Analysis of gastrocnemius from male wild type(WT) and Skn-1-deficient mice. Skn-1-deficient mice have reduced body weight with low body fat due to increased energy expenditure.
Catecholamines Facilitate Fuel Expenditure and Protect Against Obesity via a Novel Network of the Gut-Brain Axis in Transcription Factor Skn-1-deficient Mice.
Sex, Specimen part, Time
View SamplesDorsomorphin is a small molecule inhibitor of type I bone morphogenic protein receptors (BMPRs). We have found that dorsomorphin affects a wide range of T cell function. In order to obtain the bigger picture of the effects of DM in T cell activation. transcriptomic analysis was performed using mouse primary CD25-CD4+ T cells with either DM (4 M) or vehicle in the presence or absence of stimulation by anti-CD3 and -CD28 antibodies.
Differential effects of inhibition of bone morphogenic protein (BMP) signalling on T-cell activation and differentiation.
Specimen part, Treatment
View SamplesTamoxifen, a selective estrogen receptor modulator, is widely used in research and clinically in patients. Tamoxifen injection (3 consecutive days, intraperitoneal, 5mg/20g mouse body weight) causes dramatic rearrangement of the gastric mucosa with loss of > 90% of PCs, a 6-fold increase in proliferation in stem/progenitor cells, and morphological changes in the ZCs in the bases of gastric-units.
Identification of alanyl aminopeptidase (CD13) as a surface marker for isolation of mature gastric zymogenic chief cells.
Time
View SamplesGenes related to AMPK activation, cellular respiration, and metabolism are enriched in the gastric parietal cell population. Metformin is known activator of AMPK.
A Metformin-Responsive Metabolic Pathway Controls Distinct Steps in Gastric Progenitor Fate Decisions and Maturation.
Specimen part
View SamplesThe fields of drug discovery and regenerative medicine require large numbers of adult human primary hepatocytes. For this purpose, it is desirable to use hepatocyte-like cells (HLCs) differentiated from human pluripotent stem cells. To develop an efficient HLCs induction method, we constructed a red fluorescent reporter, CYP3A7R, in which DsRed is placed under the transcriptional regulation of CYP3A7 coding for a human fetus-type P450 enzyme. We created transgenic mice using mouse embryonic stem cells (mESCs) carrying a CYP3A7R transgene.
Real-time fluorometric evaluation of hepatoblast proliferation in vivo and in vitro using the expression of CYP3A7 coding for human fetus-specific P450.
Specimen part
View SamplesUsing microcell-mediated chromosome transfer (MMCT) into the mouse melanoma cell line, B16F10, we have previously found that human chromosome 5 carries a gene, or genes, that can negatively regulate TERT expression. To identify the gene responsible for the regulation of TERT transcription, we performed cDNA microarray analysis using parental B16F10 cells, telomerase negative B16F10 microcell hybrids with a human chromosome 5 (B16F10MH5), and its revertant clones (MH5R) with reactivated telomerase. Here we report the identification of PITX1, whose restoration leads to the downregulation of mouse tert (mtert) transcription, as a TERT suppressor gene. Additionally, both human TERT (hTERT) and mouse TERT (mtert) promoter activity can be suppressed by PITX1. We showed that three and one binding sites, respectively, within the hTERT and mtert promoters that express a unique conserved region are responsible for the transcriptional activation of TERT. Furthermore, we showed that PITX1 binds to the TERT promoter both in vitro and in vivo. Thus, PITX1 suppresses TERT transcription through direct binding to the TERT promoter, which ultimately regulates telomerase activity.
Identification of PITX1 as a TERT suppressor gene located on human chromosome 5.
Specimen part, Cell line
View SamplesThe change in gene expression on the 8th day of gestation was investigated using DNA microarrays.
Cystathionine β-synthase deficiency causes infertility by impairing decidualization and gene expression networks in uterus implantation sites.
Sex, Age, Specimen part
View SamplesThe change in gene expression on the 8th day of gestation was investigated using DNA microarrays. Uterine gene expression of interimplanted sites was analyzed in female mice.
Cystathionine β-synthase deficiency causes infertility by impairing decidualization and gene expression networks in uterus implantation sites.
Sex, Age, Specimen part
View SamplesLysine 9 di-methylation and lysine 27 tri-methylation of histone H3 (H3K9me2 and H3K27me3) are mostly linked to gene repression. However, functions of repressive histone methylation dynamics during inflammatory responses remain poorly understood. Here, we show that lysine demethylase 7A (KDM7A) and 6A (UTX) are rapidly transported to nuclear factor kappa-B (NF-?B) related elements in human endothelial cells in response to tumor necrosis factor (TNF)-a. KDM7A and UTX demethylate H3K9me2 and H3K27me3, respectively, and cooperatively activate NF-?B dependent inflammatory genes. Furthermore, using both in situ Hi-C and other 3C based technology, loops between super enhancers (SEs) are newly formed following TNF-a-stimuli at NF-?B-dependent inflammatory loci where KDM7A- and UTX-recruitment coincide. Collectively, these findings suggest that erasing of repressive histone marks by KDM7A and UTX within NF-?B-related elements might functionally associate with formation of SE-SE three-dimensional interactions and could be a cue signal during inflammatory responses in human endothelial cells. Overall design: Total 29 samples were derived from [1] HUVECs in the absence or presence of TNF-alpha (0, 4, and 24 hrs) to determine TNF-alpha-responsive genes during inflammation, [2] si control, siKDM7A, siUTX, or siKDM7A+siUTX transfected HUVECs under TNF-alpha-stimuli (4 hrs) to understand molecular function of KDM7A and UTX during inflammation.
Coordinated demethylation of H3K9 and H3K27 is required for rapid inflammatory responses of endothelial cells.
Subject, Time
View SamplesTo identify the targets of LBH589 treatment, we compared gene expression profiles in three different types of human cancer cell lines (H295R, HeLa and MCF-7her2) with and without LBH589 treatment. Affymetrix microarray analysis was performed to determine changes in gene expression that are unique to LBH treatment.
Inhibition of the proliferation of acquired aromatase inhibitor-resistant breast cancer cells by histone deacetylase inhibitor LBH589 (panobinostat).
Cell line, Treatment
View Samples