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Senescent melanocytes driven by glycolytic changes are characterized by melanosome transfer dysfunction [scRNA-seq]

ABSTRACT: Senescent melanocytes driven by glycolytic changes are characterized by melanosome transfer dysfunction [scRNA-seq]

PROVIDER: PRJNA950005 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR24005369_1.fastq.gz	Fastqsanger.gz
	SRR24005369_2.fastq.gz	Fastqsanger.gz

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Senescent melanocytes driven by glycolytic changes are characterized by melanosome transfer dysfunction.

Project description:Senescent melanocytes driven by glycolytic changes are characterized by melanosome transfer dysfunction.

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Senescent melanocytes driven by glycolytic changes are characterized by melanosome transfer dysfunction [RNA-seq]

Project description:Senescent melanocytes driven by glycolytic changes are characterized by melanosome transfer dysfunction [RNA-seq]

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Senescent melanocytes driven by glycolytic changes are characterized by melanosome transfer dysfunction [RNA-seq]

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Senescent melanocytes driven by glycolytic changes are characterized by melanosome transfer dysfunction [scRNA-seq]

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Senescent melanocytes driven by glycolytic changes are characterized by melanosome transport dysfunction.

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Senescent melanocytes driven by glycolytic changes are characterized by melanosome transfer dysfunction.

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

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Retinoblastoma protein promotes oxidative phosphorylation through upregulation of glycolytic genes in oncogene-induced senescent cells

Project description:Metabolism is tightly coupled with the process of aging, and tumorigenesis. However, the mechanisms regulating metabolic properties in different contexts remain unclear. Cellular senescence is widely recognized as an important tumor suppressor function and accompanies metabolic remodeling characterized by increased mitochondrial oxidative phosphorylation (OXPHOS). Here we showed retinoblastoma (RB) is required for the increased OXPHOS in oncogene-induced senescent (OIS) cells. Combined metabolic and gene expression profiling revealed that RB mediated activation of the glycolytic pathway in OIS cells, causing upregulation of several glycolytic genes and concomitant increases in the levels of associated metabolites in the glycolytic pathway. Knockdown of these genes by small interfering RNAs (siRNAs) resulted in decreased mitochondrial respiration, suggesting that RB-mediated glycolytic gene activation promotes metabolic flux into the OXPHOS pathway. These results suggest that coordinate transcriptional activation of metabolic genes by RB enables OIS cells to maintain metabolically bivalent states that both glycolysis and OXPHOS are highly active. Collectively, our findings demonstrated a previously unrecognized function of RB in OIS cells. To understand the role of RB, we investigated the effect of RB1-knockdown in the transcription profile of oncogene-induced senescent (OIS) cells. IMR90 ER:Ras cells were treated with 100 nM 4-OHT for 6 days to induce senescence. RNA was isolated 6 days after OHT treatment and hybridized to Affymetrix microarrays. SiRNA transfection (control siRNA or siRB1) was performed 4 days before RNA isolation.

2015-05-26 | E-GEOD-60652 | biostudies-arrayexpress

Retinoblastoma protein promotes oxidative phosphorylation through upregulation of glycolytic genes in oncogene-induced senescent cells

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Human Sensory Neurons Modulate Melanocytes Through Secretion of RGMB

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2022-08-08 | GSE189493 | GEO

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