Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1249223 | ENA |
REPOSITORIES: ENA
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Project description:We hypothesize that gene expression in the aging lungs of these two strains of mice are divergent thus contributing to the disparity in the phenotypes. More specifically, (1) Aging DBA/2J mice compared to aging C57BL/6 mice are known to be accelerated in their lung physiology and morphometry; (2) C57BL/6J are known to have longer natural longevity than DBA/2J mice. In order to test these hypotheses at the gene expression level, we utilized microarray analysis to examine transcriptional differences between aging lungs of both strains of mice. Keywords: comparative expression profiling
2007-08-31 | GSE6591 | GEO
Project description:We hypothesize that gene expression in the aging lungs of these two strains of mice are divergent thus contributing to the disparity in the phenotypes.re specifically, (1) Aging DBA/2J mice compared to aging C57BL/6 mice are known to be accelerated in their lung physiology andrphometry; (2) C57BL/6J are known to have longer natural longevity than DBA/2J mice. In order to test these hypotheses at the gene expression level, we utilized microarray analysis to examine transcriptional differences between aging lungs of both strains of mice. Experiment Overall Design: This study utilizes microarray analysis to test these hypotheses. Three sets of lungs were harvested from both strains at each time point (C57BL/6J: 2, 18, AND 26s; DBA/2J: 2 and 18s). RNA was isolated and used for global gene expression profiling (Affymetrixuse 430 2.0 array). Statistically significant gene expression was determined as a minimum 6 counts of 9 pairwise comparisons, minimum 1.5-fold change, and p < 0.05. Further, Absolute | FC - FC SEM | >= 1.5.
2009-04-23 | E-GEOD-6591 | biostudies-arrayexpress
Project description:To elucidate the molecular mechanisms underlying Corylin-mediated delay of aging, we employed an integrated multi-omics approach—comprising proteome, phosphoproteome, and lysine acetylome analyses—using tissue samples from quadriceps, kidney, and liver collected from both male and female C57BL/6J mice. Comparative profiling across three groups—young, aged, and aged mice treated with Corylin—enabled a systematic characterization of Corylin-induced molecular alterations associated with aging.
2026-05-07 | PXD067643 | Pride
Project description:To elucidate the molecular mechanisms underlying Corylin-mediated delay of aging, we employed an integrated multi-omics approach—comprising proteome, phosphoproteome, and lysine acetylome analyses—using tissue samples from quadriceps, kidney, and liver collected from both male and female C57BL/6J mice. Comparative profiling across three groups—young, aged, and aged mice treated with Corylin—enabled a systematic characterization of Corylin-induced molecular alterations associated with aging.
2026-05-07 | PXD067637 | Pride
Project description:To elucidate the molecular mechanisms underlying Corylin-mediated delay of aging, we employed an integrated multi-omics approach—comprising proteome, phosphoproteome, and lysine acetylome analyses—using tissue samples from quadriceps, kidney, and liver collected from both male and female C57BL/6J mice. Comparative profiling across three groups—young, aged, and aged mice treated with Corylin—enabled a systematic characterization of Corylin-induced molecular alterations associated with aging.
2026-05-07 | PXD067647 | Pride
Project description:To identify novel aging-related miRNAs, we initially established a physiological aging mouse model (20-month old male C57BL/6 mouse), compared with 2-month old male C57BL/6 mouse. Then, the Agilent miRNA microarray was performed to profile miRNA expression levels in kidney from 20-month old male C57BL/6 mouse (designated as Aging) and 2-month old male C57BL/6 mouse (designated as Young).
2018-10-01 | GSE106109 | GEO
Project description:Studies on aging have largely included one or two OMICS layers, which may not necessarily reflect the signatures of other layers. Moreover, most aging studies have often compared very young (4-5 wks) mice with old (24 months) mice which does not reflect the aging transition after the attainment of adulthood. Therefore, we aimed to study and compared muti-OMICS aging signatures across key metabolic tissues of mature adults (6 months) and old (24 months) C57BL/6J mice (the most commonly used mouse strain). Here we compared the differentially regulated genes and enriched pathways for transcriptome, proteome and epigenome (H3K27ac, H3K4me3, H3K27me3, DNA methylation) across liver, heart, and quadriceps muscle. The major aging associated pathways cross multiple layers and tissues are decreased RNA metabolism, transcription, and translation at transcript and protein levels however increased potential of transcription at DNA methylation and H3K27ac levels.
2021-11-30 | PXD011142 | Pride
Project description:Calorie restriction (CR) extends lifespan by modulating the mechanisms involved in aging. We quantified the hepatic proteome of male C57BL/6 mice exposed to graded levels of CR (0% to 40% CR) for three months, and evaluated which signaling pathways were most affected.
2023-10-24 | PXD033436 | Pride
Project description:In our study, scWES was employed on oocytes from female mice with different reproductive ages. We also performed whole exome sequencing on bluk blood samples in trios to detect de novo germline variations in oocytes. Both natural aging and accelerated reproductive aging were involved. We demonstrated that genetic alterations, including base variants and structural variations, occurred in mouse oocytes during aging. Genes harboring natural aging or accelerated aging-related de novo germline variants (DNGVs) were almost involved in Ugt1a, V2R, and Mucin gene families. A copy number variant (CNV) associated with chromatin modeling were detected in natural aging oocytes. More importantly, we shortlisted various critical biological functions, like calcium binding pathway and p53 pathways, affected by these aging-related genetic alterations. Our work is the first study to identify genetic alterations in mouse oocytes with in vivo aging and offers a new direction of dissecting the aging mechanisms in oocytes and clarifying genetic causes of lower fertility at advanced maternal age.
2019-08-01 | PRJEB28344 | EVA