The goal of this study is to identify, in the head of adult flies, mRNA species whose expresson level are altered by overexpression of the Drosophila RNA-binding protein LARK in CNS neurons.
The LARK RNA-binding protein selectively regulates the circadian eclosion rhythm by controlling E74 protein expression.
No sample metadata fields
View SamplesCircadian behaviors are regulated by intrinsic biological clocks consisting of central molecular oscillators and output pathways. Despite significant progress in elucidating the central timekeeping mechanisms, the molecular pathways coupling the circadian pacemaker to overt rhythmic behavior and physiology remain elusive. The Drosophila LARK RNA-binding protein is a candidate for such a coupling factor. Previous research indicates that LARK functions downstream of the clock to mediate behavioral outputs. To better understand the roles of LARK in the Drosophila circadian system, we sought to identify RNA molecules associated with LARK in vivo, using a novel strategy that involves capturing the RNA ligands by immunoprecipitation, visualizing the captured RNAs using whole gene microarrays, and identifying functionally relevant targets through genetic screens.
The LARK RNA-binding protein selectively regulates the circadian eclosion rhythm by controlling E74 protein expression.
No sample metadata fields
View SamplesLittle is known about the pan-microvascular transcriptome, particularly considering gene transcripts and their encoded proteins that can be considered as vascular-selective in their expression.
Identification of a core set of 58 gene transcripts with broad and specific expression in the microvasculature.
No sample metadata fields
View SamplesThis SuperSeries is composed of the SubSeries listed below.
Oncogenic NRAS signaling differentially regulates survival and proliferation in melanoma.
Specimen part, Treatment
View SamplesSince direct pharmacological inhibition of RAS has thus far been unsuccessful, we explored system biology approaches to identify synergistic drug combination(s) that can mimic direct RAS inhibition. Leveraging an inducible mouse model of NRAS-mutant melanoma, we compare pharmacological MEK inhibition to complete NRAS-Q61K extinction in vivo. NRAS-Q61K extinction leads to a complete and durable tumor regression by enhancing both apoptosis and cell cycle arrest. By contrast, MEK inhibition only produces tumor stasis at best and we find that it robustly activates apoptosis but does not significantly impede proliferation.
Oncogenic NRAS signaling differentially regulates survival and proliferation in melanoma.
Specimen part
View SamplesWe sought to understand the pathways involved in NRAS extinction over time using a doxycycline-dependent, inducible mouse model of melanoma. This data provides insights into the temporal dynamics of downstream NRAS signaling and helps to correlate differentially affected pathways.
Oncogenic NRAS signaling differentially regulates survival and proliferation in melanoma.
Specimen part, Treatment
View SamplesThis SuperSeries is composed of the SubSeries listed below.
CALR mutational status identifies different disease subtypes of essential thrombocythemia showing distinct expression profiles.
Sex, Specimen part, Disease
View SamplesPolycythemia vera (PV) and essential thrombocythemia (ET) are Philadelphia-negative myeloproliferative neoplasms (MPNs) characterized by erythrocytosis and thrombocytosis, respectively. Approximately 95% of PV and 5070% of ET patients harbour the V617F mutation in the exon 14 of JAK2 gene, while about 20-30% of ET patients carry CALRins5 or CALRdel52 mutations. These ET CARL-mutated subjects show higher platelet count and lower thrombotic risk compared to JAK2-mutated patients. Here we showed that CALR-mutated and JAK2V617F-positive CD34+ cells have different gene and miRNA expression profiles. Indeed, we highlighted several pathways differentially activated between JAK2V617F- and CALR-mutated progenitors, i.e. mTOR, MAPK/PI3K and MYC pathways. Furthermore, we unveiled that the expression of several genes involved in DNA repair, chromatin remodelling, splicing and chromatid cohesion are decreased in CALR-mutated cells. According to the low risk of thrombosis in CALR-mutated patients, we also found the down-regulation of several genes involved in thrombin signalling and platelet activation. As a whole, these data support the model in which CALR-mutated ET could be considered as a distinct disease entity from JAK2V617F-positive MPNs and may provide the molecular basis supporting the different clinical features of these patients.
CALR mutational status identifies different disease subtypes of essential thrombocythemia showing distinct expression profiles.
Sex, Specimen part, Disease
View SamplesComparison of malic enzyme 3 (ME3) depleted vs non-depleted xenograft tumors. ME3 is an isoform of ME2. Overall design: Sub-cutaneous tumors of nude mice injected with PATU-ishME3 (shRNA against ME3) and treated +/- Dox to knockdown ME3. 4 tumors off-dox and 2 tumors on-dox
Genomic deletion of malic enzyme 2 confers collateral lethality in pancreatic cancer.
Specimen part, Cell line, Subject
View SamplesThe pathogenic mechanisms of common kidney glomerular diseases, including the vast majority of cases of proteinuria, remain unknown.
Glomerular transcriptome changes associated with lipopolysaccharide-induced proteinuria.
No sample metadata fields
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