A Role for the Transcriptional Coregulator RIP140 in the Control of Muscle Endurance Fitness [RNASeq_Training_strKO_flat]
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ABSTRACT:
PROVIDER: PRJNA1223460 | ENA |
REPOSITORIES: ENA
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Project description:Poor skeletal muscle fitness contributes to many chronic disease states including obesity, heart failure, primary muscle disorders, and age-related sarcopenia. Receptor Interacting Protein 140 (RIP140) is a striated muscle-enriched nuclear receptor co-regulator. To investigate the role of RIP140 in skeletal muscle, striated muscle-specific RIP140-deficient (strNrip1-/-) mice were generated and characterized. strNrip1-/- mice display a remarkable endurance performance phenotype based on endurance treadmill performance, VO2max testing, and functional assessment of isolated muscle. RNA-sequence analysis of glycolytic fast-twitch muscle from the strNrip1-/- mice identified a broad array of differentially upregulated metabolic and structural muscle genes involved in muscle endurance fitness pathways including mitochondrial biogenesis and respiration, fatty acid oxidation, triglyceride dynamics, muscle fiber type, angiogenesis, and neuromuscular junction (NMJ) remodeling. Assessment of the structural correlates of these processes confirmed the function of RIP140 as placing a “brake” on the transcriptional network controlling these key muscle endurance fitness processes. Integration of the RNA sequence results with CUT&RUN analysis of strNrip1-/- myotubes identified direct RIP140 targets including genes involved in fatty acid metabolism and NMJ biogenesis. We conclude that RIP140 serves as a physiological “rheostat” for a broad network of genes involved in skeletal muscle fitness.
2025-08-27 | GSE289567 | GEO
Project description:Poor skeletal muscle fitness contributes to many chronic disease states including obesity, heart failure, primary muscle disorders, and age-related sarcopenia. Receptor Interacting Protein 140 (RIP140) is a striated muscle-enriched nuclear receptor co-regulator. To investigate the role of RIP140 in skeletal muscle, striated muscle-specific RIP140-deficient (strNrip1-/-) mice were generated and characterized. strNrip1-/- mice display a remarkable endurance performance phenotype based on endurance treadmill performance, VO2max testing, and functional assessment of isolated muscle. RNA-sequence analysis of glycolytic fast-twitch muscle from the strNrip1-/- mice identified a broad array of differentially upregulated metabolic and structural muscle genes involved in muscle endurance fitness pathways including mitochondrial biogenesis and respiration, fatty acid oxidation, triglyceride dynamics, muscle fiber type, angiogenesis, and neuromuscular junction (NMJ) remodeling. Assessment of the structural correlates of these processes confirmed the function of RIP140 as placing a “brake” on the transcriptional network controlling these key muscle endurance fitness processes. Integration of the RNA sequence results with CUT&RUN analysis of strNrip1-/- myotubes identified direct RIP140 targets including genes involved in fatty acid metabolism and NMJ biogenesis. We conclude that RIP140 serves as a physiological “rheostat” for a broad network of genes involved in skeletal muscle fitness.
2025-08-27 | GSE289576 | GEO
Project description:Poor skeletal muscle fitness contributes to many chronic disease states including obesity, heart failure, primary muscle disorders, and age-related sarcopenia. Receptor Interacting Protein 140 (RIP140) is a striated muscle-enriched nuclear receptor co-regulator. To investigate the role of RIP140 in skeletal muscle, striated muscle-specific RIP140-deficient (strNrip1-/-) mice were generated and characterized. strNrip1-/- mice display a remarkable endurance performance phenotype based on endurance treadmill performance, VO2max testing, and functional assessment of isolated muscle. RNA-sequence analysis of glycolytic fast-twitch muscle from the strNrip1-/- mice identified a broad array of differentially upregulated metabolic and structural muscle genes involved in muscle endurance fitness pathways including mitochondrial biogenesis and respiration, fatty acid oxidation, triglyceride dynamics, muscle fiber type, angiogenesis, and neuromuscular junction (NMJ) remodeling. Assessment of the structural correlates of these processes confirmed the function of RIP140 as placing a “brake” on the transcriptional network controlling these key muscle endurance fitness processes. Integration of the RNA sequence results with CUT&RUN analysis of strNrip1-/- myotubes identified direct RIP140 targets including genes involved in fatty acid metabolism and NMJ biogenesis. We conclude that RIP140 serves as a physiological “rheostat” for a broad network of genes involved in skeletal muscle fitness.
2025-08-27 | GSE289569 | GEO
Project description:A Role for the Transcriptional Coregulator RIP140 in the Control of Muscle Endurance Fitness
| PRJNA1223455 | ENA
Project description:A Role for the Transcriptional Coregulator RIP140 in the Control of Muscle Endurance Fitness [CUTnRUN_Ac_flat]
| PRJNA1223459 | ENA
Project description:A Role for the Transcriptional Coregulator RIP140 in the Control of Muscle Endurance Fitness [RNASeq_MyogeninCre_flat]
| PRJNA1223461 | ENA
Project description:Cell-and context-specific activities of nuclear receptors may in part be due to distinct coregulator complexes recruited to distinct subsets of target genes. RIP140 (also called NRIP1) is a ligand-dependent corepressor that is inducible with retinoic acid (RA). We have shown previously that silencing of RIP140 enhances RA-induced differentiation and enhances the induction of model RA target genes in human embryonal carcinoma cells (EC). Through use of microarray technology we sought to elucidate in a de novo fashion the global role of RIP140 in RA-dependent signaling. RIP140-dependent gene expression was largely consistent with RIP140 functioning to limit RAR signaling. Few if any genes were regulated in a manner to support a role for RIP140 in “active repression”. Interestingly, approximately half of the RA-dependent genes were unaffected by RIP140, suggesting that RIP140 may discriminate between different classes of RA target genes. RIP140 silencing also accelerated RA target gene activation and sensitized EC cells to low doses of RA. Together the data suggests that the RIP140-dependent RA target genes identified here may be particularly important in mediating RA-induced tumor cell differentiation. RIP140 may be an attractive target to sensitize tumor cells to retinoid-based differentiation therapy. Keywords: Drug treatment with siRNA
2008-03-24 | GSE7500 | GEO
Project description:This SuperSeries is composed of the SubSeries listed below.
