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Analysis of Wild Type and Siah2 KO time series liver transcriptome from male and female mice

ABSTRACT: Analysis of Wild Type and Siah2 KO time series liver transcriptome from male and female mice

PROVIDER: PRJNA758032 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR15620651.fastq.gz	Fastqsanger.gz
	SRR15620652.fastq.gz	Fastqsanger.gz
	SRR15620653.fastq.gz	Fastqsanger.gz
	SRR15620654.fastq.gz	Fastqsanger.gz
	SRR15620655.fastq.gz	Fastqsanger.gz

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Analysis of Wild Type and Siah2 KO time series liver transcriptome from male and female mice [ZT 10]

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Analysis of Wild Type and Siah2 KO time series liver transcriptome from male and female mice [ZT0-ZT21]

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Analysis of Wild Type and Siah2 KO time series liver transcriptome from male and female mice [ZT0-ZT21]

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Project description:Analysis of Wild Type and Siah2 KO time series liver transcriptome from male and female mice [ZT 10]

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Siah2-dependent gene expression profile

Project description:Gene expression profiling was performed to identify Siah2-dependent changes in cells subjected to ER stress, hypoxia, and combined glucose/oxygen deprivation. To establish the magnitude of the Siah2 effect on the ER stress response, we have compared gene expression profiles of WT and Siah1a-/-::Siah2-/- mouse embryo fibroblasts (MEFs) that were subjected to glycosylation inhibitor tunicamycin (TM), thapsigargin (TG), glucose deprivation, or glucose/oxygen deprivation. Overall, this analysis confirmed changes associated with ER stress that had not previously been associated with Siah2 signaling, substantiating Siah2 as a key coordinator of ER stress through the ATF4 and sXbp1 pathways. WT and Siah1a/Siah2 KO MEF cells were treated with TM or TG for 6 h, or subjected for 12 h to oxygen deprivation, glucose deprivation or a combination of oxygen and glucose deprivation, in duplicate.

2014-04-01 | E-GEOD-39244 | biostudies-arrayexpress

Analysis of Wild Type and Siah2 KO time series liver transcriptome from male and female mice

Project description:This SuperSeries is composed of the SubSeries listed below.

2022-06-29 | GSE182836 | GEO

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Siah2 control on tumor environment

Project description:Understanding mechanisms underlying anti-tumor immunity is pivotal for improving immune-based cancer therapies. Here we demonstrate that growth of inoculated BRAF mutant melanoma cells was inhibited in Siah2-/- mice, up to a complete loss. Melanoma grown in Siah2-/- mice exhibited increased proinflammatory immune components, signified by enhanced intra-tumoral activated T cells, along with decreased expression of Ccl17 and Ccl22, and decreased Foxp3 expression. A marked reduction in Treg proliferation was associated with inhibition of Treg cell cycle progression. Correspondingly, G1 cell cycle arrest in Siah2-/- Tregs coincided with elevated expression of the cyclin dependent kinase inhibitor p27, a Siah2 substrate. Growth of PD1-unresponsive melanoma was effectively inhibited up to complete tumor rejection in Siah2-/- mice subjected to PD1 blockade, highlighting synergy between PD1 inhibition and Siah2 loss. Siah2 regulation of Treg recruitment and cell cycle progression effectively controls melanoma development and confers synthetic lethality when combined with anti-PD1 therapy.

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Transcription profiling of mouse adult male wild-type liver (M-WT), adult female wild-type liver (F-WT), adult male liver-specific HNF4alpha knockout liver (M-KO) and adult female liver-specific HNF4alpha knockout liver (F-KO) to investigate sex-dependent and HNF4alpha-dependent gene expression

Project description:A series of dual-channel gene expression profiles obtained using Rosetta/Agilent Whole Mouse Genome oligonucleotide microarrays, 4 x 44K format, was used to identify sex-dependent and HNF4alpha-dependent differences in gene expression in adult mouse liver. This series is comprised of four sex-genotype combinations: adult male wild-type liver (M-WT), adult female wild-type liver (F-WT), adult male liver-specific HNF4alpha knockout liver (M-KO) and adult female liver-specific HNF4alpha knockout liver (F-KO). Four pools, each comprised of 4 randomly selected individual liver RNAs, were prepared for each sex-genotype combination. The pools were paired randomly to generate 4 separate experimental comparisons: M-WT:F-WT (first array comparison), M-WT:M-KO (second array comparison), F-WT:F-KO (third array comparison), and M-KO:F-KO (fourth array comparison). A total of 4994 HNF4alpha-dependent genes were identified, of which ~1000 fewer genes responded to the loss of HNF4alpha in female liver as compared to male liver. Moreover, 90% of the genes showing sex-specific expression in the liver were shown to lose sex specificity in HNF4alpha-deficient liver. Experiment Overall Design: An Alexa555-labeled cDNA sample is co-hybridized with an Alexa647-labeled cDNA sample. The samples are then dye-swapped and compared again on a second microarray chip. Together, these two mixed cDNA samples are considered a fluorescent reverse pair (dye swap). Similarly, a second fluorescent reverse pair is generated and the two pairs are averaged. The normalized expression ratio for each array is reported along with the two separate intensities. In this way, dye swaps were carried out for each of the four experimental comparisons. Thus, four microarrays, one for each mixed cDNA sample, were hybridized for each of the four fluorescent reverse pairs, giving a total of 16 microarrays.

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