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Partial reprogramming of melanoma cells confers drug resistance and increased vulnerability to calcium channel antagonists

ABSTRACT: Partial reprogramming of melanoma cells confers drug resistance and increased vulnerability to calcium channel antagonists

PROVIDER: PRJNA506248 | ENA |

REPOSITORIES: ENA

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Partial reprogramming of melanoma cells confers drug resistance and increased vulnerability to calcium channel antagonists [C790 cells]

Project description:Partial reprogramming of melanoma cells confers drug resistance and increased vulnerability to calcium channel antagonists [C790 cells]

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Partial reprogramming of melanoma cells confers drug resistance and increased vulnerability to calcium channel antagonists [4434 cells]

Project description:Partial reprogramming of melanoma cells confers drug resistance and increased vulnerability to calcium channel antagonists [4434 cells]

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Partial reprogramming of melanoma cells confers drug resistance and increased vulnerability to calcium channel antagonists

Project description:Our aim is to compare whole-genome expression profiles of partially reprogrammed C790 melanoma murine cells after induction of stem cell related genes (+ dox vs -dox)

2020-02-21 | GSE122763 | GEO

Partial reprogramming of melanoma cells confers drug resistance and increased vulnerability to calcium channel antagonists [4434 cells]

Project description:Our aim is to compare whole-genome expression profiles of partially reprogrammed 4434 melanoma murine cells after induction of stem cell related genes (+ dox vs -dox)

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Partial reprogramming of melanoma cells confers drug resistance and increased vulnerability to calcium channel antagonists [C790 cells]

Project description:Our aim is to compare whole-genome expression profiles of partially reprogrammed C790 melanoma murine cells ( - dox vs + dox) after treatment with trametinib, in order to identify potential candidates related with drug resistance.

2020-02-21 | GSE122399 | GEO

DEGs resulting from activating L-type calcium channel, CaV1.2, in mouse valvular interstitial cells (mVICs).

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Inhibiting L-type calcium channel promotes cardiomyocyte proliferation through activating canonical Wnt signaling pathway

Project description:We performed RNA-Seq analysis of neoatal rat ventricular cardiomyocytes (NRVCs) and human pluripotent stem cells derived cardiomyocytes (hPSC-CMs) which were treated with Nimodipine (NM) to investigate the moleclular mechanism of inhibiting L-type calcium channel (LTCC) to promote cardiomyocyte proliferation.

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The mutant Moonwalker TRPC3 channel links calcium signaling to lipid metabolism in the developing

Project description:The Moonwalker (Mwk) mouse is a model of dominantly inherited cerebellar ataxia caused by a gain-of-function mutation in the transient receptor potential (TRP) channel TRPC3. We report impairments in dendritic growth and synapse formation early on during Purkinje cell development in the Mwk cerebellum that are accompanied by alterations in calcium signaling.

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Sustained L-type Calcium Channel Blockade Alters Gene Regulation in the Adult Mouse Ventricle

Project description:Objective: L-type calcium channels (LTCC) homeostatically regulate calcium on a beat by beat basis, but also provide Ca that over long time scales may contribute to transcriptional regulation. We previously showed that sustained LTCC blockade (CCB) elicits LTCC remodeling in ventricular cardiac myocytes (CM). Here we hypothesize that sustained CCB has broad effects on the expression of genes involved in calcium handling. Methods and Results: Therefore, we subjected adult mice to sustained CCB for 24 hours and performed gene expression profiling. In comparison to vehicle-only control animals, 231 genes were up-regulated, and 111 genes were down-regulated by sustained LTCC blockade (p <0.01). Gene ontology analysis suggested that the CaMKIIdelta signaling pathway was up-regulated in these cells. Unexpectedly, phosphorylation of phospholamban (PLN) at threonine17 (Thr17), an index of CaMKIIdelta activity, was not changed by sustained CCB; however, the degree of phosphorylation of the neighboring PLN-Ser16 substrate site for PKA was significantly reduced by sustained CCB compared to control. Gene expression profiling suggested no change in PKA, but it showed that protein phosphatase 2A (PP2A) mRNA increased, and immunoblots demonstrated that PP2Ac-alpha protein was significantly increased by sustained CCB. Consistent with elevated PP2Ac-alpha protein expression LTCC exhibited decreased phosphorylation of the C-terminal Ser1928 PKA substrate site. Conclusions: We conclude that sustained CCB elicits a spectrum of transcriptional events, including compensatory up-regulation of LTCC and PP2Ac-alpha. Although this study is restricted to mouse, these results suggest the new hypothesis that clinically-relevant sustained LTCC blockade in humans results in changes in gene regulation in the heart. Keywords: L-type calcium channel, calcium channel blockade, verapamil

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Transcriptome profiling of liver derived from calcium channel ITPR2 KO mice

Project description:Transcriptome profiling of liver derived from calcium channel ITPR2 KO mice

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