Purpose: Investigate the molecular determinants of retinal regeneration in adult vertebrates by analyzing the gene expression profiles of control and post-lesion retina of adult zebrafish, a system that regenerates following injury.
Gene expression profiles of intact and regenerating zebrafish retina.
No sample metadata fields
View SamplesTissues from the eye primordia, lateral endoderm, and posterior
Generation of functional eyes from pluripotent cells.
No sample metadata fields
View SamplesTo understand the role of MiT in Drosophila, we set out to identify critical gene targets by looking at changes in the WT transcriptome induced by either gain or loss of MiT function. Mutant hindgut and malpighian tubules provided loss-of function tissue and nub-Gal4-driven expression of MiT in the wing epithelium was used for gain-of-function. In the wing disc experiment, 543 genes were upregulated by exogenous MiT, and 359 genes were downregulated (>1.4 fold; P value < 0.01). In the larval HG+MT, 897 genes were downregulated and 898 were upregulated (>1.4 fold; P value < 0.01) after MiT. Among these genes, 85 were both upregulated in wing discs and downregulated in mutant HG+MT, and are the common genes that regulated by MiT in both tissues.
Mitf is a master regulator of the v-ATPase, forming a control module for cellular homeostasis with v-ATPase and TORC1.
Specimen part
View SamplesThis SuperSeries is composed of the SubSeries listed below.
Loss of Ezh2 cooperates with Jak2V617F in the development of myelofibrosis in a mouse model of myeloproliferative neoplasm.
Specimen part
View SamplesInactivating EZH2 mutations have been associated with myelofibrosis (MF). Moreover, EZH2 mutations co-exist with the JAK2V617F mutation in a significant cases of MF. To determine the effects of concomitant loss of EZH2 and JAK2V617F mutation in hematopoiesis, we generated Ezh2-deficient Jak2V617F-expressing mice. To gain insights into the mechanisms by which Ezh2 deficiency promotes the development of MF in Jak2V617F knock-in mice, we performed microarray gene expression analysis on sorted LT-HSC from control, MxCre;Jak2VF/+ and MxCre;Jak2VF/+ EZH2-/- mice.
Loss of Ezh2 cooperates with Jak2V617F in the development of myelofibrosis in a mouse model of myeloproliferative neoplasm.
Specimen part
View SamplesXenopus laevis embryos were injected with mRNA for EFTFs at 2-cell stage. Animal caps collected at stage 9, cultured to the equivalent of stage 15 and RNA extracted. Four biological replicates of the EFTF-injected and GFP-injected (control) caps were used to profile transcript expression patterns using Affymetrix Xenopus Laevis GeneChip microarrays.
Generation of functional eyes from pluripotent cells.
No sample metadata fields
View SamplesThis SuperSeries is composed of the SubSeries listed below.
Effects of Acute Prenatal Exposure to Ethanol on microRNA Expression are Ameliorated by Social Enrichment.
Sex
View SamplesIn this study, we tested if miRNAs are altered in amygdala and ventral striatum as a consequence of prenatal ethanol exposure and/or social enrichment. miRNA samples from 72 male and female adolescent rats were analyzed by RNA-Seq analysis and Affymetrix miRNA arrays. Several miRNAs showed significant changes due to prenatal ethanol exposure or social enrichment in one or both brain regions. Some of the miRNA changes caused by ethanol were reversed by social enrichment. The top predicted gene targets of these miRNAs were mapped and subjected to pathway enrichment analysis. We also directly examined the evidence for modulation of target mRNAs in whole transcriptome microarray data from the same rats. Among the pathways most strongly affected were p53, CREB, Glutamate and GABA signaling. Together, our data suggest a number of novel epigenetic mechanisms for social enrichment to reverse the effects of ethanol exposure.
Effects of Acute Prenatal Exposure to Ethanol on microRNA Expression are Ameliorated by Social Enrichment.
Sex
View SamplesTranscriptional analysis of multiple brain regions in Parkinson's disease supports the involvement of specific protein processing, energy metabolism, and signaling pathways, and suggests novel disease mechanisms.
Transcriptional analysis of multiple brain regions in Parkinson's disease supports the involvement of specific protein processing, energy metabolism, and signaling pathways, and suggests novel disease mechanisms.
Sex, Age, Disease, Disease stage
View SamplesPost mortem tissue was dissected from two groups of age and gender matched groups of Parkinson and Control subjects
Transcriptional analysis of multiple brain regions in Parkinson's disease supports the involvement of specific protein processing, energy metabolism, and signaling pathways, and suggests novel disease mechanisms.
Sex, Age, Disease, Disease stage
View Samples