Bdh2 morphants displayed mitochondrial dysfunction and degradation by autophagy, as well as hypohemoglobinization. Suppression of Atg7 expression in Bdh2 morphants diminished mitochondrial clearance and partly corrected their hemoglobinization defect.
Inactivation of 3-hydroxybutyrate dehydrogenase 2 delays zebrafish erythroid maturation by conferring premature mitophagy.
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View SamplesBdh2 morphants displayed mitochondrial dysfunction and degradation by autophagy, which could be restored by ectopic Bdh2 overexpression.
Inactivation of 3-hydroxybutyrate dehydrogenase 2 delays zebrafish erythroid maturation by conferring premature mitophagy.
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View SamplesRecently, we described a new animal model of CNS primitive neuroectodermal tumors (CNS-PNET), which was generated by orthotopic transplantation of human Radial Glial (RG) cells into NOD-SCID mice’s brain sub- ventricular zone. In the current study we conducted comprehensive RNA-Seq analyses to gain some insights on the mechanisms underlying tumorigenesis in this mouse model of CNS-PNET. Here we show that the RNA-Seq profiles derived from these tumors cluster with those reported for patients’ PNETs. Overall design: RNA-seq of tumors from central nervous system primitive neuroectodermal tumor (CNS PNET) animal model
Stabilization of HIF-1α and HIF-2α, up-regulation of MYCC and accumulation of stabilized p53 constitute hallmarks of CNS-PNET animal model.
Specimen part, Disease stage, Subject
View SamplesAnalysis of human glioblastoma multiforme tumors revealed genes that are upregulated in tumors expressing EGFRvIII compared to those expressing wild-type EGFR
Sprouty2 Drives Drug Resistance and Proliferation in Glioblastoma.
Specimen part
View SamplesAnalysis of rat tumor xenografts revealed genes that are upregulated in tumors expressing EGFRvIII
Sprouty2 Drives Drug Resistance and Proliferation in Glioblastoma.
Sex
View SamplesAdar1 is an essential gene for mouse embryonic development. Adar1 null mouse embryos dies around E11.5 because of massive apoptosis. Overall design: Small RNA: 4 samples examined: wild type E11.0, ADAR1 null E11.0, wild type E11.5, ADAR1 null E11.5, mRNA-seq: wild type E11.5, ADAR1 null E11.5.
ADAR1 forms a complex with Dicer to promote microRNA processing and RNA-induced gene silencing.
Specimen part, Cell line, Subject
View SamplesSmall RNA expression was analysed in total RNA of HeLa cells treated with siRNA toward Luciferase (negative cotrol) or ADAR1. Overall design: Small RNA: 2 samples examined: HeLa cell with siLuc (negative cotrol), with siADAR1
ADAR1 forms a complex with Dicer to promote microRNA processing and RNA-induced gene silencing.
Cell line, Subject
View SamplesCTCF (CCCTC-binding factor) is a highly conserved 11-zinc finger DNA binding protein with tens of thousands of binding sites genome-wide. CTCF acts as a multifunctional regulator of transcription, having been previously associated with activator, repressor, and insulator activity. These diverse regulatory functions are crucial for preimplantation development and are implicated in the regulation of numerous lineage-specific genes. Despite playing a critical role in developmental gene regulation, the mechanisms that underlie developmental changes in CTCF recruitment and function are poorly understood. Our previous work suggested that differences in CTCF’s binding site sequence may affect the regulation of CTCF recruitment, as well as CTCF’s regulatory function. To investigate these two possibilities directly during a developmental process, changes in genome-wide CTCF binding and gene expression were characterized during in vitro differentiation of mouse embryonic stem cells. CTCF binding sites were initially separated into three classes (named LowOc, MedOc, and HighOc) based on similarity to the consensus motif. The LowOc class, with lower-similarity to the consensus motif, is more likely to show changes in binding during differentiation. These more dynamically bound sites are enriched for motifs that confer a lower in vitro affinity for CTCF, suggesting a mechanism where sites with low-binding affinity are more amenable to developmental control. Additionally, by comparing changes in CTCF binding with changes in gene expression during differentiation, we show that LowOc and HighOc sites are associated with distinct regulatory functions. In sum, these results suggest that the regulatory control of CTCF’s binding and function is dependent in part upon specific motifs within its DNA binding site. Overall design: Mouse E14 ES cells were differentiated in vitro for 4.5 days using retinoic acid. RNA-Seq was performed from cells collected before and after differentiation.
CTCF binding site sequence differences are associated with unique regulatory and functional trends during embryonic stem cell differentiation.
Specimen part, Cell line, Subject
View SamplesThe majority of NK cells (~90%) are phenotypically characterized as CD56dimCD16+, while the remaining are CD56brightCD16-. The cytotoxic CD56dimCD16+ NK subset expresses higher levels of chemokine receptors, and therefore is preferentially recruited to sites of inflammation. Encounters between CD56dimCD16+ NK cells with target cells and locally secreted inflammatory cytokines synergize to induce activation of this subset, leading to dramatically increased cytotoxic activity against target cells and abundant pro-inflammatory cytokine production often equivalent to that of the CD56brightCD16- population. The early recruitment of activation of CD56dimCD16+ NK cells to sites of inflammation raises many important questions regarding the potential immune functions of these cells that extend beyond their cytotoxic capabilities. This study has sought to elucidate the genetic profile of activated CD56dimCD16+ NK cells via a series of laboratory-based approaches coupled with a bioinformatics persective.
Gene expression profiling of the human natural killer cell response to Fc receptor activation: unique enhancement in the presence of interleukin-12.
Specimen part, Subject
View SamplesUnlike ovarian cancer, normal ovarian epithelium response to TGFb1 induced growth inhibition. This time course study tried to idenify genes that showed changes after additionof TGFb1 in immortalized ovarian surface epithelial cells (IOSE) which is derived from normal ovarian epithelial cells
An integrative ChIP-chip and gene expression profiling to model SMAD regulatory modules.
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