Depletion of PARP-2 in C2C12 cells
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ABSTRACT:
PROVIDER: PRJNA428451 | ENA |
REPOSITORIES: ENA
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Project description:Poly(ADP-ribose) polymerase-2 (PARP-2) is acknowledged as a DNA repair enzyme; however, recently metabolic properties had been attributed to it. Hereby, we examined the metabolic consequences of PARP-2 ablation in skeletal muscle.
2020-12-18 | GSE108737 | GEO
Project description:Poly(ADP-ribose) polymerase-2 (PARP-2) is acknowledged as a DNA repair enzyme; however, recently metabolic properties had been attributed to it. Hereby, we examined the metabolic consequences of PARP-2 ablation in liver. Microarray analysis of PARP-2 knockdown HepG2 cells revealed the dysregulation of lipid and cholesterol metabolism genes. Induction of cholesterol biosynthesis genes stemmed from the enhanced expression of sterol-regulatory element binding protein (SREBP)-1. We revealed that PARP-2 is a suppressor of the SREBP-1 promoter, therefore ablation of PARP-2 induces SREBP-1 expression and consequently cholesterol synthesis. PARP-2-/- mice had higher SREBP-1 expression that was translated into enhanced hepatic and serum cholesterol levels. PARP-2 silencing was performed employing shPARP-2 (small hairpin) and scPARP-2 (scrambled) shRNA by lentiviral delivery (Sigma) using 40 MOI lentiviruses coding shRNA sequence against PARP-2.
2013-12-31 | E-GEOD-43981 | biostudies-arrayexpress
Project description:Poly(ADP-ribose) polymerase-2 (PARP-2) is acknowledged as a DNA repair enzyme; however, recently metabolic properties had been attributed to it. Hereby, we examined the metabolic consequences of PARP-2 ablation in liver. Microarray analysis of PARP-2 knockdown HepG2 cells revealed the dysregulation of lipid and cholesterol metabolism genes. Induction of cholesterol biosynthesis genes stemmed from the enhanced expression of sterol-regulatory element binding protein (SREBP)-1. We revealed that PARP-2 is a suppressor of the SREBP-1 promoter, therefore ablation of PARP-2 induces SREBP-1 expression and consequently cholesterol synthesis. PARP-2-/- mice had higher SREBP-1 expression that was translated into enhanced hepatic and serum cholesterol levels.
2013-12-31 | GSE43981 | GEO
Project description:Transcriptional profiling of mouse myoblast cells comparing control vs. Mybbp1a knockdown. Stable clones of C2C12 cells harboring control or Mybbp1a-targeting shRNA were established and further pooled for analysis. Goal was to determine, based on the effects of Mybbp1a depletion on global gene expression, candidate downstream target genes of Mybbp1a, a putative transcriptional co-repressor. Two-condition experiment, control vs. Mybbp1a knockdown C2C12 cells (mixed stable clones). Biological replicates: 2.
2011-08-09 | E-GEOD-31319 | biostudies-arrayexpress
Project description:C2C12 cells are mouse skeletal muscle cells. These cells were transfected with shRNA against FoxO1, FoxO3, and FoxO4. FoxO1, FoxO3, and FoxO4 are the known paralogues expressed in this cell line. C2C12 cells are transfected with shRNA against FoxO1, FoxO3, and FoxO4, respectively. Colonies were selected for the best depletion of the target FoxOs, respectively. Cells were grown in DMEM medium. Total RNA was extracted from each line. Microarray analysis was performed by following the Affymetrix protocols. The data were analyzed by GCOS system. The target genes that we are interested in were further confirmed by qRT-PCR, reporter assay, and other biochemical and molecular biology assays.
2008-12-30 | E-GEOD-13347 | biostudies-arrayexpress
Project description:Expression data from C2C12 cells
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Project description:RNA-seq was performed in both wild type and parp1-/- ES cells to check the effect of PARP-1 depletion on gene expression profile in mESC.
2017-01-23 | GSE74111 | GEO
Project description:Study the effect of PARP-14 and its activity on Th2 differentiation ChIP seq was performed on Th2 differentiated cells isolated from PARP-14 +/+ and PARP-14 -/- treated with or without PJ34
2013-12-31 | E-GEOD-51344 | biostudies-arrayexpress
Project description:Genomic instability is one of the hallmarks of cancer. Several chemotherapeutic drugs and radiotherapy induce DNA damage to prevent cancer cell replication. Cells in turn activate different DNA damage response (DDR) pathways to either repair the damage or induce cell death. These DDR pathways also elicit metabolic alterations which can play a significant role in the proper functioning of the cells. The understanding of these metabolic effects resulting from different types of DNA damage and repair mechanisms is currently lacking. In this study, we used NMR metabolomics to identify metabolic pathways which are altered in response to different DNA damaging agents. By comparing the metabolic responses in MCF-7 cells, we identified the activation of poly (ADP-ribose) polymerase (PARP) in methyl methanesulfonate (MMS)-induced DNA damage. PARP activation led to a significant depletion of NAD+. PARP inhibition using veliparib (ABT-888) was able to successfully restore the NAD+ levels in MMS-treated cells. In addition, double strand break induction by MMS and veliparib exhibited similar metabolic responses as zeocin, suggesting an application of metabolomics to classify the types of DNA damage responses. This prediction was validated by studying the metabolic responses elicited by radiation. Our findings indicate that cancer cell metabolic responses depend on the type of DNA damage responses and can also be used to classify the type of DNA damage.
2015-08-01 | MTBLS177 | MetaboLights
Project description:Effect of depletion of FAM129B on gene expression during skeletal muscle differentiation of C2C12 cells
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