Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Aging Liver Profiles of Long Lived Pit-1 Mutant Mouse (Snell) and Wild Type Controls

ABSTRACT: To compare and contrast genetic signatures from livers of young and aged Snell dwarf mice with their wild type controls. Keywords: Aging

ORGANISM(S): Mus musculus

PROVIDER: GSE3129 | GEO | 2005/08/16

SECONDARY ACCESSION(S): PRJNA93027

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Aging Liver Profiles of the Long Lived Prop-1 Mutant Mouse (Ames) and Wild Type Controls

Project description:To compare and contrast genetic signatures from livers of young and aged Ames dwarf mice with their wild type controls. Keywords: Time Course

2005-08-18 | GSE3150 | GEO

Transcription profiling of mouse liver from long lived Prop-1 mutant (Ames) vs. wild type controls

Project description:To compare and contrast genetic signatures from livers of young and aged Ames dwarf mice with their wild type controls. SUBMITTER_CITATION: W. H. Boylston, James H. DeFord, John Papaconstantinou (2006) Identification of longevity-associated genes in long-lived Snell and Ames dwarf mice Age 28:125-144 Experiment Overall Design: 25 micrograms of liver RNA was isolated from young (5 dwarfs, 5 wildtype), middle aged (5 dwarfs, 5 wild type) and aged (5 dwarf, 6 wild type) mice for use in hybridization of Affymetrix gene chips according to Affymetrix protocols.

2008-06-12 | E-GEOD-3150 | biostudies-arrayexpress

Transcription profiling of livers from aged and young Snell dwarf mice and their wild type controls to identify genetic signatures.

Project description:To compare and contrast genetic signatures from livers of young and aged Snell dwarf mice with their wild type controls. SUBMITTER_CITATION: W. H. Boylston, James H. DeFord, John Papaconstantinou (2006) Identification of longevity-associated genes in long-lived Snell and Ames dwarf mice Age 28:125-144 Experiment Overall Design: 25 micrograms of liver RNA was isolated from each of 6 aged (3 dwarf, 3 wild type) and 8 young (4 dwarf, 4 wild type) mice for use in hybridization of Affymetrix gene chips according to Affymetrix protocols.

2007-12-01 | E-GEOD-3129 | biostudies-arrayexpress

Tracking gene expression changes following aging of C. elegans

Project description:Track down the differential gene expressions between young and aged C. elegans to build a aging metabolism map Track down the differential gene expressions between young and aged C. elegans to build a aging metabolism map

2022-08-06 | GSE210389 | GEO

The effects of aging vs. alpha7 nAChR subunit deficiency on the mouse brain transcriptome

Project description:Aging is accompanied by expression changes in multiple genes and the brain is one of the tissues most vulnerable to aging. Since the alpha7 nicotinic acetylcholine receptor (nAChR) subunit has been associated with neurodevelopmental disorders and cognitive decline during aging, we hypothesized that its absence might affect gene expression profiles in aged brains. To study whether transcriptional changes occur due to aging, alpha7 deficiency or both, we analyzed whole brain transcriptomes of young (8 week) and aged (2 year) alpha7 deficient and wild-type control mice, using Mouse Genome 430 2.0 microarray. Highly significant expression changes were detected in 47 and 1543 genes (after Bonferroni and FDR correction) in the brains of aged mice compared to young mice, regardless of their genotype. These included genes involved in immune system function and ribosome structure, as well as genes that were previously demonstrated as differentially expressed in aging human brains. Genotype-dependent changes were detected in only 3 genes, Chrna7 which encodes the alpha7 nAChR subunit, and two closely linked genes, likely due to a mouse background effect. Expression changes dependent on age-genotype interaction were detected in 207 genes (with a low significance threshold). Age-dependent differential expression levels were approved in all nine genes that were chosen for validation by real-time RT-PCR. Our results suggest that the robust effect of aging on brain transcription clearly overcomes the almost negligible effect of alpha7 nAChR subunit deletion, and that germline deficiency of this subunit has a minor effect on brain expression profile in aged mice. Total of 20 samples. 10 from young adult mice (8 weeks) and 10 from aged mice (2 years). In each age group, 5 were wild-type control mice and 5 alpha7 nAChR subunit defecient mice

2011-01-01 | E-GEOD-20411 | biostudies-arrayexpress

Young blood-derived platelet factors abate inflammation and rescue recognition in aging.

