The study of the compond PIP-RBPJ-1 function on neural stem cell. Synthetic DNA-binding inhibitors capable of gaining precise control over neurogenesis factors could obviate the current clinical barriers associated with small molecule use in regenerative medicine. Here, we show the design and bio-efficacy of a synthetic ligand PIP-RBPJ-1 to cause promoter-specific suppression of neurogenesis-associated HES1, and its downstream genes. Furthermore, PIP-RBPJ-1 alone could alter the neural system-associated notch signaling factors and remarkably induce neurogenesis with an efficiency that is comparable to a conventional approach. Here is one day treatment of the PIP-RBPJ-1 on neural stem cells.
No associated publication
Specimen part
View SamplesGene expression patterns in the brain are strongly influenced by the severity of physiological stress at death. This agonal effect, if not well controlled, can lead to spurious findings in case-control comparisons. While many recent studies match samples by tissue pH and clinically recorded agonal conditions, we found that these commonly used indicators were sometimes at odds with observed stress-related patterns of gene expression, and that matching by these criteria still sometimes results in identifying differences between cases and controls that are primarily driven by residual agonal effects. This problem is analogous to the one in genetic studies, where race and ethnicity are often imprecise proxies for complex environmental and genetic factors.
Sample matching by inferred agonal stress in gene expression analyses of the brain.
Subject
View SamplesThis data was used to determine levels of BRCA1 and BRCA2 in primary human leukemia samples. Samples were determined to be high BRCA1 and/or BRCA2 or low BRCA1 and/or BRAC2.
Personalized synthetic lethality induced by targeting RAD52 in leukemias identified by gene mutation and expression profile.
No sample metadata fields
View SamplesThe present study was constructed to confirm previous findings that mice on a high fat diet (HFD) treated by subcutaneous injection with exenatide (EXE) at 3g/kg once daily for 6 weeks develop exocrine pancreatic injury (Rouse et al. 2014). The present study included 12 weeks of EXE exposure at multiple concentrations (3, 10, or 30 g/kg) with multiple endpoints (histopathology evaluations, immunoassay for cytokines, immunostaining of the pancreas, serum chemistries and measurement of trypsin, amylase, and, lipase, and gene expression profiles). Time- and dose-dependent exocrine pancreatic injury was observed in mice associated with EXE exposure in a HFD environment. The time- and dose-dependent morphological changes identified in the pancreas involved acinar cell injury and death (autophagy, apoptosis, necrosis, and atrophy), cell adaptations (hypertrophy and hyperplasia), and cell survival (regeneration) accompanied with varying degrees of inflammatory response leading to secondary injury in pancreatic blood vessels, ducts, and adipose tissues. Gene expression profiles supported the presence of increased signaling for cell survival and altered lipid metabolism. The potential for EXE to cause acute or early chronic pancreatic injury was identified in a HFD environment. In human disease, the influence of pancreatitis risk factors or pre-existing chronic pancreatitis on this injury potential requires further investigation.
Extended exenatide administration enhances lipid metabolism and exacerbates pancreatic injury in mice on a high fat, high carbohydrate diet.
Sex, Specimen part
View SamplesGene expression profile of LysMCre/Cre and KLF2/ primary peritoneal macrophages following 6 hours of LPS treatment.
The myeloid transcription factor KLF2 regulates the host response to polymicrobial infection and endotoxic shock.
Age, Specimen part
View SamplesSpecification of germ cell fate is fundamental in development. With a highly representative single-cell microarray and rigorous quantitative-PCR analysis, we defined the genome-wide transcription dynamics that create primordial germ cells (PGCs) from the epiblast, a process that exclusively segregates them from their somatic neighbors. We also analyzed the effect of the loss of Blimp1, a key transcriptional regulator, on these dynamics. Our analysis revealed that PGC specification involves complex, yet highly ordered regulation of a large number of genes, proceeding under the strong influence of mesoderm induction with active repression of specific programs such as epithelial-mesenchymal transition, Hox gene activation, cell-cycle progression and DNA methyltransferase machinery. Remarkably, Blimp1 is essential for repressing nearly all the genes normally down-regulated in PGCs relative to their somatic neighbors, whereas it is dispensable for the activation of approximately half of the genes up-regulated in PGCs.
Complex genome-wide transcription dynamics orchestrated by Blimp1 for the specification of the germ cell lineage in mice.
No sample metadata fields
View SamplesMany organisms acquired circadian clock system to adapt daily and seasonal environmental changes. Mammals have the master clock in the brains suprachiasmatic nucleus (SCN) that synchronizes other circadian clocks in the peripheral tissues or organs. Plants also have circadian clock in their bodies, but the presence of the tissue-specific functions of circadian clock is remained elusive. The aim of this experiment is to compare tissue-specific gene expression profile using gene expression Microarray.
Tissue-specific clocks in Arabidopsis show asymmetric coupling.
Specimen part, Time
View SamplesThis SuperSeries is composed of the SubSeries listed below.
Induction of mouse germ-cell fate by transcription factors in vitro.
Sex, Specimen part
View SamplesSpermatogonial stem cells (SSCs) have pluripotent potential. However, frequency of pluripotent cell derivation is low and the mechanism of culture-induced reprogramming remains unknown. Here we report that epigenetic instability of germline stem (GS) cells, cultured SSCs, induces pluripotent cell derivation. GS cells undergo DNA demethylation in H19 differentially methylated region under low-density culture. When H19 demethylation was induced by Dnmt1 depletion, they converted into embryonic stem (ES)-like cells. Dnmt1 depletion downregulated Dmrt1 expression, whose depletion also induced pluripotency. Functional screening of Dmrt1 target gene revealed that Dmrt1 depletion upregulates Sox2, the key molecule responsible for generating induced pluripotent stem cells. Although Sox2 transfection upregulated Oct4 and produced pluripotent cells, this conversion was inhibited by Oct1 overexpression, suggesting that the balance of Oct proteins maintains SSC identity. These results suggest that culture-induced reprogramming is caused by unstable DNA methylation, and that Dmrt1-Sox2 cascade is critical for regulating pluripotency in SSCs.
Regulation of pluripotency in male germline stem cells by Dmrt1.
Specimen part, Treatment
View SamplesThis SuperSeries is composed of the SubSeries listed below.
Identification of MMP1 as a novel risk factor for intracranial aneurysms in ADPKD using iPSC models.
Sex, Specimen part, Disease stage, Subject
View Samples