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Leuenbergeria bleo

ABSTRACT: Leuenbergeria bleo overview

PROVIDER: PRJNA491553 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR6269778_1.fastq.gz	Fastqsanger.gz
	SRR6269778_2.fastq.gz	Fastqsanger.gz
	SRR7846277_1.fastq.gz	Fastqsanger.gz
	SRR7846277_2.fastq.gz	Fastqsanger.gz
	SRR7848078_1.fastq.gz	Fastqsanger.gz

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Leuenbergeria bleo

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Reproducible lung protective effects of a TGFβR1/ALK5 inhibitor in the bleomycin-induced and spirometry-confirmed mouse model of IPF

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Transcriptomic and proteomic profiling of young and old mice in the Bleo model

Project description:Transcriptomic and proteomic profiling of young and old mice in the Bleo model

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Transcription profiling of mouse parental cell line YAMC, plus bleo/Neo vector control, mp53-expressing, Ras-expressing and mp53/Ras cells reveals a synergistic response to oncogenic mutations defines gene class critical to cancer phenotype

Project description:Understanding the molecular underpinnings of cancer is of critical importance to developing targeted intervention strategies. Identification of such targets, however, is notoriously difficult and unpredictable. Malignant cell transformation requires the cooperation of a few oncogenic mutations that cause substantial reorganization of many cell features and induce complex changes in gene expression patterns. Genes critical to this multi-faceted cellular phenotype thus only have been identified following signaling pathway analysis or on an ad hoc basis. Our observations that cell transformation by cooperating oncogenic lesions depends on synergistic modulation of downstream signaling circuitry suggest that malignant transformation is a highly cooperative process, involving synergy at multiple levels of regulation, including gene expression. Here we show that a large proportion of genes controlled synergistically by loss-of-function p53 and Ras activation are critical to the malignant state. Remarkably, 14 among 24 such 'cooperation response genes' (CRGs) were found to contribute to tumor formation in gene perturbation experiments. In contrast, only one in 14 perturbations of genes responding in a non-synergistic manner had a similar effect. Synergistic control of gene expression by oncogenic mutations thus emerges as an underlying key to malignancy and provides an attractive rationale for identifying intervention targets in gene networks downstream of oncogenic gain and loss-of-function mutations. Experiment Overall Design: Contains 50 samples total, 10 replicates each of parental cell line YAMC, plus bleo/Neo vector control, mp53-expressing, Ras-expressing and mp53/Ras cells. Polysomal RNA from each sample was run on Affymetrix GeneChipÂ® Mouse Genome 430 2.0 Arrays.

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Project description:Disease-Specific Gene Expression Profiling in Multiple Models of Lung Disease We profiled lung gene expression in 12 mouse models of infection, allergy, and lung injury. A total of 24 transcripts, including many involved in inflammation and immune activation, were differentially expressed in a substantial majority (9 or more) of the models. Expression patterns distinguished three groups of models: (1) bacterial infection (n = 5), with changes in 89 transcripts, including many related to nuclear factor-B signaling, cytokines, chemokines, and their receptors; (2) bleomycin-induced diseases (n = 2), with changes in 53 transcripts, including many related to matrix remodeling and Wnt signaling; and (3) T helper cell type 2 (allergic) inflammation (n = 5), with changes in 26 transcripts, including many encoding epithelial secreted molecules, ion channels, and transporters.

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