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Transcript profiling in WT, CRTC3 KO and CRTC3-rescued B16F1 cells.

ABSTRACT: Transcript profiling in WT, CRTC3 KO and CRTC3-rescued B16F1 cells.

PROVIDER: PRJNA645146 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR12185840.fastq.gz	Fastqsanger.gz
	SRR12185841.fastq.gz	Fastqsanger.gz
	SRR12185842.fastq.gz	Fastqsanger.gz
	SRR12185843.fastq.gz	Fastqsanger.gz
	SRR12185844.fastq.gz	Fastqsanger.gz

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Transcript profiling in WT, CRTC3 KO and CRTC3-rescued B16F1 cells.

Project description:Triggering of cAMP and mitogen-activated (MAPK) pathways in response to hormonal and growth factor cues promotes melanocyte pigmentation and survival in part through induction of the master regulator MITF by cAMP-responsive factor CREB. We examined the role of CREB coactivators (CRTC1-3) in transduction of cAMP and MAPK signals in melanocytes. We found that CRTC3 knock-out in mice and B16F1 melanoma cells decreases pigmentation by directly regulating the expression of the melanosomal transporter OCA2. In addition to effects of cAMP, CRTC3 activation was also promoted by ERK1/2-mediated phosphorylation at Ser391; amounts of phosphorylated CRTC3-S391 were constitutively elevated in human melanoma cells expressing mutated BRAF or NF1. Knock-out of CRTC3 in A375 melanoma cells impaired their anchorage-independent growth, migration and invasiveness, whereas CRTC3 over-expression increased survival in response to BRAF inhibition by vemurafenib. Analysis of spontaneous CRTC3 mutations in melanomas reveals that increased activity of this co-activator associates with reduced patient survival. Our results highlight the importance of CRTC3 in pigmentation and melanoma progression.

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Transcript profiling in WT and CRTC3 KO A375 cells.

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Transcript profiling in whole skins of WT and CRTC3 KO mice.

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Analysis of CRTC3 genomic occupancy upon forskolin stimulus in B16F1 cells.

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Transcript profiling in WT and CRTC3 KO A375 cells.

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Expression data from primary astrocyte cell in CRTC3 KO and WT mice

Project description:CRTC3 is CREB regulated transcriptional co-activators and prominently expressed in astrocyte cells. CRTC3 plays a specific role in determining the social heirarchical ranking in mice by confirming social rank test in CRTC3 KO mice. Loss of CRTC3 in astrocyte induced neuronal change and caused exchanging protein expression pattern. We used microarrays to determine the astrocyte-derived factors that were regulated by CRTC3 and related with social dominance behaviours of CRTC3 KO mice. We identifed distinct factor of down-regulated gene during primary astrocyte cell in CRTC3 KO.

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Transcript profiling in whole skins of WT and CRTC3 KO mice.

Project description:Transcript profiling in whole skins of WT and CRTC3 KO mice.

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Analysis of CRTC3 genomic occupancy upon forskolin stimulus in B16F1 cells.

Project description:Analysis of CRTC3 genomic occupancy upon forskolin stimulus in B16F1 cells.

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Expression data from primary astrocyte cell in CRTC3 KO and WT mice

Project description:Expression data from primary astrocyte cell in CRTC3 KO and WT mice

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Comparison of transcriptomic profile of the murine B16F1-GFP-M melanoma cells with the derived dormant B16F1-GFP-D, B16F1-GFP-DB#1, B16F1-GFP-DB#2, B16F1-GFP-DB#3 melanoma cells

Project description:Cancer patients after successful therapy contain nested in their organs and/or circulating in the systemic fluids tumor cells that remain asymptomatic for an extended period of time. They stay dormant with no apparent immediate potential to develop into a clinically manifested tumor until activated by yet not well defined mechanisms. We previously developed tumor dormancy model of murine melanoma, a cancer with a high potential of phenotype plasticity to adapt to micro-environmental changes, in which to investigate cellular quiescence and related factors as a potential mechanism of tumour dormancy. In this study, to explore molecular mechanism responsible for cellular dormancy, we performed a comparative transcriptome analysis of dormant B16F1-GFP-D and derived dormant brain metastasis (DB) with maternal B16F1-GFP-M cells.

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