Homo sapiens
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ABSTRACT:
PROVIDER: PRJNA114951 | ENA |
REPOSITORIES: ENA
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Project description:Microarray analysis has been applied to the cell proliferation in a human colonic cel line, Caco-2. We have shown previously that a moderate riboflavin depletion around weaning has a profound impact on the structure and function of the small intestine of the rat, which is not reversible following riboflavin repletion. In this study we have modelled riboflavin deficiency in a human cell line, shown irreversible loss of cell viability associated with impaired mitosis and identified candidate effectors of riboflavin depletion in the cell. The aim of the present study is to develop a cell culture model of riboflavin depletion and analyse its behaviour using a using a combination of cell biology approaches including microarray analysis. A human colonic cell line, Caco-2, was grown in culture and treated to riboflavin depletion. Treated and untreated cells were collected at appropriate time points and isolated RNA subjected to microarray analysis.
2009-03-06 | E-GEOD-15132 | biostudies-arrayexpress
Project description:Transcriptome analysis of RNA samples from riboflavin-depleted HEK293T cells. Riboflavin is an essential component of the human diet and its derivative cofactors have an established role in oxidative metabolism. Riboflavin deficiency has been linked with various human diseases. In this study, we have modelled riboflavin deficiency in HEK293T cell line, shown remarkable increase of cell proliferation. The aim of the present study is to develop a cell culture model of riboflavin depletion and analyze its molecular mechanism of acceleration cell proliferation. So, we used Affymetrix Human Transcriptome Array 2.0 to identify genes that were differentially expressed upon riboflavin-depleted HEK293T cells.
2017-05-16 | GSE98927 | GEO
Project description:Microarray analysis has been applied to the cell proliferation in a human colonic cel line, Caco-2. We have shown previously that a moderate riboflavin depletion around weaning has a profound impact on the structure and function of the small intestine of the rat, which is not reversible following riboflavin repletion. In this study we have modelled riboflavin deficiency in a human cell line, shown irreversible loss of cell viability associated with impaired mitosis and identified candidate effectors of riboflavin depletion in the cell. The aim of the present study is to develop a cell culture model of riboflavin depletion and analyse its behaviour using a using a combination of cell biology approaches including microarray analysis.
2009-03-06 | GSE15132 | GEO
Project description:Riboflavin depletion regulates cell proliferation and cell cycle progression‑associated genes in HEK293T cells
| PRJNA386885 | ENA
Project description:Our observation suggest that ADAR may play important role to maintain GSC stemness. In order to address this hypothesis, we abrogated the expression of ADAR in GSCs using two distinct short and non-overlapping shot hairpin RNAs (shRNAs). A non-targeting control shRNA (shCONT) is used as control in these experiments. Both shRNAs significantly reduced ADAR protein expression. Depletion of ADAR impaired GSCs proliferation but did not affect matched DGCs. Similarly, lack of ADAR reduces GSC self-renewal capacity as assessed by in vitro limiting dilution assay . In order to identify the antitumor mechanisms triggered by ADAR depletion, we performed global transcriptional profiling through RNA-sequencing in GSCs upon ADAR knockdown. These analyses show that ADAR downregulation impairs the impairs the expression of genes involved in cancer proliferation, particularly those involved in cell cycle regulation
2022-07-19 | GSE153270 | GEO
Project description:Riboflavin-derived molecules such as flavin mononucleotide and flavin adenine dinucleotide comprise the most important redox coenzymes all across life kingdoms. Vibrio cholerae, a pandemic diarrheagenic bacterium, is able to synthesize riboflavin through the riboflavin biosynthetic pathway (RBP) and to internalize exogenous riboflavin using the RibN importer. This bacterium thrives in different environments such as estuarine waters and the human intestinal tract. The presence of two independent riboflavin supply pathways in this species may be related to the variable riboflavin availability and requirements across different niches. In order to gain insights into the role of the riboflavin provision pathways in the physiology of V. cholerae, we analyzed the bacterial transcriptomics response to extracellular riboflavin and to the deletions of ribD (RBP-deficient strain) or ribN. Notably, many genes responding to riboflavin have been previously reported to belong to the iron regulon. Real time PCR analysis confirmed this effect and further documented that reciprocally, iron regulates RBP and ribN genes in a riboflavin-dependent way. A subset of genes were responding to both ribD and ribN deletions. Nonetheless, a group of genes was specifically affected in the ∆ribD strain, on which the functional terms protein folding and oxidation reduction process were enriched. Also, a subset of genes was affected specifically in the ∆ribN strain, on which the cytochrome complex assembly functional term was enriched. Results indicate that iron and riboflavin interrelate to regulate its respective provision genes and suggest that both common and specific effects of biosynthesized and internalized riboflavin exist.
