Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR28465210_1.fastq.gz | Fastqsanger.gz | |||
| SRR28465210_2.fastq.gz | Fastqsanger.gz | |||
| SRR28465211_1.fastq.gz | Fastqsanger.gz | |||
| SRR28465211_2.fastq.gz | Fastqsanger.gz | |||
| SRR28465212_1.fastq.gz | Fastqsanger.gz |
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Similar Datasets
Project description:ChIP microarrays were used to investigate whether dibutylphthalate (DBP)-mediated repression of SF1-regulated genes was associated with changes in transcription factor binding to genes involved in DBP-induced testicular maldevelopment. The repressive effect of DBP on SF1 regulated gene expression in fetal testes correlates with inhibition of SF1 binding to steroidogenic gene promoters.
2013-02-28 | GSE39225 | GEO
Project description:D-site binding protein, DBP, is a clock-controlled transcription factor and drives daily rhythms of physiological processes through the regulation of an array of genes harboring a DNA binding motif, D-box. DBP protein levels show a circadian oscillation with an extremely robust peak/trough ratio, but how the temporal pattern is regulated by post-translational regulation is unclear. In this study, we found that DBP protein levels are down-regulated by the ubiquitin-proteasome pathway. We screened 19 dominant-negative forms of E2 enzymes and found that UBE2G1 and UBE2T mediate the degradation of DBP. A proteomic analysis of DBP-interacting proteins and database screening identified Tumor necrosis factor Receptor-Associated Factor 7 (TRAF7), a RING-type E3 ligase, that forms a complex with UBE2G1 and/or UBE2T. Overexpression of TRAF7 down-regulated DBP protein level, while knockdown of TRAF7 up-regulated DBP in cultured cells. Knockout of TRAF7 in NIH3T3 cells revealed that TRAF7 mediates the time-of-the-day-dependent regulation of DBP levels. Furthermore, TRAF7 has a period-shortening effect on the cellular clock. Together, TRAF7 plays an important role in circadian clock oscillation through destabilization of DBP.
2024-08-28 | PXD051884 | Pride
Project description:The spatial organization of genes in the interphase nucleus plays an important role in establishment and regulation of gene expression. The circadian expressed and clock controlled genes represent about 10% of the transcripts in the mammalian cells, however the role of genome topology in the expression of genes in a circadian manner remains to be elucidated. In this study we investigated the characteristics and dynamics of the genomic loci that contact the clock controlled gene Dbp during the circadian cycle. To do so, we combined genome-wide interaction profiling by chromosome conformation capture-on-chip (4C) technology with analyses of circadian gene expression in synchronized mouse embryonic fibroblasts (MEFs). This approach allowed us to elucidate the three-dimensional organization of the genome during the circadian cycle around the clock controlled gene Dbp, paralleling its circadian expression. We found that the Dbp genomic environment remains largely similar during the circadian cycle. However, specific DNA regions change their frequency of interaction with Dbp as the circadian cycle progresses, delineating a Dbp circadian interactome. These specific changes are not present in Bmal1-/- MEF, suggesting that the clock machinery is implicated in shaping the genomic landscape around the Dbp locus. The Dbp interactome is enriched in DNA elements related to the clock system (E boxes). We found a spatial clustering of functionally related genes. The Dbp circadian interactome contains a subset of circadian genes whose expression closely parallels that for Dbp. Taken together, our results indicate that the Dbp subnuclear environment is organized to privilege the clock directed gene expression program.
2013-08-08 | GSE49582 | GEO
Project description:Endocrine disruptors, such as phthalates, are suspected of affecting reproductive function. The Mesalamine and Reproductive Health Study (MARS) was designed to address the physiological effect of in-vivo phthalate exposure on male reproduction in patients with Inflammatory Bowel Disease (IBD). As part of this effort, sperm RNA profiles as an effect of exposure to DBP were longitudinally assessed using a cross-over cross-back design of binary, high or background, levels of DBP. As the DBP level was altered, numerous sperm RNA elements were differentially expressed, and suggest that exposure to or removal from high DBP produces effects that require longer than one spermatogenic cycle to resolve. In comparison, small RNAs are minimally affected by DBP exposure. While initial study medication (high or background) implicates different biological pathways, initiation on the high-DBP condition activated oxidative stress and DNA damage pathways. Using ejaculated sperm, this work provides insight into the male germline’s response to phthalate exposure.
