This SuperSeries is composed of the SubSeries listed below.
X chromosome control of meiotic chromosome synapsis in mouse inter-subspecific hybrids.
Specimen part
View SamplesAccording to Dobzhansky-Muller model, hybrid sterility is a consequence of independent evolution of related taxa resulting in incompatible interaction during gametogenesis of their hybrids. We proposed that asynapsis of heterospecific chromosomes in meiotic prophase provides a general and recurrently evolving trigger for the meiotic arrest of interspecific F1 hybrids. We used genome-wide expression profiling to quantify misexpression of Chr X and Chr Y genes.
Mechanistic basis of infertility of mouse intersubspecific hybrids.
Age, Specimen part
View SamplesThis SuperSeries is composed of the SubSeries listed below.
Epigenetic regulations in the IFNγ signalling pathway: IFNγ-mediated MHC class I upregulation on tumour cells is associated with DNA demethylation of antigen-presenting machinery genes.
Specimen part, Cell line
View SamplesExpression profiling of isolated populations of prepachytene spermatocytes (LP), pachytene spermatocytes (RP) and spermatids (ST) from PWD and B6 was performed to study the genome wide variation in gene expression between two mouse subspecies. To evaluate the transcriptional difference between B6 and PWD in during meiosis, we compared their transcriptomes in sorted populations of pre-pachytene primary spermatocytes (Leptonema, Zygotene and Pachytene), pachytene spermatocytes (Mid-late pachytene and diplotene) and spermatids.
X chromosome control of meiotic chromosome synapsis in mouse inter-subspecific hybrids.
Specimen part
View SamplesReversible MHC class I deficiency on tumour cells is commonly caused by coordinated silencing of antigen-presenting machinery genes and restorable by IFN. Here we describe association of DNA demethylation of selected antigen-presenting machinery gene regulatory regions located in the MHC genomic locus (TAP-1, TAP-2, LMP-2, LMP-7) upon IFN treatment with MHC class I upregulation on tumour cells. Our novel findings demonstrate that IFN acts as an epigenetic modifier upregulating the expression of antigen-presenting machinery genes through DNA demethylation. Our data also cast more light on the role of DNA methylation in tumour cell escape from specific immunity.
Epigenetic regulations in the IFNγ signalling pathway: IFNγ-mediated MHC class I upregulation on tumour cells is associated with DNA demethylation of antigen-presenting machinery genes.
Specimen part, Cell line
View SamplesReversible MHC class I deficiency on tumour cells is commonly caused by coordinated silencing of antigen-presenting machinery genes and restorable by IFN. Here we describe association of DNA demethylation of selected antigen-presenting machinery gene regulatory regions located in the MHC genomic locus (TAP-1, TAP-2, LMP-2, LMP-7) upon IFN treatment with MHC class I upregulation on tumour cells. Our novel findings demonstrate that IFN acts as an epigenetic modifier upregulating the expression of antigen-presenting machinery genes through DNA demethylation. Our data also cast more light on the role of DNA methylation in tumour cell escape from specific immunity.
Epigenetic regulations in the IFNγ signalling pathway: IFNγ-mediated MHC class I upregulation on tumour cells is associated with DNA demethylation of antigen-presenting machinery genes.
Specimen part, Cell line
View SamplesReversible MHC class I deficiency on tumour cells is commonly caused by coordinated silencing of antigen-presenting machinery genes and restorable by IFN. Here we describe association of DNA demethylation of selected antigen-presenting machinery gene regulatory regions located in the MHC genomic locus (TAP-1, TAP-2, LMP-2, LMP-7) upon IFN treatment with MHC class I upregulation on tumour cells. Our novel findings demonstrate that IFN acts as an epigenetic modifier upregulating the expression of antigen-presenting machinery genes through DNA demethylation. Our data also cast more light on the role of DNA methylation in tumour cell escape from specific immunity.
Epigenetic regulations in the IFNγ signalling pathway: IFNγ-mediated MHC class I upregulation on tumour cells is associated with DNA demethylation of antigen-presenting machinery genes.
Specimen part, Cell line
View SamplesTVB-3166, an orally available, reversible, potent, and selective FASN inhibitors, was used to investigate FASN as a cancer therapeutic target. FASN inhibition with TVB-3166 induces apoptosis, inhibits anchorage-independent cell growth under lipid-rich conditions, and inhibits in vivo xenograft tumor growth.
Inhibition of de novo Palmitate Synthesis by Fatty Acid Synthase Induces Apoptosis in Tumor Cells by Remodeling Cell Membranes, Inhibiting Signaling Pathways, and Reprogramming Gene Expression.
Treatment
View SamplesDrosophila imaginal disc growth factors (IDGFs) comprise a small protein family of six members belonging to chitinase-like proteins (CLPs), which bind to, but do not cleave chitin or similar carbohydrates. IDGF2 is the prototypical member with known structure and reported to induce the proliferation of imaginal disc cells Cl.8+ in vitro. We characterized the effects of recombinant IDGF2 on tissue culture cells in vitro. We show that it is involved in cell protection from serum deprivation, as well as from the toxic effects of some xenobiotics and metabolites, when the cells are cultivated in serum-free medium conditions. Our results revealed that IDGF2 does not activate insulin pathway. Microarray-based gene expression analysis identified several IDGF2-dependent genes, including genes implicated in innate immune response, Wnt signaling and genes involved in the response to xenobiotics. Consistently, we observed that IDGF2 can be induced in vivo by aseptic or septic injury and high concentration of IDGF2 was detected in garland and pericardial nephrocytes. Our results suggest that IDGF2 is an important and abundant component of Drosophila hemolymph, which shows cytoprotective effects on insect cells in vitro and works as a modulator of multiple signaling pathways involved in morphogenesis, homeostasis and activation of innate immune response.
No associated publication
Specimen part, Cell line, Compound
View SamplesOocyte maturation is accompanied by a transition from mRNA stability to instability. We investigated the role of DCP1A and DCP2, proteins responsible for mRNA decapping, in mRNA destabilization during mouse oocyte maturation.
Maternally recruited DCP1A and DCP2 contribute to messenger RNA degradation during oocyte maturation and genome activation in mouse.
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