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RNA changes upon glucose starvation treat with or without NAC

ABSTRACT: The adaptation of tumor cells to metabolic stress is crucial for tumordevelopment, We demonstrate that the translation of NRF2, a master regulatorof antioxidant response, is controlled by the OGDH-METTL3 axis in melanomafor glucose starvation adaptation, To elucidate the regulatory mechanism ofthe OGDH-METTL3 axis during glucose starvation,we conducted coimmunoprecipitation and mass spectrometry analysis to identify the bindingpartner of OGDH that governs both the OGDH-METTL3 axis and tumor celladaptation to qlucose deprivation.

ORGANISM(S): Homo sapiens

PROVIDER: GSE272214 | GEO | 2026/01/01

REPOSITORIES: GEO

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RNA changes upon glucose starvation

Project description:The adaptation of tumor cells to metabolic stress is crucial for tumor development. We demonstrate that the translation of NRF2, a master regulator of antioxidant response, is controlled by the OGDH-METTL3 axis in melanoma for glucose starvation adaptation. To elucidate the regulatory mechanism of the OGDH-METTL3 axis during glucose starvation, we conducted co-immunoprecipitation and mass spectrometry analysis to identify the binding partner of OGDH that governs both the OGDH-METTL3 axis and tumor cell adaptation to glucose deprivation.

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RNA changes upon glucose starvation treat with or without NAC

Project description:RNA changes upon glucose starvation treat with or without NAC

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1. Mitochondrial Protein Identification; 2. Redox Proteomics Identification; 3. Quantitative Cellular Proteomics

Project description:1. Quantitative Proteomic Analysis of Isolated Mitochondria. Each group has three replicates: Glc group: Glucose starvation group. GlcFH group: FH activity inhibition combined with glucose starvation group. 2. Quantitative proteomics analysis was performed to assess intracellular protein disulfide bond levels. The experiment included the following groups, each with three replicates:UOK group: UOK262 cells under glucose starvation; UOKFH group: UOK262 cells overexpressing FH under glucose starvation. V786O group: 786-O cells under glucose starvation; XCT786O group: 786-O cells overexpressing XCT under glucose starvation. 3. Quantitative Proteomics Analysis of Cellular Protein Expression Differences, Each group has three replicates: Glcn group: glucose starvation group. Glcp group: glucose sufficiency group

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ZBTB32 performs crosstalk with the glucocorticoid receptor and is crucial in glucocorticoid responses to starvation

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Protein Kinase A Regulates Gene-Specific Translational Adaptation in Differentiating Yeast

Project description:Cellular differentiation is driven by coordinately regulated changes in gene expression. Translational control of gene expression is increasingly recognized as pervasive and quantitatively significant, but the mechanisms responsible for widespread changes in gene-specific translation activity are largely unknown. Here we investigate the mechanisms responsible for translational reprogramming during cellular adaptation to the absence of glucose, a stimulus that induces invasive filamentous differentiation in yeast. We show that gene-specific translation efficiencies are highly adapted to cellular conditions and that glucose withdrawal is accompanied by widespread translational reprogramming at the level of translation initiation. We demonstrate that transcripts from <5% of genes make up the majority of translating mRNA in both rapidly dividing and starved cells. Moreover, the identities of these highly translated genes are growth-state specific, and they are subject to condition-dependent translational privilege. By comparing glucose starvation to other growth-attenuating stresses, we distinguish a glucose-specific translational response that regulates ribosomal protein and mitochondrial protein-coding genes. This response is mediated through signaling by protein kinase A (PKA). These findings reveal a high degree of growth-state specialization of the translatome and identify PKA as an important regulator of gene-specific translation activity. Examine translational adaptation in yeast in response to glucose starvation

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