2018-02-21 | GSE107538 | GEO
Project description:This SuperSeries is composed of the following subset Series: GSE34886: Acute depletion of Tet1-dependent 5-hydroxymethylcytosine levels impairs LIF/Stat3 signaling and results in loss of embryonic stem cell identity [expression profiling] GSE34887: Acute depletion of Tet1-dependent 5-hydroxymethylcytosine levels impairs LIF/Stat3 signaling and results in loss of embryonic stem cell identity [MRE-seq] Refer to individual Series
2012-01-04 | E-GEOD-34267 | biostudies-arrayexpress
Project description:Drought is a stressor for many soil-inhabiting organisms. Although plants have been extensively investigated for drought-adaptive mechanisms, little information is available for fungi. Antioxidants are especially relevant, since desiccation is accompanied by an excessive intracellular production of reactive oxygen species. Riboflavin (vitamin B2) is one antioxidant regulating drought tolerance in plants. A similar function may exist in fungi. Here, we examined the respiratory and transcriptional responses of Agaricus bisporus to drought and the impact of riboflavin. Mesocosm experiments with four groups were established: hyphae were treated with or without 50 µM riboflavin under drought or no drought conditions. Drought increased riboflavin content in hyphae about 5 times with, but also without, addition of riboflavin. Without addition of riboflavin, fungal respiration decreased by more than 50% at water potentials of about -20 MPa. With addition of riboflavin, respiration remained about 2-3 times higher. The transcriptional responses to only drought or only riboflavin strongly overlapped and were mainly based on factors regulating transcription and translation. This was even stronger in combined treatments. Riboflavin induced protective mechanisms in drought-stressed hyphae. Most pronounced was the methylglyoxal (cytotoxic by-product of glycolysis) detoxifying of lactoylglutathione lyase. Thus, our data suggest a stress-priming function and a role of riboflavin in drought responses of A. bisporus.
2018-03-14 | GSE73010 | GEO
Project description:Translation initiation factors have complex functions in cells which are not yet understood. We show that depletion of initiation factor eIF4GI only modestly reduces overall protein synthesis in cells, but phenocopies nutrient-starvation or inhibition of protein kinase mTOR, a key nutrient sensor. eIF4GI depletion impairs cell proliferation, bioenergetics and mitochondrial activity, thereby promoting autophagy. Translation of mRNAs involved in cell growth, proliferation and bioenergetics were selectively inhibited by reduction of eIF4GI, whereas mRNAs encoding proliferation inhibitors and catabolic pathway factors were increased. Depletion or over-expression of other eIF4G family members did not recapitulate these results. The majority of mRNAs that were translationally impaired with eIF4GI depletion were excluded from polyribosomes due to the presence of multiple upstream open reading frames and low mRNA abundance. These results suggest that the high levels of eIF4GI observed in many breast cancers might act to specifically increase proliferation, prevent autophagy and release tumor cells from control by nutrient sensing. Global regulation of transcription and polysomal association in eIF4GI-silenced cells. Experiment Overall Design: Two sets of experiments are presented. First, overall transcriptome changes were determined for control or eIF4GI silenced cells. Next, mRNAs associated with polysomes were compared between control and eIF4GI silenced cells.
2008-06-11 | E-GEOD-11011 | biostudies-arrayexpress
Project description:To address the role of JUNB in cell proliferation, we investigated the consequences of JUNB depletion using U2OS human bone osteosarcoma cells. We used microarrays to detail the programme of JUNB dependent gene expression underlying cell proliferation and identified distinct classes of up and down-regulated genes during this process.
2022-09-29 | GSE195987 | GEO