The study compares gene expression profile at 20 days post amputation of the zebrafish ventricular heart between dusp6 mutant and WT siblings. Overall design: Ventricular resection was performed and 20 dpa, hearts were extracted.
Dusp6 attenuates Ras/MAPK signaling to limit zebrafish heart regeneration.
No sample metadata fields
View SamplesPTBA has been published to increase renal tubular cell proliferation, increased survival, and increased renal functional recovery in fish and various models of murine models of acute kidney injury. Immunohistological analyses suggested increased cell proliferation is accompanied by increased epithelial-to-mesenchymal transition in the RTECs. In order to elucidate pathways responsible for the increased repair response after compound treatment, larval zebrafish were given AKI and treated with PTBA analogue, UPHD25 or DMSO. Results suggests that epithelial-related genes were downregulated while mesenchymal-related genes were upregulated with injury and compound treatment. Results further validate our immunohistological finding that our compound increase post-AKI repair by increasing EMT in renal tubular cells. Overall design: At 3dpf, larval zebrafish are given acute kidney injury with gentamicin microinjection. 2 days post injury, larvae with AKI are selected and treated with 1uM of PTBA analogue, UPHD25 or vehicle control, 1% DMSO. The fish were treated with UPHD25 or DMSO for 24 hours. Then, pronephric kidneys were collected using DDT, collagenase I, and manual collection. Total 100 larvae were collected per sample, per replicate. Each treatment group was repeated with 3 biological replicates. RNA was collected and sequenced.
Enhancing regeneration after acute kidney injury by promoting cellular dedifferentiation in zebrafish.
Specimen part, Treatment, Subject
View SamplesPlants exhibit a robust transcriptional response to gamma radiation which includes the induction of transcripts required for homologous recombination and the suppression of transcripts that promote cell cycle progression. Various DNA damaging agents induce different spectra of DNA damage as well as collateral damage to other cellular components and therefore are not expected to provoke identical responses by the cell.
High atomic weight, high-energy radiation (HZE) induces transcriptional responses shared with conventional stresses in addition to a core "DSB" response specific to clastogenic treatments.
Age, Time
View SamplesThis SuperSeries is composed of the SubSeries listed below.
Direct targets of the TRP63 transcription factor revealed by a combination of gene expression profiling and reverse engineering.
No sample metadata fields
View SamplesGenome-wide identification of bona fide targets of transcription factors in mammalian cells is still a challenge. We present a novel integrated computational and experimental approach to identify direct targets of a transcription factor. This consists in measuring time-course (dynamic) gene expression profiles upon perturbation of the transcription factor under study, and in applying a novel reverse-engineering algorithm (TSNI) to rank genes according to their probability of being direct targets. Using primary keratinocytes as a model system, we identified novel transcriptional target genes of Trp63, a crucial regulator of skin development. TSNI-predicted Trp63 target genes were validated by Trp63 knockdown and by ChIP-chip to identify Trp63-bound regions in vivo. Our study revealed that short sampling times, in the order of minutes, are needed to capture the dynamics of gene expression in mammalian cells. We show that Trp63 transiently regulates a subset of its direct targets, thus highlighting the importance of considering temporal dynamics when identifying transcriptional targets. Using this approach, we uncovered a previously unsuspected transient regulation of the AP-1 complex by Trp63, through direct regulation of a subset of AP-1 components. The integrated experimental and computational approach described here is readily applicable to other transcription factors in mammalian systems and is complementary to genome-wide identification of transcription factor binding sites.
Direct targets of the TRP63 transcription factor revealed by a combination of gene expression profiling and reverse engineering.
No sample metadata fields
View SamplesAnalysis of newborn mouse epidermis lacking the expression of Insulin receptor (IR) and Insulin like growth factor 1 receptor (IGF-1R). Results show that IR/IGF-1R signalling control epidermal morphogenesis.
Insulin/IGF-1 controls epidermal morphogenesis via regulation of FoxO-mediated p63 inhibition.
No sample metadata fields
View SamplesGenome-wide identification of bona fide targets of transcription factors in mammalian cells is still a challenge. We present a novel integrated computational and experimental approach to identify direct targets of a transcription factor. This consists in measuring time-course (dynamic) gene expression profiles upon perturbation of the transcription factor under study, and in applying a novel reverse-engineering algorithm (TSNI) to rank genes according to their probability of being direct targets. Using primary keratinocytes as a model system, we identified novel transcriptional target genes of Trp63, a crucial regulator of skin development. TSNI-predicted Trp63 target genes were validated by Trp63 knockdown and by ChIP-chip to identify Trp63-bound regions in vivo. Our study revealed that short sampling times, in the order of minutes, are needed to capture the dynamics of gene expression in mammalian cells. We show that Trp63 transiently regulates a subset of its direct targets, thus highlighting the importance of considering temporal dynamics when identifying transcriptional targets. Using this approach, we uncovered a previously unsuspected transient regulation of the AP-1 complex by Trp63, through direct regulation of a subset of AP-1 components. The integrated experimental and computational approach described here is readily applicable to other transcription factors in mammalian systems and is complementary to genome-wide identification of transcription factor binding sites.
Direct targets of the TRP63 transcription factor revealed by a combination of gene expression profiling and reverse engineering.
No sample metadata fields
View SamplesGenome-wide identification of bona fide targets of transcription factors in mammalian cells is still a challenge. We present a novel integrated computational and experimental approach to identify direct targets of a transcription factor. This consists in measuring time-course (dynamic) gene expression profiles upon perturbation of the transcription factor under study, and in applying a novel reverse-engineering algorithm (TSNI) to rank genes according to their probability of being direct targets. Using primary keratinocytes as a model system, we identified novel transcriptional target genes of Trp63, a crucial regulator of skin development. TSNI-predicted Trp63 target genes were validated by Trp63 knockdown and by ChIP-chip to identify Trp63-bound regions in vivo. Our study revealed that short sampling times, in the order of minutes, are needed to capture the dynamics of gene expression in mammalian cells. We show that Trp63 transiently regulates a subset of its direct targets, thus highlighting the importance of considering temporal dynamics when identifying transcriptional targets. Using this approach, we uncovered a previously unsuspected transient regulation of the AP-1 complex by Trp63, through direct regulation of a subset of AP-1 components. The integrated experimental and computational approach described here is readily applicable to other transcription factors in mammalian systems and is complementary to genome-wide identification of transcription factor binding sites.
Direct targets of the TRP63 transcription factor revealed by a combination of gene expression profiling and reverse engineering.
No sample metadata fields
View SamplesThe S. aureus transcriptome was assessed for strains Newman (wild type) and Newman (sarZ) during both exponential (2hr) and early stationary (5hr) cell growth.
A new oxidative sensing and regulation pathway mediated by the MgrA homologue SarZ in Staphylococcus aureus.
No sample metadata fields
View SamplesCutaneous malignant melanoma is among the most deadly human cancers, broadly resistant to most clinical therapies. A majority of patients with BRAFV600E melanomas respond well to inhibitors such as vemurafenib, but all ultimately relapse. Moreover, there are no viable treatment options available for other non-BRAF melanoma subtypes in the clinic. A key to improving treatment options lies in a better understanding of mechanisms underlying melanoma progression, which are complex and heterogeneous. In this study we perform gene expression profilling of highly and poorly malignant melanocytic tumors from genetically engineered mouse models to discover important drivers of cancer progression.
Integrated Genomics Identifies miR-32/MCL-1 Pathway as a Critical Driver of Melanomagenesis: Implications for miR-Replacement and Combination Therapy.
Specimen part
View Samples