Rattus
Ontology highlight
ABSTRACT:
PROVIDER: PRJDB16502 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Classic galactosemia (CG) is a rare inborn error of galactose metabolism caused by mutations in GALT gene. Primary ovarian insufficiency (POI) is a later complication that affects 80% of women with CG due to significant decline in ovarian follicle reserve. The definite mechanisms underlying the early onset of POI in CG patients is not fully understood. We utilized spatial transcriptomics from 10x Visium to generate spatial landscape of human ovaries from pre-pubertal girls with CG to investigate dynamic gene expression profiles in the ovarian follicles and stromal cells.
2025-02-19 | GSE268523 | GEO
Project description:During female reproductive life, the reserve of ovarian follicles is reduced by maturation and atresia until menopause ensues. Foxo3 is required to maintain the ovarian reserve in mice. We asked if overexpression of a constitutively active FOXO3 protein can increase long-lasting ovarian reproductive capacity in mice. Trangenic vs non-transgenic mice onto Foxo3+/- vs Foxo3-/- genotype
2013-06-08 | E-GEOD-45389 | biostudies-arrayexpress
Project description:Hyperhomocysteinemia (HHcy) causes cardiovascular dysfunction and is associated with many complications during pregnancy related to reduced NO bioactivity. The mechanisms of HHcy on the NO-dependent control of myocardial metabolism was compared with L-NAME, which directly inhibits NO bioavailability, treated animals. We used microarrays to detail the global programme of gene expression underlying hyperhomocysteinemia during pregnancy and identified distinct classes of differentially regulated genes. Female SD rats were mated with male SD rats. Methionine was used to generate hyperhomocysteinemia model. L-NAME was used to generate NO restricted model. After treatment, the left ventricles were harvested for RNA extraction and hybridization on Affymetrix microarrays.
2015-06-12 | E-GEOD-30308 | biostudies-arrayexpress
Project description:During female reproductive life, the reserve of ovarian follicles is reduced by maturation and atresia until menopause ensues. Foxo3 is required to maintain the ovarian reserve in mice. We asked if overexpression of a constitutively active FOXO3 protein can increase long-lasting ovarian reproductive capacity in mice.
2013-06-08 | GSE45389 | GEO
Project description:Mammalian female reproductive lifespan is typically significantly shorter than life expectancy and is associated with a decrease in ovarian NAD levels. However, the mechanisms underlying this loss of ovarian NAD are unclear. Here, we show that CD38, a NAD consuming enzyme, is expressed in the ovarian extrafollicular space, primarily in immune cells, and its levels increase with reproductive age. Reproductively young mice lacking CD38 exhibit larger primordial follicle pools, elevated ovarian NAD levels, and increased fecundity relative to wild type controls. This larger ovarian reserve results from a prolonged window of follicle formation during early development. However, the beneficial effect of CD38 loss on reproductive function is not maintained at advanced age. Our results demonstrate a novel role of CD38 in regulating ovarian NAD metabolism and establishing the ovarian reserve, a critical process that dictates a female reproductive lifespan.
| MSV000092808 | MassIVE
Project description:Mammalian female reproductive lifespan is typically significantly shorter than life expectancy and is associated with a decrease in ovarian NAD levels. However, the mechanisms underlying this loss of ovarian NAD are unclear. Here, we show that CD38, a NAD consuming enzyme, is expressed in the ovarian extrafollicular space, primarily in immune cells, and its levels increase with reproductive age. Reproductively young mice lacking CD38 exhibit larger primordial follicle pools, elevated ovarian NAD levels, and increased fecundity relative to wild type controls. This larger ovarian reserve results from a prolonged window of follicle formation during early development. However, the beneficial effect of CD38 loss on reproductive function is not maintained at advanced age. Our results demonstrate a novel role of CD38 in regulating ovarian NAD metabolism and establishing the ovarian reserve, a critical process that dictates a female reproductive lifespan.
