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Suclg2 maintains the tolerogenic function of regulatory dendritic cells by suppressing Lactb succinylation

ABSTRACT: Purpose: mRNAs sequencing of the gene expression differences in maDC and diffDC, the goals of this study are to investigate the biological effect of the metabolic enzyme succinate-CoA ligase subunit beta Suclg2 in regulating regulatory DC differentiation and function.

ORGANISM(S): Mus musculus

PROVIDER: GSE219010 | GEO | 2023/11/27

REPOSITORIES: GEO

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Suclg2 maintains the tolerogenic function of regulatory dendritic cells by suppressing Lactb succinylation [si-nc/si-Suclg2]

Project description:Purpose: mRNAs sequencing of the gene expression differences in diffDC transfected with si-nc or si-Suclg2, the goals of this study are to investigate the biological effect of the metabolic enzyme succinate-CoA ligase subunit beta Suclg2 in regulating regulatory DC differentiation and function.

2023-11-27 | GSE220055 | GEO

Suclg2 maintains the tolerogenic function of regulatory dendritic cells by suppressing Lactb succinylation [si-nc/si-Suclg2]

Project description:Suclg2 maintains the tolerogenic function of regulatory dendritic cells by suppressing Lactb succinylation [si-nc/si-Suclg2]

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Suclg2 maintains the tolerogenic function of regulatory dendritic cells by suppressing Lactb succinylation

Project description:Suclg2 maintains the tolerogenic function of regulatory dendritic cells by suppressing Lactb succinylation

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SUCLG2 Regulates Mitochondrial Dysfunction through Succinylation in Lung Adenocarcinoma.

Project description: Not available

| S-EPMC10724390 | biostudies-literature

Telomerase Dysfunction Strategy Overcomes Targeted Therapy Induced Drug Tolerant Persister in Pan-cancer via SUCLG2 downregulation

Project description:The evolution of cancer cells from a drug-tolerant persister (DTP) state into stably resistant clones is a primary barrier to the long-term efficacy of targeted therapies. Through longitudinal transcriptomic profiling across melanoma, non-small cell lung cancer (NSCLC), and colorectal cancer models, we uncover a conserved, biphasic regulation of telomerase as a fundamental driver of this process. Combining targeted therapies with telomerase inhibition (genetic or pharmacological) in melanoma and NSCLC models suppressed DTP cell formation and resistance progression in vitro and in vivo. Mechanistic dissection via RNA-seq revealed SUCLG2 as a critical downstream effector of the telomerase inhibitor 6-thio-dG; SUCLG2 knockdown phenocopied combinatorial efficacy. Complementary ATAC-seq demonstrated 6-thio-dG–induced chromatin remodelling at the SUCLG2 locus, reducing accessibility to downregulate expression and thereby impeding DTP proliferation and resistance evolution. Collectively, we establish preemptive telomerase inhibition as a vulnerability-directed strategy to ablate adaptive resistance across malignancies.

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A telomerase-SUCLG2 signaling axis drives drug resistance by protecting persister cells

Project description:The evolution of drug-tolerant persister (DTP) cells into resistant clones remains a major obstacle to targeted therapies. Transcriptomic profiling across melanoma (A375, SK-MEL-28), non-small cell lung cancer (NSCLC; HCC827, PC-9), and colorectal cancer (CRC; SW480) models revealed a conserved biphasic telomerase regulation during DTP evolution. Combining targeted therapies with the telomere-dysfunction agent 6-thio-dG effectively suppressed DTP outgrowth and resistance in vitro and in vivo. Mechanistically, 6-thio-dG induces chromatin remodeling, reducing SUCLG2 locus accessibility and downregulating this mitochondrial enzyme to disrupt DTP metabolic stability. Consistently, SUCLG2 knockdown recapitulated these therapeutic effects. Furthermore, in vivo RNAseq of HCC827 xenografts confirmed the combination coordinately suppresses mitochondrial metabolism, telomere maintenance, and persister programs. Collectively, preemptively combining 6-thio-dG with targeted therapies is a potent strategy to disrupt DTP evolution and overcome adaptive resistance across diverse malignancies.

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A telomerase-SUCLG2 signaling axis drives drug resistance by protecting persister cells [ATAC-Seq]

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Succinyl-CoA synthetase deficiency in mouse forebrain results in hyper-succinylation with perturbed neuronal transcriptional regulation and metabolism (RNA-Seq)

Project description:Lysine-succinylation is a subtype of protein acylation associated with metabolic regulation of succinyl-CoA in the TCA cycle. Deficiency of succinyl-CoA synthetase (SCS), the TCA-cycle enzyme catalyzing the reversible conversion of succinyl-CoA to succinate, leads to mitochondrial encephalomyopathy in humans and embryonic lethality in mice. This report presents a conditional forebrain-specific knock-out (KO0 mouse model of Sucla2, the gene encoding the ATP-specific beta isoform of SCS, resulting in postnatal deficiency of the entire SCS complex. Results demonstrate that the accumulation of succinyl-CoA in the absence of SCS leads to hyper-succinylation within the cerebral cortex of adult mice. With previous research identifying succinylation marks on histones, and with proteomic evidence of histone lysine-succinylation within the presented model, global chromatin accessibility was surveyed in Sucla2 mutant and control mice via ATAC-sequencing. Data show wide-scale alterations in chromatin landscape and global gene expression. Computational analysis of combined chromatin-accessibility and gene expression data reveal perturbation of neuronal transcriptional regulatory networks in the mutant forebrain, suggesting SCS-related changes in the protein succinylome and chromatin accessibility play a significant role in the neuronal pathogenesis of SCS-deficiency.

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Succinyl-CoA synthetase deficiency in mouse forebrain results in hyper-succinylation with perturbed neuronal transcriptional regulation and metabolism (ATAC-Seq)

2022-07-27 | GSE208690 | GEO

Ethylamine versus succinate cells of Methylobacterium extorquens

Project description:In order to provide global information on gene expression during growth on C2 compounds, microarray analysis of M. extorquens AM1 cells was carried out, comparing ethylamine-grown cells to succinate-grown cells. This comparison has confirmed previous observations on the inducible nature of some of the enzymes involved in C2 metabolism, such as methylamine (and ethylamine) utilization system (mau), putative enzymes for converting acetaldehyde into acetate and acetyl-CoA, and enzymes of the ethylmalonyl-CoA pathway that has been proposed to operate for assimilation of acetyl-CoA into cell biomass. RNA from ethylamine-grown cells was compared to RNA from succinate-grown cells. Four biological replicates were carried out.

2010-05-14 | E-GEOD-20365 | biostudies-arrayexpress

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