Project description:We used the microarray analysis to determine the differential gene expression profiles in mouse uterine luminal epithelium between preimplantation gestation day 3.5 and postimplantation gestation day 4.5, and investigeate the molecular mechanism of the establishment of uterine receptivity and embryo implantation. Uterine luminal epithelium (LE) is critical for the establishment of uterine receptivity during embryo implantation. Many genes are known to have differential expression in the periimplantation LE but the global profiling of the altered genes in the periimplantation LE is unknown. To fill in this knowledge gap, microarray analysis was performed in gestation day 3.5 (D3.5, preimplantation) and D4.5 (postimplantation) mouse LE from natural pregnancy. There were 382 significantly upregulated and 245 significantly downregulated genes (>2 fold, P<0.05) in the D4.5 LE. There are 6 samples. 3 for gestation day 3.5 uterine luminal epithelium, the other 3 for gestation day 4.5 uterine luminal epithelium
Project description:We report the transcriptomic profile of uterine tissues obtained from the control (Wnk1f/f) and Wnk1 cKO (PGRCre/+;Wnk1f/f) mice during pseudopregnancy day 4.5.
Project description:We report the sequencing of the uterine transcriptome sequencing of control and conditional knock-out of the Forkhead box O1 at day 4.5 of murine pseudopregnancy
Project description:To identify substrates of the ubiquitinating E3 enzyme Rsp5 we applied purified Rsp5 to duplicate protein arrays. The Rsp proteins were expressed as fusion proteins to GST. We used as a control Ubr1, a RING domain containing E3 ligase We analyzed Rsp5 from S.cerevisiae on duplicate arrays, with four control chips, two without Rsp5 and two with Ubr1.
Project description:Uterine glands are essential for pregnancy in mice and likely humans, because they secrete or transport bioactive substances that regulate uterine receptivity for blastocyst implantation. In mice, the uterus becomes receptive to blastocyst implantation on day 4, but is refractory by day 5. Here, blastocysts could be recovered from progesterone-induced uterine gland (PUGKO) but not wildtype (WT) mice on day 5 post-mating. Anti-adhesive Muc1 protein and microvilli were present on the luminal epithelium of PUGKO but not WT uteri. A number of known uterine receptivity genes and gland-specific genes were altered in the PUGKO uterus. Next, the uterus and uterine luminal fluid (ULF) were obtained from WT and PUGKO mice on day 3, 4 and 5. Transcriptome analysis revealed that 580 genes were decreased in the PUGKO uterus, however ULF secrotome analysis revealed that many proteins and several amino acids were increased in the PUGKO ULF. Of note, many proteins encoded by many gland-specific genes were not identified in the ULF of WT mice. These results support the ideas that uterine glands secrete factors that regulate ULF homeostasis and interact with other cell types in the uterus to influence uterine receptivity and blastocyst implantation for the establishment of pregnancy.
Project description:Tamoxifen, a selective estrogen receptor modulator (SERM), is an effective treatment for breast cancers. In the CD-1 mouse model, neonatal oral dosing with tamoxifen leads to the development of adenomyosis. Both 4-hydroxyestradiol and tamoxifen can form DNA-reactive metabolites and may be involved in carcinogenesis of the uterus. After comparing the uterotrophic response of several SERMs the maximal uterotrophic doses of estradiol (100mg/kg) 4-hydroxyestradiol (385mg/kg) and tamoxifen (250mg/kg) were determined. Maximal uterotrophic doses were given orally to newborn CD-1 mice on days 1 â 4 after birth and gene and pathological changes examined in the uterus at 3 months after dosing. ERKOa knockout mice were dosed orally with tamoxifen (1mg/Kg) on days 1 â 4 after birth and uterine gene expression compared with CD-1 mice. Dosing groups: Estradiol (E2): 100mg/Kg 4-hydroxyestradiol (4OHE2): 385mg/Kg Tamoxifen : 250mg/Kg ERKO mice dosed with tamoxifen (1mg/Kg) 4 dosed animals and 4 controls for each treatment group. Uteri removed at 3 months after dosing and total RNA extracted. Controls were pooled. RNA labelling, hybridisation and analysis of fluorescence was carried out as described by Turton et al (2001). Cy3/Cy5 dye swap labelling was carried out on samples from each animal. Reference: Turton NJ et. al. (Oncogene (2001) 20, 1300-1306
Project description:cea06-01_uranyl_nitrate - time course uranyl nitrate response - Dynamic analyses of transcriptomic response to urany l nitrate - Plants are grown on sand and transfert in hydroponic culture during 2 days and then expose or not to 50uM uranyl nitrate at pH 4.5 in water or only to water at pH 4.5. Roots and leaves were collected independently after 2h, 6h and 30h of treament. Keywords: organ comparison,time course,treated vs untreated comparison 20 dye-swap - CATMA arrays
Project description:We report an integrated analysis incorporating DNA copy number analyses, somatic exon mutations, mRNA expression via RNA-sequencing, and shotgun mass spectrometry analysis of protein abundance in 108 surgically resected squamous cell lung cancers (SCC) with accompanying clinical outcome, evaluation of tumor pathology, and other clinically relevant data. We identified three major subtypes of SCC at the proteomic level, with two groups associated with inflammation/immune response or oxidation-reduction biology. Inflamed tumors could be further sub-classified based on neutrophil infiltration or antigen presentation proteomes and reflected patterns of infiltrating immune cells. No gene mutations, mRNA signatures, or proteomic subclasses were associated with outcomes; however, the presence of B-cell rich tertiary lymph node structures could be associated with better patient outcomes. By integrating our proteogenomic data with publicly available RNA interference screen data, we identified TP63, PSAT1, and AKR1C3 as vulnerabilities in SCC, particularly in the redox proteomic group. This cohort and its deep molecular data serves as an important resource to better understand biology and targets associated with SCC.