Similar Datasets
Project description:CtBP2 ChIP-seq normal mouse liver
| PRJNA525001 | ENA
Project description:Liver transcriptome regulated by CtBP2
| PRJNA526541 | ENA
Project description:Feeding behavior, a vital activity in the lives of all captive animals, is orchestrated by a delicate equilibrium between the orexigenic and anorexigenic activities of neurons in the hypothalamus. This exquisite control of neuropeptides governing the feeding behavior can be a focal point in the pathogenesis of obesity, and unraveling of the intricate transcriptional systems behind this may offer clues to develop approaches for better management of obese subjects. The transcriptional corepressor, C-terminal binding protein 2 (CtBP2), has been reported to be a metabolite-sensor inactivated in liver tissues and pancreatic β-cells in obesity. Here we describe a transcriptional system regulated by CtBP2 in hypothalamus. Our global mapping of CtBP2 binding sites by ChIP-seq reveals the recruitment of CtBP2 to the promoters of those neuropeptides as well as other key genes involved in the maintenance of hypothalamic neuronal activities. Whereas the expression of CtBP2 is not altered in obese mouse models, the recruitment of CtBP2 to the promoters of those neuropeptides is diminished in obesity, suggesting allosteric inactivation of CtBP2 in the metabolic milieu in obesity in this tissue. Exogenous expression of CtBP2 in hypothalamic cells decreases NPY gene promoter activity, and loss of CtBP2 in hypothalamic neurons in mice increases expression levels of orexigenic neuropeptides. These findings illustrate a sequential event where obesity promotes orexigenic behavior through metabolic inactivation of CtBP2. Our findings underscore a previously unexplored layer within the redundant transcriptional systems that regulate the hypothalamic feeding circuitry.
2026-08-05 | GSE266964 | GEO
Project description:adenovirus mediated overexpression of wild-type CtBP2 and Rossmann fold mutant CtBP2 along with control GUS in dietary induced obese mice
2021-09-27 | GSE128145 | GEO
Project description:Feeding behavior, a vital activity in the lives of all captive animals, is orchestrated by a delicate equilibrium between the orexigenic and anorexigenic activities of neurons in the hypothalamus. This exquisite control of neuropeptides governing the feeding behavior can be a focal point in the pathogenesis of obesity, and unraveling of the intricate transcriptional systems behind this may offer clues to develop approaches for better management of obese subjects. The transcriptional corepressor, C-terminal binding protein 2 (CtBP2), has been reported to be a metabolite-sensor inactivated in liver tissues and pancreatic β-cells in obesity. Here we describe a transcriptional system regulated by CtBP2 in hypothalamus. Our global mapping of CtBP2 binding sites by ChIP-seq reveals the recruitment of CtBP2 to the promoters of those neuropeptides as well as other key genes involved in the maintenance of hypothalamic neuronal activities. Whereas the expression of CtBP2 is not altered in obese mouse models, the recruitment of CtBP2 to the promoters of those neuropeptides is diminished in obesity, suggesting allosteric inactivation of CtBP2 in the metabolic milieu in obesity in this tissue. Exogenous expression of CtBP2 in hypothalamic cells decreases NPY gene promoter activity, and loss of CtBP2 in hypothalamic neurons in mice increases expression levels of orexigenic neuropeptides. These findings illustrate a sequential event where obesity promotes orexigenic behavior through metabolic inactivation of CtBP2. Our findings underscore a previously unexplored layer within the redundant transcriptional systems that regulate the hypothalamic feeding circuitry.
2026-08-05 | GSE266966 | GEO
Project description:Feeding behavior, a vital activity in the lives of all captive animals, is orchestrated by a delicate equilibrium between the orexigenic and anorexigenic activities of neurons in the hypothalamus. This exquisite control of neuropeptides governing the feeding behavior can be a focal point in the pathogenesis of obesity, and unraveling of the intricate transcriptional systems behind this may offer clues to develop approaches for better management of obese subjects. The transcriptional corepressor, C-terminal binding protein 2 (CtBP2), has been reported to be a metabolite-sensor inactivated in liver tissues and pancreatic β-cells in obesity. Here we describe a transcriptional system regulated by CtBP2 in hypothalamus. Our global mapping of CtBP2 binding sites by ChIP-seq reveals the recruitment of CtBP2 to the promoters of those neuropeptides as well as other key genes involved in the maintenance of hypothalamic neuronal activities. Whereas the expression of CtBP2 is not altered in obese mouse models, the recruitment of CtBP2 to the promoters of those neuropeptides is diminished in obesity, suggesting allosteric inactivation of CtBP2 in the metabolic milieu in obesity in this tissue. Exogenous expression of CtBP2 in hypothalamic cells decreases NPY gene promoter activity, and loss of CtBP2 in hypothalamic neurons in mice increases expression levels of orexigenic neuropeptides. These findings illustrate a sequential event where obesity promotes orexigenic behavior through metabolic inactivation of CtBP2. Our findings underscore a previously unexplored layer within the redundant transcriptional systems that regulate the hypothalamic feeding circuitry.
2026-08-05 | GSE266965 | GEO
Project description:Using an RNA interference-based genetic screen in mouse F9 cells we identify the transcriptional corepressor CTBP2 as a coactivator critically required for retinoic acid (RA)-induced transcription. Here we perfom a whole genome transcriptome analysis in F9 cells expressing shRNA for Ctbp2 and Rxr in the absence or presence of retinoic acid (RA). A total of 2,754 genes were found to be upregulated (>2 fold) and 1518 genes were downregulated (>2 fold) in response to RA treatment in the control cells. We find that around 52% and 55% of upregulated genes are dependent on Ctbp2 and Rxr for activation respectively suggesting that Ctbp2 is a coactivator of RA signaling. Whole genome RNA-sequencing in F9 cells expressing shGFP or shCtbp2 or shRxr
2013-06-21 | E-GEOD-47708 | biostudies-arrayexpress
Project description:Using an RNA interference-based genetic screen in mouse F9 cells we identify the transcriptional corepressor CTBP2 as a coactivator critically required for retinoic acid (RA)-induced transcription. Here we perfom a whole genome transcriptome analysis in F9 cells expressing shRNA for Ctbp2 and Rxr in the absence or presence of retinoic acid (RA). A total of 2,754 genes were found to be upregulated (>2 fold) and 1518 genes were downregulated (>2 fold) in response to RA treatment in the control cells. We find that around 52% and 55% of upregulated genes are dependent on Ctbp2 and Rxr for activation respectively suggesting that Ctbp2 is a coactivator of RA signaling.
2013-06-21 | GSE47708 | GEO
Project description:CtBP2 ChIP-seq analysis was performed in a murine pancreatic beta cell line MIN6.
2023-08-08 | GSE221257 | GEO