Trimma okinawae
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ABSTRACT:
PROVIDER: PRJDB15183 | ENA |
REPOSITORIES: ENA
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Project description:PRDM16 is a 140 kDa transcriptional coregulatory protein. PRDM16 has been shown to function as a bi-directional switch in brown fat cell fate by stimulating the development of brown fat cells from myf-5 positive myoblastic precursors. We used microarrays to detail the global programme of gene expression underlying the myoblasts-brown fat conversion induced by PRDM16.
2009-07-31 | GSE15895 | GEO
Project description:Circadian rhythms are daily physiological and behavioral changes governed by an internal molecular clock, and dysfunctions in circadian rhythms have long been associated with various neurodegenerative diseases. Abnormal sleep-wake cycle often precedes the onset of cognitive and motor symptoms in patients, while the pathological changes may further exacerbate the disturbance in circadian cycle. It is unclear whether dysregulated circadian rhythm is a consequence of, or a contributing factor for, neurodegeneration. In addition, the evidence directly connecting the neurodegeneration-associated proteins to core circadian clock gene expression remains sparse. Here we show that FUS, a RNA-binding protein implicated in the pathogenesis of ALS and frontotemporal dementia, exhibits a bi-directional regulation with circadian rhythm. Our meta-analysis of RNAseq datasets and subsequent biochemical analysis revealed FUS as a gene regulated by circadian oscillation. Furthermore, NR1D1 binds the FUS promoter and regulates the amplitude of FUS oscillation. Meanwhile, FUS is recruited by transcriptional co-repressor PSF, and is found in the same complex as Bmal-Clock to repress Per2 expression. More strikingly, in cells and brain tissues from homozygous knock-in rats, the pathogenic R521C mutant FUS significantly alters the oscillation patterns of core circadian genes even at young age. Therefore, our results have revealed a novel bi-directional mechanism whereby dysregulated circadian clock and FUS expression may exacerbate neurodegeneration via mutual influence.
2017-04-12 | GSE77572 | GEO
Project description:PRDM16 is a 140 kDa transcriptional coregulatory protein. PRDM16 has been shown to function as a bi-directional switch in brown fat cell fate by stimulating the development of brown fat cells from myf-5 positive myoblastic precursors. We used microarrays to detail the global programme of gene expression underlying the myoblasts-brown fat conversion induced by PRDM16. undifferentiated C2C12 myoblasts were stably expressed with retroviral PRDM16 or vector control. Total RNAs were isolated by Trizol, and subjected to Affymetrix microarrays.
2010-03-03 | E-GEOD-15895 | biostudies-arrayexpress
Project description:Bi-directional interactions of omental adipocytes and SKOV3ip1 cells
| PRJNA986819 | ENA
Project description:Bi-sex male and female Schistosoma mansoni worms were isolated from mice 7-weeks post-infection. Bi-sex male material or female material was compared in a direct bimodal comparison to single-sex male or female material. Two independent biological batches of both bi- and single-sex males were used. One batch of single-sex female material was used in comparisons to three independent biological batches of bi-sex female material. A dye-swap hybridization was performed for each bimodal comparisons in turn.
2006-11-01 | E-MEXP-474 | biostudies-arrayexpress
Project description:To gain insights into the molecular mechanisms underpinning the reversible, bi-directional CD138- Pre-PC and CD138+ PC transition we subjected highly purified (>99%) Pre-PC - PC pairs from 9 patients to global mRNA expression profiling
2012-11-21 | E-MEXP-3772 | biostudies-arrayexpress
Project description:Directional selection in the domestication of fish species has resulted in rapid gains of growth, body size, and other production-relevant traits in relatively few generations. While there is clear evidence of genetic divergence contributing to selection-related phenotypic changes, emerging research suggests that intergenerational epigenetic inheritance may also be a relevant mechanism explaining rapid evolutionary change in domestic fish lines. Epigenetic changes have also been implicated in fish species’ responses to warming associated with climate change. Domestic lines of Brook Charr (Salvelinus fontinalis) are the primary source of fish used for recreational fisheries stocking in many parts of Eastern North America and there are concerns about how these fish will fare when stocked into lakes in the coming decades. We jointly investigated the effects of directional selection for performance traits (i.e., absence of early sexual maturation and increased growth) and exposure to elevated temperatures on DNA methylation in sperm cells of two experimental lines (hereafter: Selected and Control lines) of Brook Charr . We used whole-genome bisulfite sequencing to characterize DNA methylation at over 17 million methylated sites and identified 393 selection-related differentially methylated regions (DMR). The putative functions of genes in proximity to these DMRs are consistent with well-characterized phenotypic differences between the lines, including lipid metabolism and precocial maturation, and support the hypothesis that rapid evolution of traits may be partially mediated by epigenetic inheritance. We subsequently detected 85 warming-related DMRs in the Control line and 302 DMRs in the Selected line. None of these regions were shared between the two lines, indicating that the directional selection regime significantly altered the environmentally sensitive epigenetic landscape.
2024-03-11 | GSE227271 | GEO
Project description:To study bi-directional signaling between cancer-associated fibroblasts (CAFs) and cancer cells, we used stable isotope labeling by amino acids in cell culture (SILAC) to determine changes in tyrosine phosphorylation upon direct contact of the two cell types.
2020-05-26 | PXD003574 | Pride
Project description:Idiopathic pulmonary fibrosis (IPF) is the prototypic progressive fibrotic lung disease with a median survival of 2-4 years. Injury to and/or dysfunction of alveolar epithelium are strongly implicated in IPF disease initiation, but what factors determine why fibrosis progresses rather than normal tissue repair occurs remain poorly understood. We previously demonstrated that ZEB1-mediated epithelial-mesenchymal transition (EMT) in human alveolar epithelial type II (ATII) cells augments TGF-β-induced profibrogenic responses in underlying lung fibroblasts by paracrine signalling. Here we investigated bi-directional epithelial-mesenchymal crosstalk and its potential to drive fibrosis progression. RNA sequencing (RNA-seq) of lung fibroblasts exposed to conditioned media from ATII cells undergoing RAS-induced EMT identified many differentially expressed genes including those involved in cell migration and extracellular matrix (ECM) regulation. We confirmed that paracrine signalling between AS-activated ATII cells and fibroblasts augmented fibroblast recruitment and demonstrated that this involved a ZEB1-tissue plasminogen activator (tPA) axis. In a reciprocal fashion, paracrine signalling from TGF-β-activated lung fibroblasts or IPF fibroblasts induced RAS activation in ATII cells, at least partially via the secreted protein, SPARC. Together these data identify that aberrant bi-directional epithelial-mesenchymal crosstalk in IPF drives a chronic feedback loop that maintains a wound-healing phenotype and provides self-sustaining pro-fibrotic signals.
2021-08-19 | PXD025821 | Pride