Comparison of gene expression (hESC, PGC-like cell from hESC, SSC from testis)
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
SUBMITTER: LIM JUNG JIN
PROVIDER: E-GEOD-52302 | biostudies-arrayexpress |
REPOSITORIES: biostudies-arrayexpress
Similar Datasets
Project description:PGC-1α (Peroxisome proliferator-activated receptor gamma coactivator-1alpha) coactivators regulate adaptive gene expression in response to challenges such as cold exposure, fasting, or physical exercise to balance energy supply and demand. Transcription of a single PGC-1α gene produces different isoforms (e.g. PGC-1α1 to α4) with different biological functions. We aimed to characterize the nuclear interactome for each PGC-1α variant, in particular the transcription factors they bind to regulate gene expression. This was done by generating GST-fusions of all PGC-1a variants, expressed in an insect cell system. These were used to capture associated protein complexes from HeLa nuclear extracts.
2022-03-01 | PXD009232 | Pride
Project description:Microarray analysis to identify the similarity of gene expression between ESC-derived PGC-like cells and testis-derived SSCs
2013-11-13 | GSE52302 | GEO
Project description:Huntington's Disease (HD) is an inherited neurodegenerative disease caused by a glutamine repeat expansion in huntingtin protein. Transcriptional deregulation and altered energy metabolism have been implicated in HD pathogenesis. We report here that mutant huntingtin causes disruption of mitochondrial function by inhibiting expression of PGC-1a, a transcriptional coactivator that regulates several metabolic processes including mitochondrial biogenesis and respiration. Mutant huntingtin represses PGC-1a gene transcription by associating with the promoter and interfering with the CREB/TAF4-dependent transcriptional pathway critical for the regulation of PGC-1a gene expression. Crossbreeding of PGC-1a knockout mice with HD knock-in mice leads to increased neurodegeneration of striatal neurons and motor abnormalities in the HD mice. Importantly, expression of PGC-1a partially reverses the toxic effects of mutant huntingtin in cultured striatal neurons. Moreover, lentiviral-mediated delivery of PGC-1a in the striatum provides neuroprotection in the transgenic HD mice. These studies suggest a key role for PGC-1a in the control of energy metabolism in the early stages of HD pathogenesis. Experiment Overall Design: Total RNA was extracted from striata of 3 pgc1 KO mice and 3 littermate controls using the RNeasy Mini Kit (Qiagen) according to manufacturer's protocol. Samples were analyzed using RNA 6000 Nano LabChip kit on a 2100 Bioanalyzer (Agilent Technologies) to ensure integrity of RNA.
2007-11-13 | E-GEOD-5786 | biostudies-arrayexpress
Project description:With PNGase F digestion, PGC enrichment,OVA N-glycans were analyzed using PGC nanoLC-ESI-MS/MS.Datasets were analyzed by the N-glycan database search engine called GlycanGoggle developed in our group.
2019-01-17 | PXD006400 | Pride
Project description:Differentiated C2C12 cells adenovirally overexpressing either PGC-1alpha or PGC-1beta or GFP as control were treated with TNFalpha for 2h or left untreated. NF-kappaB- and stress-depedent gene expression was determined by a customized array.
2012-12-14 | E-MEXP-3676 | biostudies-arrayexpress
Project description:Mesenchymal stem cells (MSCs) are a multipotent cell type that can differentiate into non-hematopoietic cells, such as adipocytes. Adipocyte tissue is central to regulate energy balance. PGC-1 alpha controls several aspects of mitochondrial biogenesis. However, roles of PGC-1 alpha in brown fat differentiation of MSCs remain uncertain. To investigate roles of PGC-1 alpha in brown fat differentiation immortalized human MSCs were used for all experiments. The changes in genetic profiling between MSCs and PGC-1 alpha-expressing MSCs were analyzed by microarray analysis. The genetic profiling of PGC-1 alpha-expressing MSCs shows the significant increase of genes related to mitochondrial functions and lipid metabolism compared to that of MSCs. When expressed in MSCs, PGC-1 alpha activates a robust mitochondrial biogenesis and respiration. The expression of thermogenic markers, such as cytochrome C and complex II, was significantly increased in MSCs with treatment of adenovirus expressing PGC-1 alpha. Our microarray results also indicate that genetic pattern of PGC-1 alpha-expressing MSCs is very closed to that of adipose tissues. Bone marrow-derived MSCs were infected with Ad-GFP, or Ad-PGC-1? at a multiplicity of infection (m.o.i.) of 500 overnight.
2010-12-01 | E-GEOD-19643 | biostudies-arrayexpress
Project description:We examined global gene expression patterns in response to PGC-1 expression in cells derived from liver or muscle. As our study revealed regulation of HSF1 by PGC-1alpha, in some experiments we knocked-down HSF1 using siRNAs in addition to inducing PGC-1alpha expression. Cells were grown in 24-well plates and adenoviruses encoding either GFP ("Ad-GFP"), PGC-1alpha ("Ad-PGC-1alpha") or PGC-1beta ("Ad-PGC-1beta") were directly added to the culture medium. For experiments involving siRNA transfections, cells were transfected with the indicated siRNAs 48hr prior to infection with adenoviruses encoding either GFP ("Ad-GFP") or PGC-1alpha ("Ad-PGC-1alpha").
