Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA131441 | ENA |
REPOSITORIES: ENA
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2013-07-26 | GSE23242 | GEO
Project description:We found that TLS can work as a PGC-1alpha cofactor and this assay was carried out to test the functional dependency of TLS on PGC-1alpha on a whole genome scale Three independently-isolated cultures of primary hepatocytes from PGC-1α+/+ and PGC-1α-/- mice were infected with shTLS or control adenovirus. RNA was extracted by Trizol extraction, re-purified with RNAeasy (Invitrogen), and checked for integrity and quantity with the Agilent Bio-Analyzer QC. RNA was amplified and labeled with the One-Color Microarray-Based Gene Expression Analysis Protocol (Agilent Technologies, Palo Alto, CA, USA). Samples were hybridized to a G4122F 4x44K whole mouse genome microarray (Agilent Technologies). Arrays were scanned at 5 mm resolution with a G2565BA DNA microarray scanner (Agilent Technologies) at the default settings for 4x44k format one-color arrays. Images were analyzed using Feature Extraction software v10.1.1.1 (Agilent Technologies). Raw signals were thresholded to 1 and normalized by quantile (Bolstad et al., 2003) was performed using GeneSpring software. Data were analyzed on the log2 scale. Default flags were considered as absent, except for saturated spots that were flagged as marginal.
2013-07-26 | E-GEOD-23242 | biostudies-arrayexpress
Project description:Decreased mitochondrial mass and function in muscle of diabetic patients is associated with low PGC-1alpha, a transcriptional coactivator of the mitochondrial gene program. To investigate whether reduced PGC-1alpha and oxidative capacity in muscle directly contributes to age-related glucose intolerance, we compared the genetic signatures and metabolic profiles of aging mice lacking muscle PGC-1alpha. Microarray analysis revealed that a significant proportion of PGC-1alpha-dependent changes in gene expression overlapped with age-associated effects, and aging muscle and muscle lacking PGC-1alpha shared gene signatures of impaired electron transport chain activity and TGFbeta signalling.
2013-12-05 | GSE52550 | GEO
Project description:Decreased mitochondrial mass and function in muscle of diabetic patients is associated with low PGC-1alpha, a transcriptional coactivator of the mitochondrial gene program. To investigate whether reduced PGC-1alpha and oxidative capacity in muscle directly contributes to age-related glucose intolerance, we compared the genetic signatures and metabolic profiles of aging mice lacking muscle PGC-1alpha. Microarray analysis revealed that a significant proportion of PGC-1alpha-dependent changes in gene expression overlapped with age-associated effects, and aging muscle and muscle lacking PGC-1alpha shared gene signatures of impaired electron transport chain activity and TGFbeta signalling. Gastrocnemius muscle mRNA from young (10 week old) and old (24 month old) wild-type and knock-out (muscle-specific PGC-1alpha, myogenin-cre) C57Bl/6N/6J/129 mice
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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").
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