Browse
Submit Data
Databases
API
Help

Unknown,Transcriptomics,Genomics,Proteomics

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Expression data from mouse tissues

ABSTRACT: The role of p53 in assuring longevity through prevention of cancer is well established, but how it specifically regulates aging is still controversial. Our assumption is that distinct p53-pathways regulate tumor suppression and aging and that p66Shc is one of the master regulators of the p53 aging function. p66Shc longevity determinant protein acts as a downstream target of p53 and it is indispensable for the ability of activated p53 to induce elevation of intracellular oxidants and apoptosis. We used microarray to gain insight into the mechanism of the physiological activation of p53-p66Shc pathway Total RNA was extracted from freshly isolated thymus, liver, heart and lung of two months old mice (pool of four mice for each genotype)

ORGANISM(S): Mus musculus

SUBMITTER: Simone Minardi

PROVIDER: E-GEOD-28417 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

ACCESS DATA

Json Xml

Similar Datasets

Expression data from mouse tissues

2012-04-02 | GSE28417 | GEO

Expression data from mouse embryo fibroblast (MEFS)

2012-04-02 | GSE28416 | GEO

Expression data from mouse embryo fibroblast (MEFS)

Project description:The role of p53 in assuring longevity through prevention of cancer is well established, but how it specifically regulates aging is still controversial. Our assumption is that distinct p53-pathways regulate tumor suppression and aging and that p66Shc is one of the master regulators of the p53 aging function. p66Shc longevity determinant protein acts as a downstream target of p53 and it is indispensable for the ability of activated p53 to induce elevation of intracellular oxidants and apoptosis. We used microarray to gain insight into the mechanism through which p66Shc could regulate p53 oxidative stress dependent activity. Total RNA was extracted from Primary murine embryonic fibroblasts (MEFs) were isolated from 13.5-day-old embryos according to standard procedures from WT, p53KO and p66ShcKO mice. Treatment: Early passage (p.2) MEFs were washed twice with PBS1X solution, and then incubated in DMEM media containing 400 Î¼M of H2O2 or 0.25Î¼g/ml of Doxorubicin (SIGMA) at 37Â°C for four hours.

2012-04-01 | E-GEOD-28416 | biostudies-arrayexpress

Expression data from mouse tissues and MEFs: insights into the physiological activation of p53-p66Shc pathway

Project description:This SuperSeries is composed of the following subset Series: GSE28416: Expression data from mouse embryo fibroblast (MEFS) GSE28417: Expression data from mouse tissues Refer to individual Series

2012-04-01 | E-GEOD-28418 | biostudies-arrayexpress

Early-adulthood spike in protein translation drives aging via juvenile hormone/germline signaling

Project description:Protein translation (PT) declines with age in invertebrates, rodents, and humans. It has been assumed that elevated PT at young ages is beneficial to health and PT ends up dropping as a passive byproduct of aging. In Drosophila, we show that a transient elevation in PT during early-adulthood exerts long-lasting negative impacts on aging trajectories and proteostasis in later-life. Blocking the early-life PT elevation robustly improves life-/health-span and prevents age-related protein aggregation, whereas transiently inducing an early-life PT surge in long-lived fly strains abolishes their longevity/proteostasis benefits. The early-life PT elevation triggers proteostatic dysfunction, silences stress responses, and drives age related functional decline via juvenile hormone-lipid transfer protein axis and germline signaling. Our findings suggest that PT is adaptively suppressed after early-adulthood, alleviating later-life proteostatic burden, slowing down age-related functional decline, and improving lifespan. Our work provides a theoretical framework for understanding how lifetime PT dynamics shape future aging trajectories.

2023-10-24 | PXD044118 | Pride

Early-adulthood spike in protein translation drives aging via juvenile hormone/germline signaling

Project description:Protein translation (PT) declines with age in invertebrates, rodents, and humans1-6. It has been assumed that elevated PT at young ages is beneficial to health and PT ends up dropping as a passive byproduct of aging. In Drosophila, we show that a transient elevation in PT during early-adulthood exerts long-lasting negative impacts on aging trajectories and proteostasis in later-life. Blocking the early-life PT elevation robustly improves life-/health-span and prevents age-related protein aggregation, whereas transiently inducing early-life PT surge in long-lived fly strains abolishes their longevity/proteostasis benefits. The early-life PT elevation triggers proteostatic dysfunction, silences stress responses, and drives age-related functional decline via juvenile hormone-lipid transfer protein axis and germline signaling. Our findings suggest that PT is adaptively suppressed after early-adulthood, alleviating later-life proteostatic burden, slowing down age-related functional decline, and improving lifespan. Our work provides a novel theoretical framework for understanding how lifetime PT dynamics shape future aging trajectories.

