Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA122353 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Transcriptional profiling of cultured CD1 mouse embryonic kidneys (E13.5) comparing HDACi-treated kidneys with control drug-treated kidneys. Studies in our lab showed that pharmacological inhibition of HDAC activity in ex-vivo cultured metanephroi results in extensive defects in kidney development, including impaired UB branching, tubulogenesis, and glomerulogenesis, accompanied by cell cycle arrest and apoptosis.The goal of the microarray analysis was to elucidate the morphogenetic pathways affected by HDACi. Two-condition experiment, HDACi-treated E13.5 kidneys (Scriptaid 2.0 μg/ml x 6hrs) vs. Control drug-treated E13.5 kidneys (Nullscript 2.0 μg/ml x 6hrs). Biological replicates: 3 control replicates, 3 HDACi-treated replicates. Two-color Agilent 4x44k chips with dye-swap on 2 of 4 arrays.
2010-08-01 | E-GEOD-19581 | biostudies-arrayexpress
Project description:Transcriptional profiling of cultured CD1 mouse embryonic kidneys (E13.5) comparing HDACi-treated kidneys with control drug-treated kidneys. Studies in our lab showed that pharmacological inhibition of HDAC activity in ex-vivo cultured metanephroi results in extensive defects in kidney development, including impaired UB branching, tubulogenesis, and glomerulogenesis, accompanied by cell cycle arrest and apoptosis.The goal of the microarray analysis was to elucidate the morphogenetic pathways affected by HDACi.
2010-08-01 | GSE19581 | GEO
Project description:Mouse embryonic kidneys (E13.5): mutant (UB HDAC1,2-/-) vs. wild type
| PRJNA152771 | ENA
Project description:Transcriptional profiling of mouse embryonic kidneys (E13.5) comparing UB HDAC1,2-/- kidneys with wild type kidneys. Studies in our lab showed that histone deacetylase 1 (HDAC1) and 2 (HDAC2) perform redundant, yet essential functions in the developing mouse ureteric bud (UB) tissue. Double deletion of HDAC1 and HDAC2 in the UB results in impaired UB branching morphogenesis, followed by severe kidney dysgenesis. The goal of the microarray analysis was to identify the genetic pathways controlled by HDAC1 and 2 in the UB. Two-condition experiment: E13.5 mutant kidneys (UB HDAC1,2-/-) vs. E13.5 wild type kidneys . Biological replicates: 4 control replicates, 4 UB HDAC1,2-/- replicates. Two-color Agilent 4x44k chips with dye-swaps on 2 of 4 arrays.
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Project description:To assess the effects of histone deacetylase (HDAC) inhibitor, HDACi 4b, treatment on muscle function on a molecular level, we performed microarray analysis on skeletal muscle (gastrocnemius) samples from wt and N17182Q mice treated with the HDAC inhibitor 4b for 3 months (50 mg/kg; s.c. injection 3x weekly; n=4 per group). The transcriptome pattern in N17182Q mice compared to wt controls consisted of deficits in the expression of genes related to mitochondrial function and oxidative metabolism. In addition, we noted that numerous genes associated with basal contractile function were altered in HD N17182Q mice. These include genes related to the muscle contractile complex, Tnnt3 and Myh8, as well as several additional myosin genes: myosin heavy chain genes, Myh10 and Myh4, and myosin light chain genes, Myl1, Mylc2 and Mylk. These findings implicate deficits in the underlying contractile function in skeletal muscle from HD mice. Further, we found robust effects of 4b treatment on the expression of genes in skeletal muscle, with 556 genes showing significantly altered expression, at p<0.005, in 4b-treated N17182Q muscle compared to vehicle-treated control mice. n=4 vehicle-treated WT mice, n=5 HDACi 4b-treated WT mice, n=4 vehicle-treated N17182Q transgenic mice, and n=3 HDACi 4b-treated N17182Q transgenic mice.
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