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Different response of WT and Ts keratinocyte to TPA treatment

ABSTRACT: Ts keratinocyte has increased proliferation compare to WT keratinocyte upon TPA treatment. This result showed the different transcription regulation in Ts and WT keratinocyte upon TPA treatment.

ORGANISM(S): Mus musculus

PROVIDER: GSE40382 | GEO | 2013/06/01

SECONDARY ACCESSION(S): PRJNA173818

REPOSITORIES: GEO

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Different response of WT and Ts keratinocyte to TPA treatment

Project description:Ts keratinocyte has increased proliferation compare to WT keratinocyte upon TPA treatment. This result showed the different transcription regulation in Ts and WT keratinocyte upon TPA treatment. Total RNA extracted from WT or Ts keratinocytes, not treated or treated with TPA for 12 hours.

2013-06-01 | E-GEOD-40382 | biostudies-arrayexpress

Mus musculus

Project description:Different response of WT and Ts keratinocyte to TPA treatment

| PRJNA173818 | ENA

Differentially expressed genes induced by TPA stimulation between the P2ry6+/+ and P2ry6-/- mice

Project description:We report that P2ry6-deficient mice exhibit marked resistance to 7,12-dimethylbenzanthracene (DMBA)/12-O-tetradecanoylphorbol-13-acetate (TPA)-induced two-stage skin papilloma formation compared with wild-type mice. Consistent with these findings, epidermal hyperplasia in response to TPA stimulation was suppressed in the P2ry6 knockout or MRS2578 (P2RY6 antagonist)-treated mice. The dramatic decrease in hyperplasia and tumorigenesis due to P2ry6 disruption was associated with the suppression of TPA-induced keratinocyte proliferation and inflammatory reactions.We have employed whole genome microarray expression profiling as a discovery platform to identify genes with the potential to distinguish differentially expressed genes induced by TPA stimulation between the P2ry6+/+ and P2ry6-/- mice. Notably, P2ry6 deletion prevented the TPA-induced increase in YAP nuclear accumulation and hence its downstream gene expression in an MST/LATS1-dependent manner.

2021-11-26 | GSE189478 | GEO

Metabolic enhancement of developmental pausing (TS cells)

Project description:Embryonic stem (ES) cells and embryos reversibly pause via chemical mTOR inhibition. In this study, we investigate the tissue-specific response to mTORi-induced pausing in ES and trophoblast stem (TS) cells. To resolve the sequential rewiring of the proteome, we conducted a time-series proteomics experiment at 1, 3, 6, 12, 24, and 48 hours upon induction of pausing, and at 1, 3, 6, 12, 24, and 48 hours upon release of pausing in ES and TS cells. We find that ES, but not TS cells pause reversibly. To optimise developmental pausing conditions, we reasoned that by understanding the difference in pausing response of ES and TS cells, we could identify which pathways are essential for pausing. We found that KEGG pathways related to amino acid degradation, fatty acid degradation, and DNA repair are upregulated in ES cells, but downregulated in TS cells during entry into pausing. Moreover, by targeted metabolomics, we found a depletion of short chain carnitines in the paused ES cells. To extend the length of developmental pausing, we supplemented paused embryos with L-carnitine. The L-carnitine supplementation facilitates lipid usage and prolongs the pausing length by 19 days through the establishment of a more dormant state.

2023-11-06 | PXD033798 | Pride

Expression profiles of human primary keratinocytes differentiated with TPA

Project description:Human primary keratinocytes were left untreated or treated for 48 hr with 12-O-tetradecanoylphorbol-13-acetate (TPA) and expression profiles were compared to find long ncRNAs expressed and differentially regulated upon differentiation. 4 replicates of minus TPA and 3 of plus TPA with dye-swap. Custom-made microarray from Agilent.

2011-04-12 | E-GEOD-28552 | biostudies-arrayexpress

ESCC KYSE150 cells: TPA treatment vs. control

Project description:Complete lncRNA and mRNA expression profile of ESCC KYSE150 cells and TPA-treatment KYSE150 cells

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TS-seq

Project description:TS-seq

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Vav proteins orchestrate a keratinocyte auto/paracrine program critical for skin tumorigenesis.

Project description:Cutaneous squamous tumors rely on autocrine/paracrine loops for proper fitness. Targeting this Achilles’ heel is therefore considered a potential avenue for patient treatment. However, the mechanisms that engage and sustain such programs during tumor ontogeny are poorly understood. Here, we show that two Rho/Rac activators, the exchange factors Vav2 and Vav3, control the expression of an epithelial autocrine/paracrine program that regulates keratinocyte survival and proliferation as well as the creation of an inflammatory microenvironment. Vav proteins are also critically involved in some of the subsequent autocrine signaling loops activated in keratinocytes. The genetic inactivation of both Vav proteins reduces tumor multiplicity without hampering skin homeostasis, thus suggesting that pan-specific Vav therapies may be useful in skin tumor prevention and treatment. The dorsal skin of WT and DKO mice (Vav2-/-;Vav3-/-) were treated with either one or four applications of phorbol ester 12-O-tetradecanoylphorbol-13 acetate (TPA) (6.8 nmol in 200 μl acetone) two days after shaving. As control, we applied 200 μl of acetone. Animals were euthanized 24 hours after treatment.

2013-07-30 | E-GEOD-40849 | biostudies-arrayexpress

Deletion of DUSP5 affects the expression of a subset of TPA-inducible genes

Project description:This experiment was designed to determine if deletion of the dual-specificity MAP kinase phosphatase encoded by DUSP5 had any effect on the pattern of gene expression in cells treated with the phorbol ester tumour promoter TPA. Sex matched primary WT and DUSP5 knockout MEFs were isolated from littermate embryos and cultured. Cells were then exposed to TPA for 0, 1 and 3h before isolation of RNA prior to microarray hybrdisation and data analysis. Our results show that the transcript levels of a subset of TPA-inducible genes are altered in cells that lack DUSP5.

2014-10-17 | GSE62433 | GEO

Expression profiles of human primary keratinocytes differentiated with TPA

2011-04-12 | GSE28552 | GEO

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