This SuperSeries is composed of the SubSeries listed below.
Hippo pathway activity influences liver cell fate.
Specimen part, Time
View SamplesHippo signaling is highly associated with activity in the stem cell compartment of many epithelial tissues. In this study, we examined if Hippo signaling inhibition (by inducing Yap expression) could convert differentiated cells into a progenitor like phenotype. Organoid cells derived from mouse livers under various conditions, wild-type, Yap ON (Plus Dox), and Yap ON then OFF (Minus Dox) was examined.
Hippo pathway activity influences liver cell fate.
Specimen part
View SamplesHippo signaling is highly associated with activity in the stem cell compartment of many epithelial tissues. In this study, we examined if Hippo signaling inhibition (by inducing Yap expression) could convert differentiated cells into a progenitor like phenotype.
Hippo pathway activity influences liver cell fate.
Specimen part, Time
View SamplesCurrent models imply that the FERM domain protein Merlin, encoded by the tumor suppressor NF2, inhibits mitogenic signaling at or near the plasma membrane. Here, we show that the closed, growth inhibitory form of Merlin accumulates in the nucleus, binds to the E3 ubiquitin ligase CRL4DCAF1, and suppresses its activity. Depletion of DCAF1 blocks the promitogenic effect of inactivation of Merlin. Conversely, enforced expression of a Merlin-insensitive mutant of DCAF1 counteracts the antimitogenic effect of Merlin. Re-expression of Merlin and silencing of DCAF1 induce a similar, tumor-suppressive program of gene expression. Tumor-derived mutations invariably disrupt Merlins ability to interact with or inhibit CRL4DCAF1. Finally, depletion of DCAF1 inhibits the hyperproliferation of Schwannoma cells from NF2 patients and suppresses the oncogenic potential of Merlin-deficient tumor cell lines. We propose that Merlin suppresses tumorigenesis by translocating to the nucleus to inhibit CRL4DCAF1.
Merlin/NF2 suppresses tumorigenesis by inhibiting the E3 ubiquitin ligase CRL4(DCAF1) in the nucleus.
Specimen part
View SamplesHuntingtons disease (HD) is a devastating disease for which currently no therapy is available. It is a progressive autosomal dominant neurodegenerative disorder that is caused by a CAG repeat expansion in the HD gene, resulting in an expansion of polyglutamines at the N-terminal end of the encoded protein, designated huntingtin, and the accumulation of cytoplasmic and nuclear aggregates. Not only is there a loss of normal huntingtin function, upon expansion of the CAG repeat there is also a gain of toxic function of the huntingtin protein and this affects a wide range of cellular processes. To identify groups of genes that could play a role in the pathology of Huntingtons disease, we studied mRNA changes in an inducible PC12 model of Huntingtons disease before and after aggregates became visible. This is the first study to show the involvement Nrf2-responsive genes in the oxidative stress response in HD. Oxidative stress related transcripts were altered in expression suggesting a protective response in cells expressing mutant huntingtin at an early stage of cellular pathology. Furthermore, there was a down-regulation of catecholamine biosynthesis resulting in lower dopamine levels in culture. Our results further demonstrate an early impairment of transcription, the cytoskeleton, ion channels and receptors. Given the pathogenic impact of oxidative stress and neuroinflammation, the Nrf2-ARE signaling pathway is an attractive therapeutic target for neurodegenerative diseases.
Mutant huntingtin activates Nrf2-responsive genes and impairs dopamine synthesis in a PC12 model of Huntington's disease.
No sample metadata fields
View SamplesTo better understand the scale of gene expression changes that occur during the formation of mature adipocytes from preadipocytes, we compared and characterised the transcriptome profile of mesenchymal stromal cells derived from human adipose tissue, otherwise known as adipose-derived stromal cells (ASCs), undergoing adipocyte differentiation on day 1, 7, 14 and 21 (representing the early to late stage process of adipogenesis). Microarray technique was systematically employed to study gene expression in adipose-derived stromal cells during adipogenic differentiation over a 21 day period to identify genes that are important in driving adipogenesis in humans.
Genome-wide analysis of gene expression during adipogenesis in human adipose-derived stromal cells reveals novel patterns of gene expression during adipocyte differentiation.
Sex, Age, Specimen part, Subject
View SamplesmRNA used for the analysis of these microarrays were previously analyzed for 34 genes by reverse transcription - polymerase chain reaction in Desai BJ et al., J.Orthop.Trauma 17: 689-698, 2003. These two data sets were subsequently studied to compare the results from these two different methods for mRNA quantitation. The comparison was publised in "Comparison of mRNA gene expression by RT-PCR and DNA microarray" by W. Etienne, M.H. Meyer, J. Peppers, and R.A. Meyer, Jr., BioTechniques 36 (4): 618-626, April 2004.
Comparison of mRNA gene expression by RT-PCR and DNA microarray.
No sample metadata fields
View SamplesWe compared different mouse cancer cell lines to identify their unique cell signatures.
Mutant KRAS promotes malignant pleural effusion formation.
Specimen part, Cell line
View SamplesWe compared different mouse cancer cell lines to identify their unique cell signatures.
Mutant KRAS promotes malignant pleural effusion formation.
Specimen part, Cell line
View SamplesWe isolated mouse epithelial trachea cells from FVB mice in order to identify their transcriptomic signature.
Mutant KRAS promotes malignant pleural effusion formation.
Specimen part
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