2023-08-01 | GSE239506 | GEO

Whole-Genome Sequencing of a Healthy Aging Cohort.

Project description:Studies of long-lived individuals have revealed few genetic mechanisms for protection against age-associated disease. Therefore, we pursued genome sequencing of a related phenotype-healthy aging-to understand the genetics of disease-free aging without medical intervention. In contrast with studies of exceptional longevity, usually focused on centenarians, healthy aging is not associated with known longevity variants, but is associated with reduced genetic susceptibility to Alzheimer and coronary artery disease. Additionally, healthy aging is not associated with a decreased rate of rare pathogenic variants, potentially indicating the presence of disease-resistance factors. In keeping with this possibility, we identify suggestive common and rare variant genetic associations implying that protection against cognitive decline is a genetic component of healthy aging. These findings, based on a relatively small cohort, require independent replication. Overall, our results suggest healthy aging is an overlapping but distinct phenotype from exceptional longevity that may be enriched with disease-protective genetic factors.

| EGAS00001002306 | EGA

Transcriptional profiling by array of ovaries from aged mice

Project description:We transcriptionally profiled ovaries harvested from young and middle-aged outbred CD1 mice to elucidate mechanisms and identify novel markers of ovarian aging.

2018-12-15 | E-MTAB-7493 | biostudies-arrayexpress

Heat-killed probiotic Levilactobacillus brevis MRKAK9 downregulates insulin-signaling pathway and improves proteostasis and autophagy to promote longevity and immunity in Caenorhabditis elegans

Project description:Probiotics play important role in maintaining the health and extend longevity in their host. Previous studies reported several live probiotic bacteria in enhancing longevity and improving diverse feature of the host’s health. In this study, we reported a new potential heat- killed probiotic bacterium Levilactobacillus brevis strain MRKAK9 improved longevity and different features of healthy aging, including age-associated physical activity, improved resistance to biotic and abiotic stress in C. elegans. The mechanistic investigations showed that heat-killed strain MRKAK9 promoted longevity and healthy aging by downregulating insulin-signaling pathway resulting in improved proteostasis, autophagy and preserving lysosomal functionality in C. elegans. Heat-killed strain MRKAK9-mediated downregulation of insulin signaling pathway was regulated by the miRNA mir-243, suggesting that mir-243 partially involved in enhancing longevity of C. elegans. Additionally, the structural component exopolysaccharide of the strain heat-killed MRKAK9 also downregulated insulin- signaling mechanisms, increased the expression of genes involved in proteostatsis, autophagy as well as improved expression of mir-243. This study indicates that heat-killed strain MRKAK9 improves longevity and healthy aging, suggesting its candidature as a novel postbiotic.

2024-08-10 | PXD041237 | Pride

Proteome analysis of rice seeds during artificial aging treatment for understanding the role of antioxidant machinery

Project description:Seed longevity is a crucial trait in agriculture as it determines the ability of seeds to maintain viability during dry storage. However, the molecular mechanism underlying seed aging and reduced seed longevity are currently not well understood. Here we report the comparative proteome and metabolome profiling of three rice cultivars varying in aging tolerance including an aging tolerant indica cultivar Dharial, an aging sensitive japonica cultivar Ilmi, and a moderately aging tolerant cultivar A2 that was generated by crossing between Dharial and Ilmi. Results obtained from comparative proteome and metabolome profiling suggest that aged seeds of all the cultivars utilize ubiquitin proteasome-mediated protein degradation which results in the accumulation of free amino acids in Ilmi while tolerant cultivars utilize those for energy production and synthesis of heat shock proteins, especially hsp20/alpha crystallin family protein. Additionally, aging tolerant cultivar seems to activate brassinosteroid signalling and suppress jasmonate signaling to initiate a signaling cascade that allows efficient detoxification of aging induced ROS to maintain the seed longevity during aging. Taken together, these results provide an in-depth understand of aging induced changes in rice seeds.

2024-01-10 | PXD043955 | Pride

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data