This SuperSeries is composed of the SubSeries listed below.
Phf8 histone demethylase deficiency causes cognitive impairments through the mTOR pathway.
Age, Specimen part
View SamplesWe used microarrays to detail the global programme gene expression of Phf8 knock out and wild type mice
Phf8 histone demethylase deficiency causes cognitive impairments through the mTOR pathway.
Age, Specimen part
View SamplesEnvironmental cadmium, with a high average dietary intake, is a severe public health risk. However, the long-term health implications of environmental exposure to cadmium in different life stages remain unclear.
Sex-Dependent Effects of Cadmium Exposure in Early Life on Gut Microbiota and Fat Accumulation in Mice.
Sex, Specimen part
View SamplesThe CCAAT/enhancer-binding proteins (CEBPs) are transcription factors involved in hematopoietic cell development and induction of several inflammatory mediators. Here, we generated CEBP-beta (CEBPB) and CEBP-epsilon (CEBPE) double-knockout (bbee) mice and compared their phenotypes to those of single-deficient (bbEE and BBee) and wild-type (BBEE) mice.
In vivo deficiency of both C/EBPβ and C/EBPε results in highly defective myeloid differentiation and lack of cytokine response.
Sex, Specimen part, Treatment
View SamplesTo comprehensively reflect the impact of RPL11 deficiency on the transcriptome of zebrafish embryos, we collected 40–50 RPL11-deficient and MO control zebrafish embryos at 48 hpf from separate experiments and constructed two mRNA-seq sequencing libraries in parallel. High-throughput sequencing was performed on the Hi-Seq2000 sequencing platform in parallel. The number of sequenced gene transcript reads was 35–40 million. We found that hemoglobin biosynthetic and hematological defects in RPL11-deficient zebrafish were related to dysregulation of iron metabolism-related genes, including tfa, tfr1b, alas2 and slc25a37, which are involved in heme and hemoglobin biosynthesis. In addition, we found reduced expression of the hematopoietic stem cells (HSC) marker c-myb and HSC transcription factor tal1 and hoxb4a in RPL11-deficient zebrafish embryos, indicating that the hematopoietic defects may be related to impaired HSC differentiation and proliferation. However, RPL11 deficiency did not affect the development of other blood cell lineages such as granulocytes and myelocytes. Overall design: Compare 2 different transcriptomes of RPL11-deficient and MO control zebrafish embryos
Transcriptome analysis of Rpl11-deficient zebrafish model of Diamond-Blackfan Anemia.
No sample metadata fields
View SamplesThis SuperSeries is composed of the SubSeries listed below.
Zebrafish Pou5f1-dependent transcriptional networks in temporal control of early development.
No sample metadata fields
View SamplesZebrafish embryo were analyzed at 30 and 60 % epiboly for changes in transcriptome of wild-type and MTspg mutant embryos
Zebrafish Pou5f1-dependent transcriptional networks in temporal control of early development.
No sample metadata fields
View SamplesIn this study, we generated a zebrafish model of DBA with RPL5 morphants and implemented high-throughput RNA-seq and miRNA-seq to identify key genes, lncRNAs, and miRNAs during zebrafish development and hematopoiesis. We found that RPL5 is required for both primitive and definitive hematopoiesis processes that are partially mediated by the P53 pathway. Several genes such as cirh1a, noc2l, tars, and nol6 and miRNAs such as dre-miR-10a*, dre-miR-722, dre-miR-737, and dre-miR-142a-3p were significantly deregulated, and these changes may play a crucial role in hematopoiesis, ribosome biogenesis and development process. We also characterized the lncRNome in zebrafish with RPL5 deficiency. By constructing a comprehensive regulatory network, we identified central node genes in the network connected to the P53 pathway, almost all of which were targeted by the significantly deregulated miRNAs listed above. Our results therefore establish a regulatory network for critical genes and miRNAs involved in the RPL5-deficient zebrafish model and provide a comprehensive basis for the molecular pathogenesis of RPL5-mediated DBA and other ribosomopathies. Overall design: Determine the differences of transcriptome between RPL5-deficient and MO control zebrafish embryos for understanding the complex molecular pathogenesis of mutant RPL5-mediated human diseases
Transcriptome analysis reveals a ribosome constituents disorder involved in the RPL5 downregulated zebrafish model of Diamond-Blackfan anemia.
No sample metadata fields
View SamplesWe present a robust serum-free system for the rapid and efficient reprogramming of mouse somatic cells by Oct4, Sox2 and Klf4. The elimination of fetal bovine serum and oncogene c-Myc allowed reprogramming cells to be detected as early as Day 2 and reached greater than 10% of the population at Day 7 post retroviral transduction. The resulting iPS colonies were isolated with high efficiency to establish pluripotent cell lines. Based on this method, we further developed iPS-SF1 as a dedicated reprogramming medium for chemical screening and mechanistic investigations.
Towards an optimized culture medium for the generation of mouse induced pluripotent stem cells.
Specimen part
View SamplesObjective Previous studies showed that genetic deletion or pharmacological blockade of the Receptor for Advanced Glycation Endproducts (RAGE) prevents the early structural changes in the glomerulus associated with diabetic nephropathy (DN). To overcome limitations of mouse models that lack the progressive glomerulosclerosis observed in humans, we studied the contribution of RAGE to DN in the OVE26 type 1 mouse, a model of progressive glomerulosclerosis and decline of renal function.
Deletion of the receptor for advanced glycation end products reduces glomerulosclerosis and preserves renal function in the diabetic OVE26 mouse.
Sex, Age, Specimen part, Disease, Disease stage
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