Gene expression profiling of Ercc1-/- and age-matched wt pancreata
Ontology highlight
ABSTRACT:
INSTRUMENT(S): Illumina NovaSeq 6000
ORGANISM(S): Mus musculus
SUBMITTER: George Garinis
PROVIDER: E-MTAB-10393 | biostudies-arrayexpress |
REPOSITORIES: biostudies-arrayexpress
Similar Datasets
Project description:Transcriptome analysis of epididymal white adipose tissue (WAT) depots in Ercc1 animals: To further elucidate the role of ERCC1 in WAT we scanned the transcriptome of 15 day old wt and Ercc1 epididymal WAT.
2013-11-04 | E-MEXP-3930 | biostudies-arrayexpress
Project description:Gene expression profiling of Ercc1-/- and age-matched wt pancreata
| PRJEB44570 | ENA
Project description:DNA damage and metabolic disorders are intimately linked with premature disease onset but the underlying mechanisms remain poorly understood. Persistent DNA damage accumulation in tissue-infiltrating macrophages carrying an ERCC1-XPF DNA repair defect (Er1F/-) riggers Golgi dispersal, dilation of endoplasmic reticulum, autophagy and exosome biogenesis leading to the secretion of extracellular vesicles (EVs) in vivo and ex vivo.
2019-11-04 | E-MTAB-8439 | biostudies-arrayexpress
Project description:Background: Several genetic defects of the nucleotide excision repair (NER) pathway, including deficiency of the Excision Repair Cross-Complementing rodent repair deficiency, complementation group 1 (ERCC1), result in pre-mature aging, impaired growth, microcephaly and delayed development of the cerebellum. Such a phenotype also occurs in ERCC1-knockout mice which survive for up to 4 weeks after birth. Therefore, we analyzed cerebellar and hippocamapal transcriptomes of these animals at 3 weeks of age to identify the candidate mechanisms underlying brain consequences of reduced ERCC1 activity. Results: In the cerebellum, the most prominent change was upregulation of genes that are associated with gliosis. Although Purkinje cell degeneration has been reported in some mouse strains with NER impairment, Purkinje cell transcriptome was mostly unaffected by the ERCC1 knockout. In the hippocampus, the gliosis response was minimal. Instead, there was an extensive downregulation of genes related to lipid metabolism including several enzymes of the cholesterol biosynthesis pathway as well as lipoproteins and plasma membrane proteins. Reduced expression of the cholesterol biosynthesis pathway genes was also present in the neocortex of adult mice whose ERCC1 gene was replaced by a mutant allele with a partial activity. Conclusions: Downregulation of forebrain cholesterol biosynthesis genes is a newly identified consequence of ERCC1 deficiency. Its presence in adult mice suggests that it is not a secondary consequence of brain growth impairment. Instead, reduced cholesterol biosynthesis may contribute to such an impairment as well as affect function of mature synapses.
2011-08-16 | GSE31199 | GEO
Project description:Analysis of oncogenic Kras expressing mouse pancreata in comparison to pancreata with concomitant RelA deletion
2015-08-15 | E-MTAB-3436 | biostudies-arrayexpress
Project description:The XPF-ERCC1 endonuclease is required for repair of helix-distorting DNA damage and interstrand crosslinks. Here we have engineered a severe mutation in Ercc1 gene (in which the last 7 amino acids are missing; named as "Ercc1-delta") leading to extreme sensitivity to DNA crosslinks and progeria.To investigate whether a disturbance in growth and metabolism could explain the pronounced accelerated organismal deterioration seen in Ercc1 delta mice, we evaluated the liver transcriptome of 16-week-old wt and mutant mice (n=6). At this age, the Ercc1-delta mice have not yet become cachectic.
2008-06-01 | E-MEXP-1503 | biostudies-arrayexpress
Project description:Pancreata were excised from offspring of time-mated Wistar rats age 10-11 weeks (Taconic, Lille Skensved, Denmark) at embryonic day 20 (E20), immediately after birth (P0) and two days after birth (P2). After decapitation, individual pancreata were quickly dissected and placed directly in ice cold TRIReagent (Sigma-Aldrich, St Louis, MO, USA). RNA from individual pancreata was kept separately in order to verify the array results in pools of RNA as well as in individual animals by real time qPCR. 0.5 M-5g of RNA from each of 3 male and 3 female littermates were pooled at each time-point (E20, P0 and P2). This was repeated in each of three biological independent replicate experiments giving a total of 9 pooled samples, three at each time points
2012-02-01 | E-MEXP-3174 | biostudies-arrayexpress
Project description:Using these samples, it has been shown that the transcriptional landscape in glomeruli of Ercc1[-/Δ] mice at a rather young age of 14 weeks mimics that of mice which have undergone real-life renal aging. Thus, young Ercc1[-/Δ] mice can be used as a model system for glomerular aging in future studies.
2012-12-21 | GSE43061 | GEO
Project description:Zfp800 was identified by Gene Co-expression Network analysis to be an interesting candidate gene involved in endocrine specification and β-cell maturation. We found that Zfp800 null mice exhibited early post-natal lethality, and at E18.5 their pancreata exhibited a reduced number of pancreatic endocrine cells, alterations in exocrine cell morphology, and marked changes in genes involved in protein translation, hormone secretion, and developmental pathways in the pancreas.
2021-03-02 | E-MTAB-9538 | biostudies-arrayexpress
Project description:Background: Several genetic defects of the nucleotide excision repair (NER) pathway, including deficiency of the Excision Repair Cross-Complementing rodent repair deficiency, complementation group 1 (ERCC1), result in pre-mature aging, impaired growth, microcephaly and delayed development of the cerebellum. Such a phenotype also occurs in ERCC1-knockout mice which survive for up to 4 weeks after birth. Therefore, we analyzed cerebellar and hippocamapal transcriptomes of these animals at 3 weeks of age to identify the candidate mechanisms underlying brain consequences of reduced ERCC1 activity. Results: In the cerebellum, the most prominent change was upregulation of genes that are associated with gliosis. Although Purkinje cell degeneration has been reported in some mouse strains with NER impairment, Purkinje cell transcriptome was mostly unaffected by the ERCC1 knockout. In the hippocampus, the gliosis response was minimal. Instead, there was an extensive downregulation of genes related to lipid metabolism including several enzymes of the cholesterol biosynthesis pathway as well as lipoproteins and plasma membrane proteins. Reduced expression of the cholesterol biosynthesis pathway genes was also present in the neocortex of adult mice whose ERCC1 gene was replaced by a mutant allele with a partial activity. Conclusions: Downregulation of forebrain cholesterol biosynthesis genes is a newly identified consequence of ERCC1 deficiency. Its presence in adult mice suggests that it is not a secondary consequence of brain growth impairment. Instead, reduced cholesterol biosynthesis may contribute to such an impairment as well as affect function of mature synapses. We analyzed the hippocampus and cerebellum from three Ercc1-/- and three WT littermates using the Affymetrix Mouse Genome 430_2.0. Data was analyzed using the dChip DNA-Chip analyzer software .
2011-08-15 | E-GEOD-31199 | biostudies-arrayexpress