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Comparative analysis of murine Th17 cell transcriptomes in the presence of Smo inhibitor cyclopamine or carrier control

ABSTRACT: Comparative analysis of murine Th17 cell transcriptomes in the presence of Smo inhibitor cyclopamine or carrier control

PROVIDER: PRJNA847939 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR19621815.fastq.gz	Fastqsanger.gz
	SRR19621816.fastq.gz	Fastqsanger.gz
	SRR19621817.fastq.gz	Fastqsanger.gz
	SRR19621818.fastq.gz	Fastqsanger.gz
	SRR19621819.fastq.gz	Fastqsanger.gz

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Comparative analysis of murine Th17 cell transcriptomes in the presence of Smo inhibitor cyclopamine or carrier control

Project description:T helper 17 (Th17) cells play a key role in barrier protection against fungal and bacterial pathogens but are also pathological drivers of many inflammatory diseases. We find that Hh signaling inhibition through Smoothened inhibitor cyclopamine selectively inhibits Th17 lineage differentiation but not the development of Th1, Th2, or iTreg CD4+ Th cells. In these experiments we analysed the transcriptomes of Th17 cells that had been polarized in the presence of cyclopamine or carrier control to profile the global transcriptome of Th17 cells in which the Hh pathway had been blocked. The aim of this analysis was to identify the target genes downstream of Smo that may be important for Th17 polarisation.

2022-06-13 | GSE205848 | GEO

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Project description:Analysis of gene expression levels in response to inhibition of Hh signaling in HT-29 cells using a cDNA microarray technique. Microarray analyses revealed that different genes after treatment with both cyclopamine (an antagonist of SMO) and GANT61 (a specific, small-molecular molecule inhibitor of Glis).

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SMO variants explain the majority of drug resistance in basal cell carcinoma [Target Sequencing]

Project description:Advanced basal cell carcinomas (BCCs) frequently acquire resistance to Smoothened (SMO) inhibitors through unknown mechanisms, providing a unique opportunity to study human tumor evolution. Here, we identify SMO mutations in 50% (22/44) of resistant BCCs compared with 5.6% (2/36) of untreated BCCs (p<0.0001), and show that these mutations maintain Hedgehog signaling in the presence of SMO inhibitors. Alterations include four ligand binding pocket (LBP) mutations that define sites of inhibitor binding and four variants that confer constitutive activity and inhibitor resistance, thus defining pivotal residues of SMO that ensure receptor autoinhibition. Finally, we show that both classes of SMO variants respond to the aPKC-ι/λ inhibitor PSI and GLI2 antagonist ATO that operate downstream of SMO

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Carrier Subclass

Project description:Carrier Subclass

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Whole Retina RNAseq after injury and Cyclopamine(C) treatment in zebrafish

Project description:several genes are being regulated after injury at various time points and after cyclopamine treatment.

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RNA sequencing of Foxd1Cre;Smo(flox/-) mutant kidneys

Project description:Purpose: To analyze the mRNA content of Foxd1Cre;Smo(flox/-) mutant kidneys. Methods: We collected E13.5 wildtype and Foxd1Cre;Smo(flox/-) mutant kidneys and isolated RNA to do RNA-Seq. Results: Identified differentially expressed transcripts in Foxd1Cre;Smo(flox/-) mutant kidneys compared to wildtype controls. Conclusions: Our work provides novel insight into how Hedgehog signaling from stromal cells influences renal development.

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Analysis of Th17 gene signature in the presence of CD28 costimulation in human CD4 naïve T cells

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Expression data from TH17 cells cultured in the presence or absence of glutamine

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