Project description:We show that platelet factors transfer rejuvenating effects of young plasma to the aging brain. Proteomic analysis of plasma from young and aged mice identified age-related changes in platelets. Systemic exposure of aged animals to the platelet fraction of young plasma decreased hippocampal neuroinflammation at a transcriptional and cellular level and ameliorated cognitive impairments. We identified the platelet-derived chemokine CXCL4/Platelet Factor-4 (PF4) as a pro-youthful circulating factor. Systemic PF4 administration decreased age-related neuroinflammation, restored the aging peripheral immune system to a more youthful state, and improved hippocampal-dependent learning and memory in aged mice.

2023-06-20 | GSE173254 | GEO

A Quantitative Yeast Aging Proteomics Analysis Reveals Novel Aging Regulators

Project description:Extending lifespan from yeast to mammals, calorie restriction (CR) is the most conserved longevity intervention. Numerous conserved pathways regulating aging and mediating CR have been identified; however, the overall proteomic changes during these conditions remain largely unexplored. We compared proteomes between young and replicatively aged yeast cells under normal and CR conditions using SILAC quantitative proteomics and discovered distinct signatures in the aging proteome. We found remarkable similarities between aged and CR cells, including induction of stress response pathways, providing evidence that CR pathways are engaged in aged cells. These observations also uncovered aberrant changes in mitochondria membrane proteins as well as a proteolytic cellular state in old cells. These proteomics analyses also help identify potential genes and pathways that have causal effects on longevity.

2022-02-15 | PXD018917 | Pride

Transcriptomic analysis of mouse brain microglia on aging-associated changes in response to cerebral ischemia

Project description:Senescence-associated alterations in microglia may have profound impact on cerebral homeostasis and stroke outcomes. However, the lack of a transcriptome-wide comparison between young and aged microglia in the context of ischemia limits our understanding of aging-related mechanisms. Herein, we performed bulk RNA sequencing analysis of microglia purified from cerebral hemispheres of young adult (10-week-old) and aged (18-month-old) mice 5 days after distal middle cerebral artery occlusion or sham operation. Considerable transcriptional differences were observed between young and aged microglia in healthy brains, indicating heightened chronic inflammation in aged microglia. Following stroke, the overall transcriptional activation was more robust in young microglia than in aged microglia. Gene clusters with functional implications in immune inflammatory responses, immune cell chemotaxis, tissue remodeling, and cell-cell interactions were markedly activated in microglia of young but not aged stroke mice. These alterations in microglial gene response may contribute to aging-driven vulnerability and poorer recovery after ischemic stroke.

2020-05-31 | GSE145265 | GEO

P-selectin identifies molecularly and functionally aged long-term hematopoietic stem cells in Mus musculus C57BL/6 female mice

Project description:Aged hematopoietic stem cells (HSCs) display myeloid-biased differentiation and reduced regenerative potential. In this study, we uncover that P-selectin (Selp) marks a subset of aged HSCs with reduced repopulation capacity. This population of HSCs expresses a prominent aging transcriptome. Overexpression of Selp in young HSCs impaired long-term reconstitution potential and repressed erythropoiesis. We show that IL-1β is elevated in aged bone marrow and administration of IL-1β induces expression of Selp and other aging-associated genes in HSCs. Finally, we demonstrate that transplantation of aged HSCs into young recipients restores a young-like transcriptome, specifically by repressing pro-inflammatory pathways, highlighting the important role of the bone marrow microenvironment in HSC aging.

2023-01-02 | GSE194273 | GEO

Global quantitative proteomics of mouse brain structures reveals significant alterations in expression of proteins involved in neuronal plasticity during aging

Project description:Aging is believed to be the result of alterations of protein expression and accumulation of changes in biomolecules. Although there are numerous reports demonstrating changes in protein expression in brain during aging, only few of them describe global changes in the protein level. Here, we present a deepest quantitative proteomic analysis of three brain regions, hippocampus, cortex and cerebellum, in mice aged 1 and 12 months, using the total protein approach technique. In all the brain regions, both in young and in middle-aged animals, we identified over 6,700 proteins. We found that although the total protein expression in middle-aged brain structures is practically unaffected by aging, there are significant differences between young adult and middle-aged mice in the expression of some receptors and signaling cascade proteins proven to be significant for learning and memory formation. Our analysis demonstrates that hippocampus is the most unstable structure during natural aging and that the first symptoms of weakening of neuronal plasticity may be observed on protein level in middle-aged animals.

2018-07-03 | PXD009792 | 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