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Profile of gene expression signatures on DT40 cell for bursal-derived peptides

ABSTRACT: To further elucidate the mechanism of bursal-derived bioactive peptides on avian B cell proliferation on the broad molecular level, we have employed whole genome microarray expression profiling as a discovery platform to examine gene expression patterns during BP5 and BSP-II treatment in DT40 cell culture system. Analysis of our expression microarray data in this manner defined 3163 genes up-regulated and 3539 genes down-regulated by BP5 treatment and 3117 genes up-regulated and 3531 genes down-regulated by BSP-II treatment at 95% confidence, with a commonly regulated gene set of 2253 upregulated genes and 2083 downregulated genes. Various pathways were significantly impacted by BP5 and BSP-II treatment, and gene Ontology annotations show changes in the expression of molecules involved in DT40 cell with BP5 and BSP-II treatment. Expression of 12 genes (FGF3, RAP1B, TCEB1, CSNK2A1, DNMT1, HIF1A, HDAC1, FZR1, GDF3, FGF8, IRF7, and SKP1) from this signature was quantified in the RNA samples by QRT-PCR, confirming low variability between the predicted response patterns.

ORGANISM(S): Gallus gallus

PROVIDER: GSE30396 | GEO | 2011/07/06

SECONDARY ACCESSION(S): PRJNA143399

REPOSITORIES: GEO

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Profile of gene expression signatures on DT40 cell for bursal-derived peptides

Project description:To further elucidate the mechanism of bursal-derived bioactive peptides on avian B cell proliferation on the broad molecular level, we have employed whole genome microarray expression profiling as a discovery platform to examine gene expression patterns during BP5 and BSP-II treatment in DT40 cell culture system. Analysis of our expression microarray data in this manner defined 3163 genes up-regulated and 3539 genes down-regulated by BP5 treatment and 3117 genes up-regulated and 3531 genes down-regulated by BSP-II treatment at 95% confidence, with a commonly regulated gene set of 2253 upregulated genes and 2083 downregulated genes. Various pathways were significantly impacted by BP5 and BSP-II treatment, and gene Ontology annotations show changes in the expression of molecules involved in DT40 cell with BP5 and BSP-II treatment. Expression of 12 genes (FGF3, RAP1B, TCEB1, CSNK2A1, DNMT1, HIF1A, HDAC1, FZR1, GDF3, FGF8, IRF7, and SKP1) from this signature was quantified in the RNA samples by QRT-PCR, confirming low variability between the predicted response patterns. BP5 and BSP-II induced gene expressions in DT40 cell were measured at 4 hours after exposure to doses of 0.02ug/ml and 2ug/ml, respectively. Two independent experiments were performed using different cells for each experiment.Three independently generated populations of cells were used for these experiments.

2011-07-06 | E-GEOD-30396 | biostudies-arrayexpress

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2011-02-17 | GSE27340 | GEO

Development of gene expression signatures on immunity for bursal peptide BSP-II

2011-02-17 | E-GEOD-27340 | biostudies-arrayexpress

N6-methyladenosine-enhanced FZR1 translation contributes to gemcitabine insensitivity in pancreatic cancer via quiescence maintenance [m6A-seq]

Project description:Herein, by detecting the global m6A profile in a panel of gemcitabine-sensitive and gemcitabine-insensitive PDAC cells, we identified the key role of hyper-m6A modification of the master G0/G1 regulator Fizzy and Cell Division Cycle 20 Related 1 (FZR1) in regulating gemcitabine sensitivity. Targeting m6A modification of FZR1 improves the gemcitabine treatment response of gemcitabine-insensitive PDAC cells in vitro and in vivo. Mechanistically, Gem Nuclear Organelle Associated Protein 5 (GEMIN5) was identified as a novel m6A mediator that specifically binds to m6A-modified FZR1 and recruits the eIF3 translation initiation complex to accelerate FZR1 translation. Upregulation of FZR1 maintains the G0/G1 quiescent state and impairs gemcitabine sensitivity of PDAC cells. Further clinical analysis showed that both high levels of FZR1 m6A modification and FZR1 protein indicated a poor response to gemcitabine.

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N6-methyladenosine-enhanced FZR1 translation contributes to gemcitabine insensitivity in pancreatic cancer via quiescence maintenance [PAR-CLIP-Seq]

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Photoperiod associated genes in the poplar bark

Project description:The role of bark storage proteins (BSPs) in seasonal N storage and cycling has been well documented. However, the regulatory mechanisms and pathways associated with this physiological process are poorly understood. The objective of this study is to investigate global patterns of gene expression associated with photoperiod regulated BSP accumulation and to identify candidate genes, pathways and regulatory factors governing N storage and cycling in poplar. In this study, differential expression of protease inhibitors, proteases, transcription factors, and other genes coincided with increased BSP gene expression, suggesting a complex regulatory network that might play an important role in BSP accumulation. Bark of Populus trichocarpa (Nisqually-1) was collected at weekly intervals for 6 weeks from plants treated with short-day (SD) photoperiods at 20Â°C as well as from long-day (LD) grown plants immediately before the SD treatment.

2014-03-01 | E-GEOD-49983 | biostudies-arrayexpress

Photoperiod associated genes in the poplar bark

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Project description:Pancreatic ductal adenocarcinoma (PDAC) is the most lethal cancer with limited therapeutic options, and gemcitabine insensitivity remains a major challenge. N6-methyladenosine (m6A) is a prevalent nucleotide modification in mRNA that has been linked to various biological processes in human diseases, yet its role in drug sensitivity of cancer remains largely unknown. Herein, by detecting the global m6A profile in a panel of gemcitabine-sensitive and gemcitabine-insensitive PDAC cells, we identified the key role of hyper-m6A modification of the master G0/G1 regulator Fizzy and Cell Division Cycle 20 Related 1 (FZR1) in regulating gemcitabine sensitivity. Targeting m6A modification of FZR1 improves the gemcitabine treatment response of gemcitabine-insensitive PDAC cells in vitro and in vivo. Mechanistically, Gem Nuclear Organelle Associated Protein 5 (GEMIN5) was identified as a novel m6A mediator that specifically binds to m6A-modified FZR1 and recruits the eIF3 translation initiation complex to accelerate FZR1 translation. Upregulation of FZR1 maintains the G0/G1 quiescent state and impairs gemcitabine sensitivity of PDAC cells. Further clinical analysis showed that both high levels of FZR1 m6A modification and FZR1 protein indicated a poor response to gemcitabine. These findings unveil the critical function for m6A modification in regulating gemcitabine sensitivity in PDAC and identify the m6A-FZR1 axis as a potential target to enhance gemcitabine response.

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2012-07-31 | E-GEOD-30790 | biostudies-arrayexpress

Optimized amplification and single-cell analysis identify GnRH-mediated activation of Rap1b in primary rat gonadotropes.

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