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Links from GEO DataSets

Items: 17

1.
Full record GDS5195

nuo-6;ced-4 double mutation effect on young adults

Analysis of nuo-6;ced-4 double mutants. ced-4 mutation in the intrinsic apoptosis signaling pathway suppresses the longevity of electron transport chain mutant nuo-6. Results provide insight into molecular mechanisms underlying lifespan expansion.
Organism:
Caenorhabditis elegans
Type:
Expression profiling by array, transformed count, 4 genotype/variation sets
Platform:
GPL200
Series:
GSE54024
13 Samples
Download data: CEL
2.

Expression Data of Reactive Oxygen Species Signalling in C. elegans

(Submitter supplied) We have shown that worms that possess mutations in two electron transport chain subunits live longer due to mtROS signalling. Wild type worms can also live longer by treatment with the pro-oxidant paraquat. Paraquat treatment is not additive to the mutations in the ETC subunits. We aimed to determine the underlying changes in gene expression that were common to both paraquat treatment and the two mutations. more...
Organism:
Caenorhabditis elegans
Type:
Expression profiling by array
Datasets:
GDS5193 GDS5194 GDS5195
Platform:
GPL200
22 Samples
Download data: CEL
Series
Accession:
GSE54024
ID:
200054024
3.
Full record GDS5194

isp-1;ced-4 double mutation effect on young adults

Analysis of isp-1;ced-4 double mutants. ced-4 mutation in the intrinsic apoptosis signaling pathway suppresses the longevity of electron transport chain mutant isp-1. Results provide insight into molecular mechanisms underlying lifespan expansion.
Organism:
Caenorhabditis elegans
Type:
Expression profiling by array, transformed count, 4 genotype/variation sets
Platform:
GPL200
Series:
GSE54024
13 Samples
Download data: CEL
4.
Full record GDS5193

isp-1 and nuo-6 mutants and paraquat-treated wildtype young adults

Analysis of wildtype worms treated with the pro-oxidant paraquat and electron transport chain mutants isp-1 and nuo-6. Results provide insight into common molecular mechanisms underlying the increased longevity in all three conditions.
Organism:
Caenorhabditis elegans
Type:
Expression profiling by array, transformed count, 3 genotype/variation, 3 protocol sets
Platform:
GPL200
Series:
GSE54024
13 Samples
Download data: CEL
5.

RNA-sequencing of C.elegans isp-1 mutant and superoxide dismutase-isp-1 double mutants

(Submitter supplied) isp-1;sod double mutants have decreased lifespan, increased resistance to oxidative stress and slow physiologic rates. We performed RNA sequencing to compare gene expression between isp-1 mutants and isp-1;sod-3 and isp-1;sod-5 double mutants
Organism:
Caenorhabditis elegans
Type:
Expression profiling by high throughput sequencing
Platform:
GPL19757
12 Samples
Download data: TXT
Series
Accession:
GSE95240
ID:
200095240
6.

Role of mitochondrial unfolded protein response transcription fatcor ATFS-1 in lifespan of long-lived mitochondrial mutants

(Submitter supplied) In this work, we examined the effect of the transcription factor ATFS-1 in the long lifespan of the nuo-6 mitochondrial mutant. We also examined the effect of the hypoxia transcription factor hif-1. We sequenced both atfs-1 deletion mutants and atfs-1 gain-of-function point mutants in which the mitochondrial localization sequence of ATFS-1 is disrupted. Note that sequencing batch 2 was previously uploaded as part of GSE93724.
Organism:
Caenorhabditis elegans
Type:
Expression profiling by high throughput sequencing
Platform:
GPL19757
43 Samples
Download data: TXT
Series
Accession:
GSE110984
ID:
200110984
7.

Expression data from wildtype and C. elegan mutants

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.
Organism:
Caenorhabditis elegans
Type:
Expression profiling by array
Platform:
GPL200
20 Samples
Download data: CEL
Series
Accession:
GSE9967
ID:
200009967
8.

Expression data from 2 wildtype and 8 C. elegans ETC mutants

(Submitter supplied) Utilizing C. elegans as a model of mitochondrial dysfunction provides insight into cellular adaptations which occur as a consequence of genetic alterations causative of human disease. We characterized genome-wide expression profiles of hypomorphic C. ele Our goal was to detect concordant changes among clusters of genes that comprise defined metabolic pathways utilizing gene set enrichment analysis. more...
Organism:
Caenorhabditis elegans
Type:
Expression profiling by array
Dataset:
GDS3453
Platform:
GPL200
10 Samples
Download data: CEL
Series
Accession:
GSE9897
ID:
200009897
9.

