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O-GlcNAcylation regulates c-Myc/PDK2 axis to rewire TCA cycle and promote colorectal tumor growth

ABSTRACT: O-GlcNAcylation regulates c-Myc/PDK2 axis to rewire TCA cycle and promote colorectal tumor growth

PROVIDER: PRJNA971495 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR24502603_1.fastq.gz	Fastqsanger.gz
	SRR24502603_2.fastq.gz	Fastqsanger.gz
	SRR24502604_1.fastq.gz	Fastqsanger.gz
	SRR24502604_2.fastq.gz	Fastqsanger.gz
	SRR24502605_1.fastq.gz	Fastqsanger.gz

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O-GlcNAcylation regulates c-Myc/PDK2 axis to rewire TCA cycle and promote colorectal tumor growth

Project description:To investigate the function OGT in the regulation of colorectal tumor growth, we established HT-29 cell lines in which OGT has been knocked down by shRNA.

2024-05-10 | GSE232258 | GEO

Gene expression analysis of a double knockout of TCA cycle enzymes IDH and KDH

Project description:New antimalarial drugs are urgently needed to control drug resistant forms of the malaria parasite, Plasmodium falciparum. Although mitochondrial metabolism is the target of both existing drugs and new lead compounds, the role of the mitochondrial tricarboxylic acid (TCA) cycle remains poorly understood. Herein, we describe 11 genetic knockout parasite lines that delete six of the eight TCA cycle enzymes. Although all TCA knockouts grew normally in asexual blood stages, these metabolic deficiencies halted lifecycle progression in later stages. Specifically, aconitase knockout parasites arrested as late gametocytes, whereas α-ketoglutarate dehydrogenase deficient parasites failed to develop oocysts in the mosquitoes. Mass-spectrometry analysis of 13C isotope-labeled TCA mutant parasites showed that P. falciparum has significant flexibility in TCA metabolism. This flexibility manifested itself through changes in pathway fluxes and through altered exchange of substrates between cytosolic and mitochondrial pools. Our findings suggest that mitochondrial metabolic plasticity is essential for parasite development . Two parallel timecourses resulting in a total of 16 samples (8 wildtype, Isocitrate Dehydrogenase/alpha-Ketogluterate Dehydrogenase double knockout) were hybridized against a Cy3-labeled reference pool of 3D7 mixed stage parasites on a two-color array.

2014-08-01 | E-GEOD-59015 | biostudies-arrayexpress

ABHD11 mediated deglutarylation regulates the TCA cycle and T cell metabolism

Project description:Glutarate is an intermediate of amino acid catabolism and an important metabolite for reprogramming T cell immunity, exerting its effects by inhibition of histone demethylase enzymes or through glutarylation. However, how distinct glutarate modifications are regulated is unclear. Here, we uncover a deglutarylation pathway that couples amino acid catabolism to tricarboxylic acid (TCA) cycle function. By examining how glutarate can form conjugates with lipoate, an essential mitochondrial modification for the TCA cycle, we find that Alpha Beta Hydrolase Domain 11 (ABHD11) protects against the formation of glutaryl-lipoyl adducts. Mechanistically, ABHD11 acts as a thioesterase to selectively remove glutaryl adducts from lipoate, maintaining integrity of the TCA cycle. Functionally, ABHD11 influences the metabolic reprogramming of human T cells, increasing central memory T cell formation and attenuating oxidative phosphorylation. These results uncover ABHD11 as a selective deglutarylating enzyme and highlight that targeting ABHD11 offers a potential approach to metabolically reprogramme cytotoxic T cells.

