Caveolin-1 knockout liver and gonadal adipose tissue
Ontology highlight
ABSTRACT:
ORGANISM(S): Mus musculus
SUBMITTER: Thomas Person
PROVIDER: E-GEOD-35431 | biostudies-arrayexpress |
REPOSITORIES: biostudies-arrayexpress
Similar Datasets
Project description:mRNA expression was compared in between wild type and caveolin-1 knockout livers mRNA expression was compared in between wild type and caveolin-1 knockout gonadal adipose tissue
2012-01-31 | GSE35431 | GEO
Project description:Caveolin-1 knockout liver and gonadal adipose tissue
| PRJNA152769 | ENA
Project description:Gonadectomy (GDX) induces sex steroid-producing adrenocortical tumors in certain mouse strains and in the domestic ferret. Complementary approaches, including DNA methylation mapping and microarray expression profiling, were used to identify novel genetic and epigenetic markers of GDX-induced adrenocortical neoplasia in female DBA/2J mice. Markers were validated by quantitative RT-PCR, laser capture microdissection, in situ hybridization, and immunohistochemistry. Two genes with hypomethylated promoters, Igfbp6 and Foxs1, were upregulated in post-GDX adrenocortical neoplasms. The neoplastic cells also exhibited hypomethylation of the fetal adrenal enhancer of Sf1, an epigenetic signature that typifies descendants of fetal adrenal rather than gonadal cells. Expression profiling demonstrated upregulation of gonadal-like genes, including Spinlw1, Insl3, and Foxl2, in GDX-induced adrenocortical tumors of the mouse. One of these markers, FOXL2, was detected in adrenocortical tumor specimens from gonadectomized ferrets. These new markers may prove useful for studies of steroidogenic cell development and for diagnostic testing. Total RNA extracted from whole adrenal glands of gonadectomized and non-gonadectomized mice.
2014-07-31 | E-GEOD-54393 | biostudies-arrayexpress
Project description:SUMMARY: Basal breast cancer has been associated with mutations in a number of specific tumor suppressor genes, however, the mechanism by which these tumors express a basal lineage remains unknown. Notch signaling suppresses mammary stem cell (MaSC) self-renewal, while promoting luminal cell fate specification. Here we show that Lfng, a sugar transferase that facilitates Notch activation, suppresses mammary stem/bipotent progenitor cell proliferation. Targeted deletion of Lfng in mammary epithelium induces basal tumors with reduced expression of Notch targets, amplification of the Met/Caveolin gene locus, and elevated Met and Igf-1R signaling. Human basal breast cancer, a disease associated with elevated MET receptor signaling and Caveolin protein, express low levels of LFNG. Thus, reduced LFNG expression cooperates with a Met/ Caveolin amplicon to promote basal breast disease. SIGNIFICANCE: Anti-Notch therapy is currently being tested for efficacy against basal-like breast cancer in humans. Here we report that LFNG, which controls Notch receptor activation, is consistently expressed at a low level in basal tumors and that deletion of this gene in the mouse mammary gland reduces Notch signaling, increases proliferation and induces basal mammary tumors in cooperation with amplification of the Met/Caveolin gene locus. These mutations interact to promote basal gene expression by decreasing Notch pathway activation, as well as to enhance Met and Igf-1R signaling. These pathways can be targeted at multiple levels in humans harboring basal breast cancer with amplification of MET and CAV1/2 32 array samples
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Project description:Three congenic mouse strains were profiled with microarrays and were analyzed using a QTL/Microarray approach to identify candidate genes that regulate biometric phenotypes: HG2D (HG.CAST-(D2Mit329-D2Mit457)), HG11 (HG.CAST-(D11Mit260-D11Mit255, MGI reference: 3771218), and HG17 (HG.CAST-(D17Mit196-D17Mit190); MGI reference: 3771215). All these congenic strains isolate CAST/EiJ (CAST) alleles in a C57BL/6Jhg/hg (C57) background and bare the hg deletion in the high growth locus on chromosome 10. F2 animals from intercrossing congenic males and C57 control females were profiled for gene expresion on brain, liver and gonadal white fat. To detect differential expression produced by allelic effects of biometric QTLs on chromosomes 2, 11, and 17. Three strains were profiled: HG2D, HG11, and HG17, isolating CAST alleles in a high growth (HG) background on chromosomes 2, 11, and 17 respectively. Four biological replicates were assayed per strain for brain, liver and gonadal white adipose tissue. Experiments for each chromosomes were done independently. Only genotype comparisons within tissue in each strain were performed.
