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Dynamic synthesis and transport of phenazine-1-carboxylic acid to boost extracellular electron transfer rate

ABSTRACT: Dynamic synthesis and transport of phenazine-1-carboxylic acid to boost extracellular electron transfer rate

PROVIDER: PRJNA1222813 | ENA |

REPOSITORIES: ENA

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Dynamic synthesis and transport of phenazine-1-carboxylic acid to boost extracellular electron transfer rate

Project description:We employed RNA-sequencing (RNA-seq) and transcriptomic analysis to analyze cell metabolism and electrophysiology, enabling systematically elucidate the mechanisms underlying phenazine-1-carboxylic acid (PCA)-boosted EET. As a result, the PCA-induced transcriptional response of the EET-related genes could be categorized into three groups: (i) lactate catabolism; (ii) c-Cyts biosynthesis; and (iii) biofilm formation.

2025-02-13 | GSE289377 | GEO

Mitochondrial reverse electron transport in myeloid cells perpetuates neuroinflammation

Project description:Sustained smouldering, or low grade, activation of myeloid cells is a common hallmark of several chronic neurological diseases, including multiple sclerosis. Distinct metabolic and mitochondrial features of myeloid cells guide diverse functional states. How these features act to perpetuate neuroinflammation is currently unknown. Using a multiomics approach, we identify a new molecular signature that perpetuates the activation of microglia by the reverse electron transport through complex I and the subsequent production of reactive oxygen species. Blocking reverse electron transport in pro-inflammatory myeloid cells protects against neurotoxic damage and improves functional outcomes in animal disease models in vivo. Our data show that reverse electron transport in myeloid cells is a potential new therapeutic target to foster neuroprotection in smouldering inflammatory central nervous system diseases.

2025-01-31 | GSE224366 | GEO

Genes expressed in age-induced mitochondrial DNA deletion mutation containing / Electron Transport abnormal cells

2013-03-01 | GSE35607 | GEO

Rewiring the Mitochondrial Electron Transport Chain Enhances Tumor Immunogenicity

Project description:Rewiring the Mitochondrial Electron Transport Chain Enhances Tumor Immunogenicity

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Mitochondrial reverse electron transport in myeloid cells perpetuates neuroinflammation

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Genes expressed in age-induced mitochondrial DNA deletion mutation containing / Electron Transport abnormal cells

Project description:Muscle tissue was longitudinally characterized histologically for electron transport function by staining 1mm of quadriceps muscle at 70 micron intervals for the activities of two complexes in the mitochondrial electron transport chain, Cytochrome C Oxidase and Succinate Dehydrogenase. Unstained serial cryosections were prepared for Laser Capture Microdissection. Target cells from the serial sections were isolated and pooled for RNA extraction, amplification and hybridization on Affymetrix microarrays. We selected homogeneous populations of muscle fibers for expression profiling based upon the presence/absence of electron transport dysfunction caused by the somatic accumulation of mitochondrial DNA deletion mutations. The design of this experiment is limited by the source tissue which is individually identified cells harboring intracellular clonal expansions of mitochondrial DNA deletion mutations. These unique and rare cells were identified in rat Vastus lateralis tissue in an aged 36-month old F344xBN F1 hybrid rat by exhaustive serial sectioning and subsequent histological characterization. Unstained serial sections where isolated by LCM and the purified RNA was amplified by 2 rounds of RNA based transcription prior to fragmentation and hybridization on rat genome affymetrix chips. Two populations of cells were analyzed, Electron transport deficient and normal control cells from the same animal.

2013-03-01 | E-GEOD-35607 | biostudies-arrayexpress

Rewiring the Mitochondrial Electron Transport Chain Enhances Tumor Immunogenicity

Project description:Although tumor growth requires the mitochondrial electron transport chain (ETC), the relative contribution of Complex I (CI) and II (CII), the gatekeepers for initiating electron flow, remains unclear. Here, we report that loss of CII, but not CI, reduces melanoma tumor growth by increasing antigen presentation and T cell-mediated killing. This is driven by succinate-mediated transcriptional and epigenetic activation of major histocompatibility complex I-antigen processing and presentation (MHC-APP) genes that is independent of interferon signaling. Furthermore, knock-out of MCJ, to promote electron entry preferentially via CI, provides proof-of-concept of ETC rewiring to achieve anti-tumor responses without side effects associated with an overall reduction in mitochondrial respiration in non-cancer cells. Our results hold therapeutic potential for tumors that have reduced MHC-APP expression, a common mechanism of cancer immunoevasion.

2024-05-01 | GSE235311 | GEO

Mitochondrial electron transport chain is necessary for NLRP3 inflammasome activation

Project description:Mitochondrial electron transport chain is necessary for NLRP3 inflammasome activation

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Laboratory evolution of synthetic electron transport system variants reveals a larger metabolic respiratory system and its plasticity

Project description:We generated four strains of Escherichia coli K12 MG1655 with distinct proton motive force generation potential and performed the adaptive laboratory evolution of these strains to study how the system adapts to the loss of alternate electron transfer pathways of the Electron Transport System. RNA-Seq was performed to examine the underlying transcriptional rewiring.

2022-05-06 | GSE202144 | GEO

Short-term effect of Boost versus Radical doses of Intraoperative electron Radiotherapy in breast cancer tumor bed using high-throughput approaches

Project description:Importance: Intra-operative electron Radiation Therapy as a partial-breast single high dose radiotherapy, leads to decrease the local recurrence through tumor bed modification. Objective: This study designed to investigate short-term effect of the dose- dependent and -independent molecular mechanisms and biological pathway of tumor bed modification induced by Intra-operative electron Radiation Methods: Six random selected breast cancer patients entered into our study and all patients by referee to their pathological report were treated by doses of 12Gy as a Boost dose and 21Gy as a Radical dose and the samples were categorized into three groups which included: Margin Before irradiation, Margin After immediately irradiation and Margin 24 hours After irradiation. Resluts: Using mRNA-sequencing, ~6 Giga base clean data (20 Million Reads, 150 base pair) per individual sample and totally 125.3 million reads of transcriptome sequence were generated from the patient samples. Discussion: Appropriate Intra-operative electron Radiation Therapy short-term effects of molecular mechanisms in tumor bed seems to be dose-independent.

2018-08-30 | GSE119204 | GEO

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