This SuperSeries is composed of the SubSeries listed below.
Identification of putative TAL effector targets of the citrus canker pathogens shows functional convergence underlying disease development and defense response.
Age, Specimen part, Time
View SamplesMicroarray analyses of sweet orange epicotyls transiently transfected with the pthA2, pthA4 or pthC1 gene, relative to epicotyls transfected with the uid gene (GUS)
Identification of putative TAL effector targets of the citrus canker pathogens shows functional convergence underlying disease development and defense response.
Age, Specimen part, Time
View SamplesMicroarray analyses of sweet orange leaves infiltrated with Xc in the presence or absence of Ch, or Ch alone
Identification of putative TAL effector targets of the citrus canker pathogens shows functional convergence underlying disease development and defense response.
Specimen part, Time
View SamplesThis SuperSeries is composed of the SubSeries listed below.
DIDO as a Switchboard that Regulates Self-Renewal and Differentiation in Embryonic Stem Cells.
Specimen part
View SamplesExperimental in vtiro approach to molecular pathways implicated in Apert Syndromes craniosynostosis through transcriptomics techniques. FGFR2 activation requires a tridimensional configuration between ligand, receptor and heparan sulfate(HS). Mutations in the extracellular region of this receptor affect the balance between proliferation and differentiation of osteoprogenitor cells, leading to craniosynostosis as Apert Syndrome (AS). We postulate that the degradation of HS in periosteal tissue in patients with AS can modify the gene expression profile and modulate cell behavior. Based on previous evidence we propose that the treatment with an enzyme that degrades HS, as Idursulfase, in periosteal tissue of patients with AS, could be affect the formation of the ternary complex (FGF / FGFR / HS), triggering changes in gene profiles expression in several molecular pathways, regarding their basal state with the mutated receptor.
No associated publication
Sex, Specimen part, Disease
View SamplesResistance to chemotherapy is one of the most relevant aspects of treatment failure in cancer. Cell lines are used as models to study resistance. We analyze the transcriptional profile of two multidrug resistant (MDR) cell lines (Lucena 1 and FEPS) derived from the same drug-sensitive cell K562. Microarray data identified 130 differentially expressed genes (DEG) between K562 vs Lucena, 1,932 between K562 vs FEPS, and 1,211 between Lucena 1 versus FEPS. The NOTCH pathway was affected in FEPS with overexpression of NOTCH2 and HEY1. The highly overexpressed gene in MDR cell was ABCB1, and both presented the ABCB1 promoter unmethylated.
No associated publication
Cell line
View SamplesTransition from symmetric to asymmetric cell division requires precise coordination of differential gene expression. Embryonic stem cells (ESC) strongly express Dido3, whose C-terminal truncation impedes ESC differentiation while retaining self-renewal. We show that Dido3 binds to its gene locus via H3K4me3 and RNA pol II and, at differentiation onset, induces expression of its splice variant Dido1, which then leads to Dido3 degradation and downregulation of stemness genes. We propose that Dido isoforms act as a switchboard to regulate genetic programs for ESC transition from pluripotency maintenance to promotion of differentiation.
DIDO as a Switchboard that Regulates Self-Renewal and Differentiation in Embryonic Stem Cells.
Specimen part
View SamplesThis SuperSeries is composed of the SubSeries listed below.
No associated publication
Sex, Specimen part, Cell line, Subject
View SamplesHuman alveolar epithelial cells were exposed to cigarette smoke extract (CSE) for 1, 3 and 5 weeks at 1%, 5% and 10%, and gene expression was evaluated by complete transcriptome microarrays.
Cigarette Smoke Enhances the Expression of Profibrotic Molecules in Alveolar Epithelial Cells.
Cell line, Time
View SamplesSeveral copy number altered regions (CNA) have been identified in the genome of cervical cancer, especially amplifications of 3q and 5p. However, the contribution of those alterations to cervical carcinogenesis is still a matter of debate, since genome-wide, there is a lack of correlation between CNAs and gene expression. In this study, we investigated whether the CNAs in cell lines (CaLo, CasKi, HeLa, SiHa), at a gene-by-gene level, are related to changes in gene expression. On average 19.2% of the whole genome of cell lines had CNA. However, only 2.4% consisted of minimal recurrent regions (MRR), common to all cell lines. Whereas 3q had just some sparse common gains (13%), 5p was entirely duplicated recurrently. Genome-wide, only 11% of genes located in CNAs changed gene expression. In contrast, the rate increased over 3 fold times in MRRs. Chr 5p was confirmed entirely amplified by FISH. In spite of this, at most 32.9% of the explored genes in 5p (n=202) were de-regulated. In 3q, the rate was just 11.8%. Even in 3q26, which had five MRRs and 38.7% of SNPs was gained recurrently, the rate rose slightly to 13.6% (10 out of 73). Interestingly, up to 16% of de-regulated genes in 5p and 80% in 3q26 were down-regulated, suggesting additional factors are involved in gene repression. The de-regulated genes in 3q and 5p were found in clusters, suggesting local chromatin factors may also influence gene expression. In regions amplified discontinuously, the rate of down-regulated genes rose steadily as the number of amplified SNPs increased (p<0.01, Spearman's correlation). This suggests partial gene amplification as a mechanism of silencing gene expression. Additional genes were identified up- or down-regulated in 5p and 3q, which could be involved in cervical carcinogenesis, especially implicated in apoptosis. Those include CLPTM1L, AHRR, PDCD6 and DAP in 5p and TNFSF10 and ECT2 in 3q. Overall, the gene expression and copy number profiles suggest other factors, like epigenetic or chromatin domains, may influence gene expression within the entirely amplified genome segments. Further studies are needed to elucidate how these mechanisms regulate gene expression.
No associated publication
Sex, Cell line
View Samples