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Project description:Currently, the mechanisms behind the anti-aging effects of exercise are not understood. The presented study conducted a microarray on hippocampal samples from adult (3.5 month-old) and aged (18 month-old) male BALB/c mice that were individually housed with or without running wheels for 8 weeks. Results showed that aging altered genes related to chromatin remodeling, cell growth, immune activity, and synapse organization compared to adult mice. Exercise was found to modulate many of the genes altered by aging, but in the opposite direction. For example, wheel running increased expression of genes related to cell growth and attenuated expression of genes involved in immune function and chromatin remodeling. Collectively, findings show that even late-onset exercise may attenuate age-related changes in gene expression and identifies possible pathways through which exercise may exert its beneficial effects. In total 20 samples (4 aged exercise, 4 aged sedentary, 6 adult exercise, and 6 adult sedentary) plus 4 technical replicates (24 total) were analyzed.
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Project description:Impact of protein ingestion following 1 h intense cycling on the induced transcriptome and signaling in biopsy samples from endurance-trained men, relative to isocaloric control Single blind, randomized, crossover design comprising two experimental blocks. During the blocks, exercise and diet were controlled and the intervention consisted of the ingestion of a protein-enriched and control beverage, with outcome measures obtained from skeletal muscle tissue collected following a bout of intense cycling. Total RNA were obtained from quadriceps. Each of the two serves were isocaloric and provided 0.2 g/kg fat (freeze dried canola oil) with either 1.2 g/kg carbohydrate (1:1 maltodextrin:fructose) and 0.4 g/kg protein (2:1 milk protein concentrate:whey isolate); or 1.6 g/kg carbohydrate (1:1 maltodextrin:fructose).
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Project description:MiRNA expression is known to be deregulated in chronic lymphocytic leukemia (CLL). To get insight into miRNA expression pattern in CLL, we compaired miRNA expression profiling of peripheral blood-derived CLL cells and the healthy donor, peripheral blood-derived B-lymphocytes. A set of differentially expressed miRNAs was revealed. MiRNA expression profiling was performed on 18 CLL samples and one sample, which is a pool of 5 RNA samples of healthy donor peripheral blood-derived B-lymphocytes
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Project description:Ongoing, lifelong neurogenesis maintains the neuronal population of the olfactory epithelium in the face of piecemeal neuronal turnover and restores it following wholesale loss. The molecular phenotypes corresponding to different stages along the progression from multipotent globose basal cell (GBC) progenitor to differentiated olfactory sensory neuron are poorly characterized. We used the transgenic expression of GFP and cell surface markers to FACS-isolate Sox2-GFP(+) GBCs, Neurog1-GFP(+) GBCs and immature neurons, and OMP-GFP(+) mature neurons from normal adult mice. In addition, the latter two populations were also collected 3 weeks after olfactory bulb ablation, a lesion that results in persistently elevated neurogenesis. Global profiling of mRNA from the populations indicates that all stages of neurogenesis share a cohort of >2100 genes that are upregulated compared to sustentacular cells. A further cohort of >1200 genes are specifically upregulated in GBCs as compared to sustentacular cells and differentiated neurons. The increased rate of neurogenesis caused by olfactory bulbectomy had little effect on the transcriptional profile of the Neurog1-GFP(+) population. In contrast, the abbreviated lifespan of OMP-GFP(+) neurons born in the absence of the bulb correlated with substantial differences in gene expression as compared to the mature neurons of the normal epithelium. Detailed examination of the specific genes upregulated in the different progenitor populations revealed that the chromatin modifying complex proteins LSD1 and coREST were expressed sequentially in upstream Sox2-GFP(+) GBCs and Neurog1-GFP(+) GBCs/immature neurons. The expression patterns of these proteins are dynamically regulated after activation of the epithelium by methyl bromide lesion. Total RNA was isolated from dissected, dissociated and FACS-purified olfactory mucosal cells from normal adult mice or mice 3 weeks after unilateral bulbectomy. Cells were purified with FACS using endogenous GFP fluorescence from various transgenic lines and cell surface labeling. Two to seven adult mice were used per replicate and three replicates per condition were performed using Illumina bead arrays. 21 samples from olfactory mucosa were analyzed in this series and 3 samples were from a commercially available reference RNA sample. Universal mouse reference RNA from Stratagene was used as a general control and Normal olfactory mucosa was used as a tissue specific control.
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