The 12-hour clock coordinates lipid homeostasis, energy metabolism and stress rhythms via the transcriptional regulator XBP1. However, the biochemical and physiological basis for integrated control of the 12-hour clock and diverse metabolic pathways remains unclear. Here, we show that steroid receptor coactivator SRC-3 coactivates XBP1 transcription and regulates hepatic 12-hour cistrome and gene rhythmicity. Mice lacking SRC-3 show abnormal 12-hour rhythms in hepatic transcription, metabolic functions, systemic energetics, and rate-limiting lipid metabolic processes including triglyceride, phospholipid and cardiolipin pathways. Notably, 12-hour clock coactivation is not only preserved, with its cistromic activation priming ahead of the zeitgeber cue of light, but concomitant with rhythmic remodeling in the absence of food. These findings reveal that SRC-3 integrates the mammalian 12-hour clock, energy metabolism, and membrane and lipid homeostasis, and demonstrates a role for the 12-hour clock machinery as an active transcriptional mechanism in anticipating physiological and metabolic energy needs and stresses.

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Integrin α5-SRC signaling induces TET1 mediated hydroxymethylation of genes critical for maintenance of hepatic polarity.

Project description:Conclusions:1、 ITGα5-SRC signalling regulates the CLDN1 expression and hepatic polarity.2、ITGα5-SRC signalling regulates the TET catelyzed DNA 5hmc/5mc level. 3、Itgα5 regulates hydroxymethylation level of genes critical for polarity in vivo. 4、Excessive deposition of ECM blocks the regulatory effect of ITGα5 on CLDN1 in vitro and in vivo.

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Integrin α5-SRC signaling induces TET1 mediated hydroxymethylation of genes critical for maintenance of hepatic polarity

Project description:Conclusions: 1. ITGα5-SRC signalling regulates the CLDN1 expression and hepatic polarity. 2. ITGα5-SRC signalling regulates the TET catelyzed DNA 5hmc/5mc level. 3. Itgα5 regulates hydroxymethylation level of genes critical for polarity in vivo. 4. Excessive deposition of ECM blocks the regulatory effect of ITGα5 on CLDN1 in vitro and in vivo.

2022-11-10 | GSE162409 | GEO

The TGF-β/SMAD pathway upregulates SRC

Project description:The non-receptor tyrosine kinase SRC is upregulated in various human cancers and plays crucial roles in cancer progression by promoting invasion and metastasis. We show that the transforming growth factor beta (TGF-β/SMAD pathway directly upregulates SRC during the epithelial-mesenchymal transition. In human epithelial MCF10A cells, TGF-β1 treatment markedly upregulated mRNA expression of SRC. Knockout of SMAD4 suppressed upregulation of SRC by TGF-β1. ChIP-sequencing analysis revealed that SRC was transcribed from the SRC1A promoter, which interacted with SMAD2 and SMAD4, in response to TGF-β1. These findings demonstrate that a direct interaction of the activated SMAD complex with the SRC1A promoter directly upregulates SRC and suggest that TGF-β contributes to SRC upregulation in the tumor microenvironment, where TGF-β-mediated tumor progression takes place.

2023-11-20 | GSE122913 | GEO

Genomic analysis of SRC-2/TIF2 regulated genes in breast cancer cells_

Project description:We have characterized the global program of transcription in SRC-2-depleted MCF-7 breast cancer cells using short-hairpin RNA technology, and in MCF-7 cells exposed to PKA activating agents. In order to identify genes that may be regulated through PKA-induced downregulation of SRC-2, overlapping transcriptional targets in response to the respective treatments were characterized. MCF-7 human breast cancer cells transduced with shRNA targeting SRC-2 (SRC-2 shRNA) or infected with control shRNA vector (Ctr shRNA) were seeded in 9,2 cm petri dishes, 2,0 x106 cells in each dishes, in DMEM supplemented with 5% charcoaled stripped FBS and 10 nM 17b-estradiol. After 48 hours a selection of the Ctr shRNA cells were treated with cAMP analog (8-CPT-cAMP, 150 µM) and cAMP elevating agents (Forskolin (10 µM) and IBMX (50 µM)) The cells were then incubated for another 24 hour in the cell incubator. Cells were harvested by washing them twice with 8 ml PBS (37 oC), before adding 1,5 ml 0,25 % trypzine. The trypzine reaction was stopped after 5 minutes by adding 2,5 ml DMEM to the cells. Trypzine and cell medium was removed by centrifugating the cell suspensions at 1000 rpm for 3 minutes. The cells were then washed with 400 µl PBS, before addition of 350 µl RLT buffer to the cell pellets. The cells were then homogenized by vortexing for 1 minute and then freezed in -80 oC.

2013-05-15 | E-MTAB-1662 | biostudies-arrayexpress

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