We have generated transgenic mice expressing constitutively activated aryl hydrocarbon receptor (CA-AhR) to examine the biological consequences of AhR activation..
A novel role for the dioxin receptor in fatty acid metabolism and hepatic steatosis.
Specimen part
View SamplesThis SuperSeries is composed of the SubSeries listed below.
Genomic evolution of the placenta using co-option and duplication and divergence.
Specimen part
View SamplesWe used full genome microarrays to profile the full lifetime of the mouse placenta from embryonic day 8.5 (e8.5), at the time of chorioallantoic fusion, until postnatal day 0 (P0).
Genomic evolution of the placenta using co-option and duplication and divergence.
Specimen part
View SamplesWe used full genome microarrays to profile the full lifetime of the mouse placenta from embryonic day 8.5 (e8.5), at the time of chorioallantoic fusion, until postnatal day 0 (P0). For these samples, at each stage the fetal placenta and maternal decidual tissues were dissected and profiled separately (See series 1).
Genomic evolution of the placenta using co-option and duplication and divergence.
Specimen part
View SamplesThis SuperSeries is composed of the SubSeries listed below.
Transcriptomic response of murine liver to severe injury and hemorrhagic shock: a dual-platform microarray analysis.
Sex, Specimen part
View SamplesA dual platform microarray analysis was used to characterize the temporal transcriptomic response in the mouse liver following trauma and hemmorhagic shock
Transcriptomic response of murine liver to severe injury and hemorrhagic shock: a dual-platform microarray analysis.
Sex, Specimen part
View SamplesSV40 large T antigen (TAg) contributes to cell transformation, in part, by targeting two well characterized tumor suppressors, pRb and p53. TAg expression affects the transcriptional circuits controlled by Rb and by p53. We have performed a microarray analysis to examine the global change in gene expression induced by wild-type TAg and TAg-mutants, in an effort to link changes in gene expression to specific transforming functions. For this analysis we have used enterocytes from the mouse small intestine expressing TAg. Expression of TAg in the mouse intestine results in hyperplasia and dysplasia. Our analysis indicates that practically all gene expression regulated by TAg in enterocytes is dependent upon its binding and inactivation of the Rb-family proteins.
Simian virus 40 T-antigen-mediated gene regulation in enterocytes is controlled primarily by the Rb-E2F pathway.
Sex, Age, Specimen part
View SamplesThe lung host immune responses following M.tuberculosis infection in the mouse model of tuberculosis were assayed by studying the gene expression profiles at day 0, day 12, 15 and 21 post infection
Profiling early lung immune responses in the mouse model of tuberculosis.
Specimen part, Time
View SamplesPurpose: To identify the changes in postnatal mouse conjunctival forniceal gene expression and their regulation by Klf4 around eye opening stage when the goblet cells first appear.
Mouse conjunctival forniceal gene expression during postnatal development and its regulation by Kruppel-like factor 4.
No sample metadata fields
View SamplesTCPOBOP (1,4-Bis [2-(3,5-Dichloropyridyloxy)] benzene) is a constitutive androstane receptor (CAR) agonist that induces robust hepatocyte proliferation and hepatomegaly without any liver injury or tissue loss. TCPOBOP-induced direct hyperplasia has been considered to be CAR-dependent with no evidence of involvement of cytokines or growth factor signaling. Receptor tyrosine kinases (RTKs), MET and EGFR, are known to play a critical role in liver regeneration after partial hepatectomy, but their role in TCPOBOP-induced direct hyperplasia, not yet explored, is investigated in the current study. Disruption of the RTK-mediated signaling was achieved utilizing MET KO mice along with Canertinib treatment for EGFR inhibition. Combined elimination of MET and EGFR signaling [MET KO + EGFRi], but not individual disruption, dramatically reduced TCPOBOP-induced hepatomegaly and hepatocyte proliferation. TCPOBOP-driven CAR activation was not altered in [MET KO + EGFRi] mice, as measured by nuclear CAR translocation and analysis of typical CAR target genes. However, TCPOBOP induced cell cycle activation was impaired in [MET KO + EGFRi] mice due to defective induction of cyclins, which regulate cell cycle initiation and progression. TCPOBOP-driven induction of FOXM1, a key transcriptional regulator of cell cycle progression during TCPOBOP-mediated hepatocyte proliferation, was greatly attenuated in [MET KO + EGFRi] mice. Interestingly, TCPOBOP treatment caused transient decline in HNF4 expression concomitant to proliferative response; this was not seen in [MET KO + EGFRi] mice. Transcriptomic profiling revealed vast majority (~40%) of TCPOBOP-dependent genes mainly related to proliferative response, but not to drug metabolism, were differentially expressed in [MET KO + EGFRi] mice. Conclusion: Taken together, combined disruption of EGFR and MET signaling lead to dramatic impairment of TCPOBOP-induced proliferative response without altering CAR activation.
TCPOBOP-induced hepatomegaly & hepatocyte proliferation is attenuated by combined disruption of MET & EGFR signaling.
No sample metadata fields
View Samples