2025-08-27 | GSE289578 | GEO
Project description:Cell-and context-specific activities of nuclear receptors may in part be due to distinct coregulator complexes recruited to distinct subsets of target genes. RIP140 (also called NRIP1) is a ligand-dependent corepressor that is inducible with retinoic acid (RA). We have shown previously that silencing of RIP140 enhances RA-induced differentiation and enhances the induction of model RA target genes in human embryonal carcinoma cells (EC). Through use of microarray technology we sought to elucidate in a de novo fashion the global role of RIP140 in RA-dependent signaling. RIP140-dependent gene expression was largely consistent with RIP140 functioning to limit RAR signaling. Few if any genes were regulated in a manner to support a role for RIP140 in â??active repressionâ??. Interestingly, approximately half of the RA-dependent genes were unaffected by RIP140, suggesting that RIP140 may discriminate between different classes of RA target genes. RIP140 silencing also accelerated RA target gene activation and sensitized EC cells to low doses of RA. Together the data suggests that the RIP140-dependent RA target genes identified here may be particularly important in mediating RA-induced tumor cell differentiation. RIP140 may be an attractive target to sensitize tumor cells to retinoid-based differentiation therapy. Experiment Overall Design: The current investigation sought to determine the global effects of RIP140 on RA-dependent and RAâ??independent gene expression. A dose of siRNA of 90 nM was chosen. Twelve independent hybridizations were performed from mRNA isolated from 12 independent samples. One scrambled and two independent RISC-free siRNA transfections and transfections with three distinct RIP140 siRNAs were performed in NT2/D1 cells. Each siRNA treatment was further treated with either 10 μM RA or DMSO control for 24 hours. Hence, the design consisted of four groups, the three siRNA controls treated with vehicle, Group 1; the siRNA controls treated with RA, Group 2; siRNA to RIP140 treated with vehicle, Group 3; and siRNA to RIP140 treated with RA, Group 4 . Experiment Overall Design: The treatments were done in the presence of normal sera, since charcoal absorption of sera removes many small hydrophobic ligands to the nuclear receptor family in addition to retinoids. This measure was taken with the aim to perhaps identify target genes of other nuclear receptors including orphan receptors that could be regulated by RIP140 in the presence of low levels of their cognate ligands. RA treatment of 10 μM for 24 hours was chosen since previous experience with NT2/D1 cells indicated that a reasonably sized set of altered genes would be obtained. In addition, NT2/D1 cells commit to RA-induced differentiation by 48 hours and RIP140 repression enhances and accelerates the effects of RA in these cells. Therefore, the 24-hour time point is well-within the range of the RA commitment â??windowâ?? and a larger percentage of direct RA-target genes could be expect to be uncovered compared to later time points. Experiment Overall Design: Based on the current understanding of the properties of RIP140, a number of potential outcomes were anticipated: 1) RIP140 may limit RA target gene activation by negative-feedback inhibition upon RA addition, 2) RIP140 may participate in â??active repressionâ?? of gene expression upon RA addition, 3) an unexpected outcome that RIP140 may participate in the activation of a subset of target genes, 4) RIP140 may regulate the transcription of target genes of other nuclear receptors or even non-nuclear receptor transcription factors. Experiment Overall Design: Total RNA was purified using RNeasy columns (Qiagen). Hybridizations were performed according to Affymetrix guidelines at the Dartmouth College Microarray Shared Resource using an Affymetrix GeneChip Workstation. Biotin-labeled cRNA was generated from 5 μg of total RNA and hybridized to the Human Genome (HG) U133 Plus 2.0 chip A total of 12 hybridizations were performed comprising 12-independent biologic samples organized into the four groups of three.
2008-04-04 | E-GEOD-7500 | biostudies-arrayexpress
Project description:Title: Gene Expression analysis of the role of RIP140 in adipocyte differentiation<br/> Description: RIPKO cells are mouse embryo fibroblasts (MEF) that were derived from <br/> RIP140-knockout mice and have been established as a RIP140 null cell line,<br/> while RIPKO-L7 and RIPKO-L16 are RIPKO cells for which the expression of<br/> RIP140 has been reintroduced using a lentiviral expression system. <br/> Using an established standard cocktail of hormones that includes IBMX, <br/> insulin, dexamethasone and a PPAR gamma agonist the cells were <br/> differentiated into adipocytes and RNA isolated at day 0 and day 10 <br/> after the addition of the cocktail.
2013-01-30 | E-MIMR-42 | biostudies-arrayexpress