2019-09-06 | GSE129216 | GEO
Project description:Chronic renal failure (CRF) is associated with a decrease in drug metabolism. The present study investigated the repercussions of CRF on liver cytochrome P450 (CYPs), but the mechanisms have been little explored. On the other hand, the expression of several CYP genes exhibits circadian rhythm. Here we report that downregulation of hepatic CYP3A11 (the murine homolog to human CYP3A4; the most decrease in 5/6Nx using microarray analysis) by suppressing the expression of clock gene; D-site binding protein (DBP). In vivo experiments, the mRNA levels of hepatic CYP3A11 exhibit circadian rhythm regulated by DBP and E4BP4, and significantly decreased in 5/6Nx. Microarray analysis revealed that the general transcription factors of CYP3A11 did not changed. However, DBP were downregulated and several CYP genes controlled by DBP also significantly decreased in 5/6Nx. These downregulations were not observed in angiotensin II type 1alpha receptor (AT II R1a) deficient 5/6Nx because serum TGF-beta was not upregulate. In vitro experiments, the RNA levels of CYP3A11 and DBP were downregulated in wild-type mouse hepatocytes incubated with serum from 5/6Nx, but did not changed in Id2 (-/-) hepatocytes. In fact, hepatic Id2 was upregulated and caused the downregulation of DBP in 5/6Nx. Hepatocyte treated with SD208 (TGF-beta receptor 1 selectivity inhibitor) recovered CYP3A11, DBP and Id2 to control levels. Furthermore, 5/6Nx treated with tranilast (inhibitor of TGF-beta production or isolation) or candesartan (ARBs) also recovered CYP3A11 levels. Our findings define that DBP has effects on downregulation of CYP3A11. In CRF conditions, TGF-beta is upregulated by angiotensin II receptor in renal and downregulates DBP and CYP3A11 levels mediated by Id2 in liver. Furthermore, downregulation of CYP3A11 can prevent by tranilast or candesartan.
2013-08-01 | GSE35135 | GEO
Project description:ChIP microarrays were used to investigate whether dibutylphthalate (DBP)-mediated repression of SF1-regulated genes was associated with changes in transcription factor binding to genes involved in DBP-induced testicular maldevelopment. The repressive effect of DBP on SF1 regulated gene expression in fetal testes correlates with inhibition of SF1 binding to steroidogenic gene promoters. Comparison of control- and DBP- in utero 500mg/Kg treated fetal rat testes
2013-02-28 | E-GEOD-39225 | biostudies-arrayexpress
Project description:This study investigates the effects of dibutyl phthalate (DBP)—a plasticizer commonly detected in surface waters worldwide—on zebrafish (Danio rerio) embryos exposed to a concentration gradient from 0 to 120 hours post-fertilization (’protuding mouth’ stage). The primary objective was to assess the utility of integrating concentration gradients into transcriptomic analyses to uncover the mechanisms of action of environmental contaminants, such as DBP. Using this experimental design, dose-response modelling was applied to estimate the sensitivity and shape of transcriptomic responses across the DBP gradient. Following optimized over-representation analysis, we revealed that the retinoid signaling pathway may be the most sensitive pathway affected by DBP during zebrafish development, potentially leading to significant morphological changes.
2024-12-18 | GSE283957 | GEO
Project description:Despite the involvement of several serine hydrolases (SHs) in the metabolism of xenobiotics such as dibutyl phthalate (DBP), no study has focused on mapping this enzyme class in zebrafish, a model organism frequently used in ecotoxicology. Here, we survey and identify active SHs in zebrafish larvae and search for biological markers of SH type after exposition to DBP. Zebrafish were exposed to 0, 5, and 100 µg/L DBP from 4 to 120 h post-fertilization. A significant decrease in vitellogenin expression level of about 2-fold compared to the control was found in larvae exposed to 100 µg/L DBP for 120h. The first comprehensive profiling of active SHs in zebrafish proteome was achieved with an activity-based protein profiling (ABPP) approach. Among 49 SHs identified with high confidence, one was the carboxypeptidase ctsa overexpressed in larvae exposed to 100 µg/L DBP for 120h. To the best of our knowledge, this is the first time that a carboxypeptidase has been identified as deregulated following exposure to DBP. The overall results indicate that targeted proteomics approaches such as ABPP can therefore be an asset for understanding the mechanism of action related to xenobiotics in ecotoxicology.
2023-03-11 | PXD038229 | Pride
Project description:Dibutyl phthalate (DBP) and diisobutyl phthalate (DiBP) have been reported to exhibit reproductive toxicity and may pose a threat to their offspring. However, the combined effect of DBP and DiBP on offspring remains unclear, especially for aquatic organisms. The aims of this study were to assess the effects of parental combined exposure to DBP and DiBP on early development of zebrafish offspring, and to explore the potential molecular mechanisms involved. The early developmental indicators and transcriptomic profiles of F1 larvae were examined after parental exposure to DBP, DiBP and their mixtures (Mix) for 30 days. Results showed that parental exposure to DBP and DiBP, alone or in combination, resulted in increasing hatchability at 48 hpf and heart rate at 96 hpf, and affected the malformation and mortality in F1 larvae. Generalized linear model (GLM) indicated that the interactive effects between DBP and DiBP on the mortality and malformation of F1 larvae was antagonistic. The transcriptomic analysis predicted that the molecular mechanisms of parental combined exposure were different from those of either chemical alone, disruption of the molecular function involving unfolded protein binding, E-box binding and photoreceptor activity in F1 larvae could be the mechanism of action after parental combined exposure.
2020-12-29 | GSE147715 | GEO