Expression data from wildtype and gas-1 mitochondrial mutant C. elegans

(Submitter supplied) Utilizing C. elegans as a model of mitochondrial dysfunction provides insight into cellular adaptations which occur as a consequence of genetic alterations causative of human disease. We characterized genome-wide expression profiles of hypomorhpic C. elegans mutants in nuclear-encoded subunits of respiratory chain complexes I, II and III. Our goal was to detect concordant changes among clusters of genes that comprise defined metabolic pathways utilizing gene set enrichment analysis. more...
Organism:
Caenorhabditis elegans
Type:
Expression profiling by array
Dataset:
GDS3452
Platform:
GPL200
10 Samples
Download data: CEL
Series
Accession:
GSE9896
ID:
200009896
10.
Full record GDS3453

Nematode models of primary mitochondrial dysfunction: complex I, II, and III mutants

Analysis of 8 different electron transport chain (ETC) subunit mutants (3 missense and 5 RNAi-induced) in complexes I, II, and III. Results from this validation set provide insight into the contributions of individual complexes or subunits to primary mitochondrial dysfunction.
Organism:
Caenorhabditis elegans
Type:
Expression profiling by array, transformed count, 4 genotype/variation, 4 protocol sets
Platform:
GPL200
Series:
GSE9897
10 Samples
Download data: CEL
11.
Full record GDS3452

Nematode model of primary mitochondrial dysfunction: complex I mutants

Analysis of gas-1(fc21) electron transport chain complex I mutants. The gas-1(fc21) mutation affects the 49 kD subunit of complex I, decreasing the rate of complex I-dependent oxidative phosphorylation. Results provide insight into molecular mechanisms underlying primary mitochondrial disease .
Organism:
Caenorhabditis elegans
Type:
Expression profiling by array, transformed count, 2 genotype/variation sets
Platform:
GPL200
Series:
GSE9896
10 Samples
Download data: CEL
12.

Impaired Insulin-/IGF1-Signaling Extends Life Span by Promoting Mitochondrial L-Proline Catabolism to Induce a Transient ROS-Signal

(Submitter supplied) Transcriptome profiling of three models with impaired insulin/IGF1 signaling. 1. Deep sequencing of endogenous mRNA from Caenorhabditis elegans N2 var. Bristol (wildtype) and daf-2(e1370) mutant; 2. Deep sequencing of endogenous mRNA from murine embryonic fibroblasts (MEF) wildtype and irs1-/- knockout; 3. Deep sequencing of endogenous mRNA from murine embryoinic fibroblast (MEF) insr+/- -lox and insr+/- knockout Jena Centre for Systems Biology of Ageing - JenAge (www.jenage.de)
Organism:
Mus musculus; Caenorhabditis elegans
Type:
Expression profiling by high throughput sequencing
Platforms:
GPL11002 GPL13776
14 Samples
Download data: CSV
Series
Accession:
GSE36041
ID:
200036041
13.

CEST-2.2 stimulates lipid metabolism and promotes longevity in mitochondrial mutant animals

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.
Organism:
Caenorhabditis elegans
Type:
Expression profiling by high throughput sequencing; Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL19757
19 Samples
Download data: BW, TSV
Series
Accession:
GSE168502
ID:
200168502
14.

CEST-2.2 stimulates lipid metabolism and promotes longevity in mitochondrial mutant animals (RNA-Seq)

(Submitter supplied) Intestine-specific transcriptome of wild-type. gas-1(fc21) and gas-1(fc21); cest-2.2 OE Caenorhaditis elegans in order to gain insight into how cest-2.2 overexpression ameliorates Complex I deficiency
Organism:
Caenorhabditis elegans
Type:
Expression profiling by high throughput sequencing
Platform:
GPL19757
15 Samples
Download data: FA, TSV, TXT, XLSX
Series
Accession:
GSE168501
ID:
200168501
15.

CEST-2.2 stimulates lipid metabolism and promotes longevity in mitochondrial mutant animals (ChIP-Seq)

(Submitter supplied) ChIP-Seq of H3.3 loading on promoters of genes in short-lived and long-lived mitochondrial mutant nematodes identifies genes which could potentially regulate longevity
Organism:
Caenorhabditis elegans
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL19757
4 Samples
Download data: BW
Series
Accession:
GSE168500
ID:
200168500
16.

Effect of lutein on worms lacking complex I subunit nuo-5 (ortholog of human NDUFS1)

(Submitter supplied) To gain insight into the pathways accounting for the deleterious effects associated with severe mitochondrial dysfunction, we compared the transcriptomic profile in control L3 larvae with that of strong (arrested) nuo-5 RNAi. We also found that the natural compound lutein was able to rescue some of the defective phenotypes we characterized in nuo-5-depleted animals therefore we compared also the transcriptomic profile of stage-matched (L3) cohorts of C. more...
Organism:
Caenorhabditis elegans
Type:
Expression profiling by array
Platform:
GPL19230
12 Samples
Download data: CEL, TXT
Series
Accession:
GSE144574
ID:
200144574
17.

Effect of knocking down complex I subunit nuo-5 (ortholog of the human NDUFS1) in C.elegans

(Submitter supplied) In this study we compared the transcriptomic profile in control L3 larvae with that of mild or strong (arrested) nuo-5 RNAi. The two treatment (mild and strong) in fact lead to two very different phenotype. The mild supperssion of nuo-5 induces improved healthspand and has pro longevity effect. The strong suppression of the same gene has, on the contrary, deleterious effects such as arrested development.
Organism:
Caenorhabditis elegans
Type:
Expression profiling by array
Platform:
GPL19230
12 Samples
Download data: CEL
Series
Accession:
GSE144573
ID:
200144573
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Supplemental Content

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