2025-05-23 | GSE292544 | GEO

MYC sensitises cells to apoptosis by driving energetic demand

Project description:The MYC oncogene is a potent driver of growth and proliferation but also sensitises cells to apoptosis, which limits its oncogenic potential. MYC induces several biosynthetic programmes and primary cells overexpressing MYC are highly sensitive to glutamine withdrawal suggesting that MYC-induced sensitisation to apoptosis may be due to an imbalance of metabolic/energetic supply and demand. Here we show that MYC elevates global transcription and translation, even in the absence of glutamine, revealing metabolic demand without corresponding supply. Glutamine withdrawal from MRC-5 fibroblasts depleted key TCA cycle metabolites and, in combination with MYC activation, led to AMP accumulation and nucleotide catabolism indicative of energetic stress. Further analyses revealed that glutamine supports viability through TCA cycle energetics rather than asparagine biosynthesis and that TCA cycle inhibition confers tumour suppression on MYC- driven lymphoma in vivo. In summary, glutamine supports the viability of MYC- overexpressing cells through an energetic rather than a biosynthetic mechanism.

2022-08-11 | PXD034517 | Pride

Gene expression analysis of a double knockout of TCA cycle enzymes IDH and KDH

2014-08-01 | GSE59015 | GEO

MITF controls the TCA cycle to modulate the melanoma hypoxia response

Project description:MITF controls the TCA cycle to modulate the melanoma hypoxia response

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ABHD11 mediated deglutarylation regulates the TCA cycle and T cell metabolism

Project description:ABHD11 mediated deglutarylation regulates the TCA cycle and T cell metabolism

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GlcNAcylation of histone H2B facilitates its monoubiquitination

Project description:This SuperSeries is composed of the following subset Series: GSE33049: GlcNAcylation of histone H2B facilitates its monoubiquitination [Illumina Genome Analyzer data] GSE33050: GlcNAcylation of histone H2B facilitates its monoubiquitination [Affymetrix data] Refer to individual Series

2011-10-26 | E-GEOD-33051 | biostudies-arrayexpress

EGR2 O-GlcNAcylation Orchestrates the Development of Protumoral Macrophages to Limit CD8+ T Cell Antitumor Responses.

Project description:Tumor associated macrophages (TAMs) exihibit a high capacity to take up glucose, however, how metabolic cues derived from glucose uptake rewire TAMs remains unclear. Here, we report that glucose metabolism-driven protein O-GlcNAcylation shapes the differentiation of protumoral TAMs, thereby accelerating tumor progression. We constructed O-GlcNAc transferase (OGT) conditional-deletion mice to examine MC38 tumor growth.

2025-06-10 | GSE276300 | GEO

Integration of the tricarboxylic acid (TCA) cycle with cAMP signaling and Sfl2 pathways in the regulation of CO2 sensing, filamentation, and virulence in Candida albicans

Project description:Candida albicans is the most common opportunistic fungal pathogen of humans and is also a benign member of the gastrointestinal (GI) tract microbiota. Morphological transitions and metabolic regulation are critical for C. albicans to adapt to the changing host environment. We generated a library of central metabolic pathway mutants in the tricarboxylic acid (TCA) cycle, and investigated the functional consequences of these gene deletions on C. albicans biology. Inactivation of the TCA cycle impairs the ability of C. ablicans to utilize non-fermentable carbon sources and dramatically attenuates cell growth rates under several culture conditions. Through integrations with the Ras1-cAMP signaling pathway and the heat shock factor-type transcription regulator Sfl2, we found that the TCA cycle plays fundamental roles in the regulation of CO2 sensing and filamentation. The TCA cycle and cAMP signaling pathways form a regulatory feedback loop, in which ATP and CO2 may function as molecular linkers. We further demonstrate that inactivation of the TCA cycle leads to lowered intracellular ATP and cAMP levels and thus affects the activation of the Ras1-regulated cAMP signaling pathway. In turn, the Ras1-cAMP signaling pathway controls the TCA cycle through both Efg1- and Sfl2-mediated transcriptional regulation in response to elevated CO2 levels. The protein kinase A (PKA) catalytic subunit Tpk1, but not Tpk2, may play a major role in this regulation. Sfl2 specifically binds to several TCA cycle and filamentation-associated genes under high CO2 conditions. Global transcriptional profiling experiments indicate that Sfl2 is indeed required for the gene expression changes occurring in response to these elevated CO2 levels. Finally, we also demonstrate that several key genes of the TCA cycle are essential for virulence and successful colonization of the GI tract in two mouse infection models.

2017-10-04 | GSE102039 | GEO

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