557227dc-4796-4e3e-b470-16fa68852b5a - samples
Ontology highlight
ABSTRACT:
PROVIDER: EGAD00001009756 | EGA |
REPOSITORIES: EGA
Similar Datasets
Project description:Complimation of variants calls from three idependent cohorts, allowing for calls of rare and common vairants. All samples derived from a Danish research projects with recruitment of individuals of Danish origin (N> 8000).
Minor allele counts below 5 are masked to keep information de-identified level s.
| EGAS00001006786 | EGA
Project description:RNA was extracted from adult male and adult female Drosophila melanogaster with reversed sex-chromosome parent-of-origin (e.g. maternal-X/paternal-Y vs. paternal-X/maternal-Y) Parent-of-origin effects were assayed in X/Y males, XY/Y males, and XY/X females. Direct comparisons were made between individuals with the same karyotype (e.g. X/Y males or XY/Y males) incorporating dye-swaps.
2013-11-01 | E-GEOD-51942 | biostudies-arrayexpress
Project description:We investigated parent-of-origin and allele-specific expression effects on obesity and hepatic gene expression in reciprocal crosses between the Berlin Fat Mouse Inbred line (BFMI) and C57Bl/6NCrl (B6N). We sequenced mRNA extracted from liver tissue of 10 M. Musculus individuals. 4 liver samples were collected from 10 week old inbred strains (1 male and 1 female Berlin Fat Mouse Inbred line (BFMI), 1 male and 1 female C57Bl/6NCrl (B6N)) and 6 liver samples collected from 10 week old F1 males using a reciprocal cross design (3 paternal BFMI (patBFMI) vs 3 maternal BFMI (matBFMI)). Reciprocal crosses were generated from the Berlin Fat Mouse Inbred line BFMI860-12/Hber (BFMI) and C57BL/6NCrl (B6N). Seven BFMI males were mated with seven B6N females and six B6N males with six BFMI860 females to generate 48 F1 animals (deemed patBFMI and matBFMI, respectively). Each reciprocal F1 offspring groups consisted of 12 males and 12 females. From these animals three F1 males from three BFMI females and three F1 males from three B6N females were used for RNA-seq measurements. One high fat diet raised male and female from each inbred parental strain (BFMI and B6N) were used as parental strain control animals and measured via RNA-seq as well.
2015-11-11 | E-GEOD-74889 | biostudies-arrayexpress
Project description:The prevalence of some autoimmune diseases (AID) is greater in females compared with males, notwithstanding that disease severity is often greater in males. The reason for this sexual dimorphism (SD) is unknown, but may reflect negative selection of Y chromosome (ChrY) bearing sperm during spermatogenesis or male fetuses early in the course of conception/pregnancy. Previously, we showed that the SD in experimental autoimmune encephalomyelitis (EAE) is associated with copy number variation (CNV) in ChrY multicopy genes. Here, we test the hypothesis that CNV in ChrY multicopy genes influences the paternal parent-of-origin effect on EAE susceptibility in female mice. We show that C57BL/6J consomic strains of mice possessing an identical ChrX and CNV in ChrY multicopy genes exhibit a female biased sex-ratio and sperm head abnormalities, consistent with X-Y intragenomic conflict arising from an imbalance in CNV between homologous ChrX:ChrY multicopy genes. These males also display paternal transmission of EAE to female offspring and differential loading of miRNAs within the sperm nucleus. These findings provide evidence for a genetic mechanism at the level of the male gamete that contributes to the SD in EAE and paternal parent-of-origin effects in female mice, raising the possibility that a similar mechanism may contribute to the SD in MS. Three biological replicates for each strain were pooled from the axillary, brachial, and inguinal lymph nodes from 5 mice for each replicate. RNA was isolated from CD4+TCRB+ FAC sorted cells.
2015-01-16 | E-GEOD-65038 | biostudies-arrayexpress
Project description:This batch of data is for three independent projects. Since in this three projects, the mouse strains are all CD1/ICR, the sex are both female, and the mouse ages are all two-month-old, three projects shared control data to save expenditure legitimately. But in our hand we couldn't segregate the raw data into two parts corresponding to two projects, so we uploads all raw data. However, we also provided researcher-analyzable excel files including the expression of all phosphorylated proteins. The concise description of these three projects are as follow: Project 1: We found that in Chronic Resistant Stress (CRS)-treated mice, the fertility and oocyte quality significantly decreased, and plenty of biochemical indexes significantly changed, so we guessed that the overall physical health of CRS mice was severely impacted. As one major strategy to investigate the mechanism how CRS impact the physical health, We chose TMT-labeled quantitative ovarian phosphoproteomics service from Hangzhou PTM Bio Co. We sent two repeats of two-month-old CRS CD1/ICR mouse ovaries and two repeats of control ovaries for characterization of differentially phosphorylated proteins. Each repeat contained about 60 ovaries from 30 female mice, about 300 mg. Project 2: We found that in High Salt (HS)-treated mice, the fertility and oocyte quality significantly decreased, and plenty of biochemical indexes significantly changed, so we guessed that the overall physical health of HS mice was severely impacted. As one major strategy to investigate the mechanism how HS impact the physical health, We chose TMT-labeled Quantitative ovarian phosphoproteomics service from Hangzhou PTM Bio Co. We sent two repeats of two-month-old HS CD1/ICR mouse ovaries and two repeats of control ovaries for characterization of differentially phosphorylated proteins. Each repeat contained about 60 ovaries from 30 female mice, about 300 mg. Project 3: We found that in arecoline (Are)-treated mice, the fertility and oocyte quality significantly decreased, and plenty of biochemical indexes significantly changed, so we guessed that the overall physical health of Are mice was severely impacted. As one major strategy to investigate the mechanism how Are impact the physical health, We chose TMT-labeled Quantitative ovarian phosphoproteomics service from Hangzhou PTM Bio Co. We sent two repeats of two-month-old Are CD1/ICR mouse ovaries and two repeats of control ovaries for characterization of differentially phosphorylated proteins. Each repeat contained about 60 ovaries from 30 female mice, about 300 mg. Two repeats of control samples and data were shared among project 1, 2 and 3. Gross protein levels were also examined and used to normalize the protein phosphorylation level.