| MSV000092808 | GNPS
Project description:Individuals with a single functional copy of the BRCA2 tumor suppressor have elevated risks for breast, ovarian, and other solid tumor malignancies. The exact mechanisms of carcinogenesis due to BRCA2 haploinsufficiency remain unclear, but one possibility is that at-risk cells are subject to acute periods of decreased BRCA2 availability and function ("BRCA2-crisis"), which may contribute to disease. Here, we establish an in vitro model for BRCA2-crisis that demonstrates chromatin remodeling and activation of an NF-κB survival pathway in response to transient BRCA2 depletion. Mechanistically, we identify BRCA2 chromatin binding, histone acetylation, and associated transcriptional activity as critical determinants of the epigenetic response to BRCA2-crisis. These chromatin alterations are reflected in transcriptional profiles of pre-malignant tissues from BRCA2 carriers and, therefore, may reflect natural steps in human disease. By modeling BRCA2-crisis in vitro, we have derived insights into pre-neoplastic molecular alterations that may enhance the development of preventative therapies.
2019-08-07 | GSE107280 | GEO
Project description:Individuals with a single functional copy of the BRCA2 tumor suppressor have elevated risks for breast, ovarian, and other solid tumor malignancies. The exact mechanisms of carcinogenesis due to BRCA2 haploinsufficiency remain unclear, but one possibility is that at-risk cells are subject to acute periods of decreased BRCA2 availability and function ("BRCA2-crisis"), which may contribute to disease. Here, we establish an in vitro model for BRCA2-crisis that demonstrates chromatin remodeling and activation of an NF-κB survival pathway in response to transient BRCA2 depletion. Mechanistically, we identify BRCA2 chromatin binding, histone acetylation, and associated transcriptional activity as critical determinants of the epigenetic response to BRCA2-crisis. These chromatin alterations are reflected in transcriptional profiles of pre-malignant tissues from BRCA2 carriers and, therefore, may reflect natural steps in human disease. By modeling BRCA2-crisis in vitro, we have derived insights into pre-neoplastic molecular alterations that may enhance the development of preventative therapies.
2019-08-07 | GSE107103 | GEO
Project description:Individuals with a single functional copy of the BRCA2 tumor suppressor have elevated risks for breast, ovarian and other solid tumor malignancies. The exact mechanisms of carcinogenesis due to BRCA2 haploinsufficiency remain unclear, but one possibility is that at-risk cells are subject to acute periods of decreased BRCA2 availability and function (“BRCA2-crisis”), which may contribute to disease. Here we establish an in vitro model for BRCA2-crisis that demonstrates novel epigenetic remodeling and activation of an NF-κB survival pathway in response to transient BRCA2-depletion. Mechanistically, we identify BRCA2 chromatin binding, histone acetylation and associated transcriptional activity as critical determinants of the epigenetic response to BRCA2-crisis. These epigenetic alterations are reflected in transcriptional profiles of pre-malignant tissues from BRCA2-carriers and therefore may reflect natural steps in human disease. By modeling BRCA2-crisis in vitro we have derived insights into pre-neoplastic molecular alterations that may enhance the development of preventative therapies.
2019-08-07 | GSE133728 | GEO
Project description:Individuals with a single functional copy of the BRCA2 tumor suppressor have elevated risks for breast, ovarian, and other solid tumor malignancies. The exact mechanisms of carcinogenesis due to BRCA2 haploinsufficiency remain unclear, but one possibility is that at-risk cells are subject to acute periods of decreased BRCA2 availability and function ("BRCA2-crisis"), which may contribute to disease. Here, we establish an in vitro model for BRCA2-crisis that demonstrates chromatin remodeling and activation of an NF-κB survival pathway in response to transient BRCA2 depletion. Mechanistically, we identify BRCA2 chromatin binding, histone acetylation, and associated transcriptional activity as critical determinants of the epigenetic response to BRCA2-crisis. These chromatin alterations are reflected in transcriptional profiles of pre-malignant tissues from BRCA2 carriers and, therefore, may reflect natural steps in human disease. By modeling BRCA2-crisis in vitro, we have derived insights into pre-neoplastic molecular alterations that may enhance the development of preventative therapies.
2019-08-07 | GSE133450 | GEO