2015-09-19 | E-GEOD-51498 | biostudies-arrayexpress
Project description:This dataset is part of the manuscript titled "The metabolic regulator ERRalpha, a downstream target of HER2/IGF1, as a therapeutic target in breast cancer" (in review). The expression data obtained in human mammary epithelial cells were used to generate a list of ERRalpha-regulated genes that was later refined in clinical breast cancer datasets to generate a clinically relevant signature of ERalpha activity (referred to as Cluster 3 signature). Using this signature of the estrogen-related receptor alpha (ERRa) to profile more than eight-hundred breast tumors, we found that patients with tumors exhibiting higher ERRa activity were predicted to have shorter disease free survival. Further, the ability of an ERRa antagonist, XCT790, to inhibit breast cancer cell proliferation correlates with the cellâs intrinsic ERRa activity. These findings highlight the potential of using the ERRa signature and antagonists in targeted therapy for breast cancer. Using a chemical genomic approach we determined that activation of the HER2/IGF1 signaling pathways upregulates the expression of PGC-1b, an obligate cofactor for ERRa activity. Knockdown of PGC-1b in HER2 positive breast cancer cells impaired ERRa signaling and reduced cell proliferation, implicating a functional role of PGC1b/ERRa in the pathogenesis HER2 positive breast cancer. Primary human mammary epithelial cells were a gift from Dr. J. Marks (Duke University, Durham, NC) and cultured in MEBM (Cambrex, East Rutherford, NJ) with MEGM bullet kit and supplemented with 5mg/ml transferrin and 10-5M isoproterenol. To generate ERR-alpha signature, hMECs were serum starved for 36h followed by infection with MOI=150 of adenoviruses expressing two variants of PGC1alpha, a protein ligand for ERRalpha: PGC-1alpha2x9 or PGC-1alpha L2L3M. PGC-1-2x9 is specific to ERRalpha, while PGC-1-L2L3M lacks the NR box and does not interact with ERRalpha or other nuclear receptors. The generation and purification of variant PGC-1alpha viruses were described previously (Gaillard et al., Molecular Cell 24:5, 2006). Comparable expression levels of the two PGC-1alpha variants were verified by Western immonoblot analysis (data not shown). RNA was collect 16h after infection and purified using RNeasy mini kit (Qiagen, Valencia, CA). Ten independent biological replicates from each virus infection were collected.
2010-11-01 | E-GEOD-23061 | biostudies-arrayexpress
Project description:The transcriptional coactivator peroxisome proliferator-activated receptor-gamma coactivator 1 alpha (PGC-1α) is a chief activator of the mitochondrial and metatolic program in skeletal muscle (skm) and prevents atrophy. Here we tested whether PGC-1α overexpression could restructure the transcriptome and metabolism of cultured human skeletal myotubes, which display an athropic phenotype. An oligonucleotide microarray analysis was used to reveal PGC-1α effects on the whole transcriptome, and the possible impact on fuel metabolism reprogramming was examined. Fifty-three different genes displayed changed expression levels in response to PGC-1α: 42 upregulated and 11 downregulated. Main associations of gene ontologies (GO) for the upregulated genes were mitochondrial components and processes and this correlated with an increase in COX activity, an indicator of mitochondrial content. Palmitate and lactate oxidation to CO2 was enhanced, but not glucose oxidation. The other most significant GO associations of upregulated genes were chemotaxis and cytokine activity, and accordingly, several cytokines, including IL8, CXCL6, CCL5 and CCL8, were within top induced genes. Among the most regulated genes were also potential metabolic regulators of fatty acid and glucose storage. FITM1/FIT1 induction was associated with an increased number of lipid droplets with smaller area, while triglyceride levels were modestly increased in oleate-incubated cells. Downregulation of CALM1, the calcium-modulated δ subunit of phosphorylase kinase, was linked to inactivation of glycogen phosphorylase and greater accumulation of glycogen. The most upregulated gene was PVALB, which is also related to calcium signaling. In conclusion, only the deficient mitochondrial transcriptional program of cultured myotubes is rescued by PGC-1α. New PGC-1α gene targets and pathways arise, some of which may mediate its activating effects in processes such as lipid and carbohydrate storage and angiogenesis. 6 samples from 3 different skeletal muscle cell cultures were used: 3 were transfected with adenovirus containing PGC-1aplha and 3 with adenovirus containing GFP (control). The 3 PGC-1alpha samples were compared against the control samples.
2012-03-15 | E-GEOD-28206 | biostudies-arrayexpress
Project description:Skeletal muscle tissue shows an extraordinary cellular plasticity, but the underlying molecular mechanisms are still poorly understood. Here we use a combination of experimental and computational approaches to unravel the complex transcriptional network of muscle cell plasticity centered on the peroxisome proliferator-activated receptor M-NM-3 coactivator 1M-NM-1 (PGC-1M-NM-1), a regulatory nexus in endurance training adaptation. By integrating data on genome-wide binding of PGC-1M-NM-1 and gene expression upon PGC-1M-NM-1 over-expression with comprehensive computational prediction of transcription factor binding sites (TFBSs), we uncover a hitherto underestimated number of transcription factor partners involved in mediating PGC-1M-NM-1 action. In particular, principal component analysis of TFBSs at PGC-1M-NM-1 binding regions predicts that, besides the well-known role of the estrogen-related receptor M-NM-1 (ERRM-NM-1), the activator protein-1 complex (AP-1) plays a major role in regulating the PGC-1M-NM-1-controlled gene program of hypoxia response. Our findings thus reveal the complex transcriptional network of muscle cell plasticity controlled by PGC-1M-NM-1. We performed ChIP-Seq experiments to identify all DNA recruitment sites for PGC-1alpha in C2C12 cells on genome-wide scale. The experiment was performed in duplicate and the Whole Cell Extract (WCE; =input DNA) was used as background condition.
2014-06-16 | E-GEOD-51178 | biostudies-arrayexpress