2024-05-22 | PXD028932 | Pride
Project description:Female breast cancer patients who underwent surgery for breast cancer as part of the Danish Center for Translational Breast Cancer Research program were included from 2003 to 2012. Patient inclusion criteria were: (1) a unifocal tumor with an estimated size of more than 20 mm in diameter, (2) none of the patients had a history of breast surgery and (3) none received preoperative treatment. Patients were defined as high risk according to the Danish Breast Cooperative Group (www.dbcg.dk) and were followed after surgery.
2018-11-16 | E-MTAB-7201 | biostudies-arrayexpress
Project description:The prevalence of some autoimmune diseases (AID) is greater in females compared with males, notwithstanding that disease severity is often greater in males. The reason for this sexual dimorphism (SD) is unknown, but may reflect negative selection of Y chromosome (ChrY) bearing sperm during spermatogenesis or male fetuses early in the course of conception/pregnancy. Previously, we showed that the SD in experimental autoimmune encephalomyelitis (EAE) is associated with copy number variation (CNV) in ChrY multicopy genes. Here, we test the hypothesis that CNV in ChrY multicopy genes influences the paternal parent-of-origin effect on EAE susceptibility in female mice. We show that C57BL/6J consomic strains of mice possessing an identical ChrX and CNV in ChrY multicopy genes exhibit a female biased sex-ratio and sperm head abnormalities, consistent with X-Y intragenomic conflict arising from an imbalance in CNV between homologous ChrX:ChrY multicopy genes. These males also display paternal transmission of EAE to female offspring and differential loading of miRNAs within the sperm nucleus. These findings provide evidence for a genetic mechanism at the level of the male gamete that contributes to the SD in EAE and paternal parent-of-origin effects in female mice, raising the possibility that a similar mechanism may contribute to the SD in MS.
2015-01-16 | GSE65047 | GEO
Project description:The prevalence of some autoimmune diseases (AID) is greater in females compared with males, notwithstanding that disease severity is often greater in males. The reason for this sexual dimorphism (SD) is unknown, but may reflect negative selection of Y chromosome (ChrY) bearing sperm during spermatogenesis or male fetuses early in the course of conception/pregnancy. Previously, we showed that the SD in experimental autoimmune encephalomyelitis (EAE) is associated with copy number variation (CNV) in ChrY multicopy genes. Here, we test the hypothesis that CNV in ChrY multicopy genes influences the paternal parent-of-origin effect on EAE susceptibility in female mice. We show that C57BL/6J consomic strains of mice possessing an identical ChrX and CNV in ChrY multicopy genes exhibit a female biased sex-ratio and sperm head abnormalities, consistent with X-Y intragenomic conflict arising from an imbalance in CNV between homologous ChrX:ChrY multicopy genes. These males also display paternal transmission of EAE to female offspring and differential loading of miRNAs within the sperm nucleus. These findings provide evidence for a genetic mechanism at the level of the male gamete that contributes to the SD in EAE and paternal parent-of-origin effects in female mice, raising the possibility that a similar mechanism may contribute to the SD in MS.
2015-01-16 | GSE65038 | GEO
Project description:The prevalence of some autoimmune diseases (AID) is greater in females compared with males, notwithstanding that disease severity is often greater in males. The reason for this sexual dimorphism (SD) is unknown, but may reflect negative selection of Y chromosome (ChrY) bearing sperm during spermatogenesis or male fetuses early in the course of conception/pregnancy. Previously, we showed that the SD in experimental autoimmune encephalomyelitis (EAE) is associated with copy number variation (CNV) in ChrY multicopy genes. Here, we test the hypothesis that CNV in ChrY multicopy genes influences the paternal parent-of-origin effect on EAE susceptibility in female mice. We show that C57BL/6J consomic strains of mice possessing an identical ChrX and CNV in ChrY multicopy genes exhibit a female biased sex-ratio and sperm head abnormalities, consistent with X-Y intragenomic conflict arising from an imbalance in CNV between homologous ChrX:ChrY multicopy genes. These males also display paternal transmission of EAE to female offspring and differential loading of miRNAs within the sperm nucleus. These findings provide evidence for a genetic mechanism at the level of the male gamete that contributes to the SD in EAE and paternal parent-of-origin effects in female mice, raising the possibility that a similar mechanism may contribute to the SD in MS. miRNA expression was analyzed in epidydimal sperm pooled from 5 mice for each replicate per strain.
2015-01-16 | E-GEOD-65047 | biostudies-arrayexpress