Mitochondrial dihydrolipoamide dehydrogenase (mtLPD1) is a central enzyme in primary carbon metabolism, since its function is required to drive four multienzymes involved in photorespiration, the tricarboxylic acid (TCA) cycle, and the degradation of branched-chain amino acids. However, in illuminated, photosynthesizing tissue a vast amount of mtLPD1 is necessary for glycine decarboxylase (GDC), the key enzyme of photorespiration. In light of the shared role, the functional characterization of mtLPD1 is necessary to understand how the three pathways might interact under different environmental scenarios. This includes the determination of the biochemical properties and all potential regulatory mechanisms, respectively. With regards to the latter, regulation can occur through multiple levels including effector molecules, cofactor availability, or posttranslational modifications (PTM), which in turn decrease or increase the activity of each enzymatic reaction. Gaining a comprehensive overview on all these aspects would ultimately facilitate the interpretation of the metabolic interplay of the pathways within the whole subcellular network or even function as a proof of concept for genetic engineering approaches. Here, we describe the typical workflow how to clone, express, and purify plant mtLPD1 for biochemical characterization and how to analyze potential redox regulatory mechanisms in vitro and in planta.
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http://dx.doi.org/10.1007/978-1-0716-3802-6_5 | DOI Listing |
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December 2024
State Key Laboratory of Systems Medicine for Cancer, Center for Single-Cell Omics, School of Public Health, Shanghai Jiao Tong University School of Medicine, Shanghai, 200025, P. R. China.
Cuproptosis, a newly defined cell death process, represents a novel modality with significant therapeutic potential in cancer treatment. Nevertheless, the modest concentration and transient half-life of copper ions in the bloodstream constrain their efficient delivery into tumor cells. In this study, a copper-based prussian blue nanostructure loaded with serine metabolic inhibitor (NCT-503@Cu-HMPB) is constructed for selectively inducing cuproptosis combined with disrupting serine metabolism.
View Article and Find Full Text PDFActa Biomater
December 2024
School of Life Sciences, Tianjin University, Tianjin, 300072, PR China; Tianjin Key Laboratory of Function and Application of Biological Macromolecular Structures, School of Life Sciences, Tianjin University, Tianjin, 300072, PR China. Electronic address:
Neurol Neuroimmunol Neuroinflamm
January 2025
From the Department of Immunology (A.J.), CHU Montpellier; Institut de Génomique Fonctionnelle (A.J., J.E.-B., G.T., J.D.), Université de Montpellier, CNRS, INSERM; and Department of Neurology (G.T.), CHU Montpellier, France.
Objectives: Dihydrolipoamide S-acetyltransferase (DLAT), the E2 component of the mitochondrial pyruvate dehydrogenase complex (PDC-E2), has recently been suggested to be a biomarker of chronic inflammatory demyelinating polyneuropathy (CIDP). It was particularly associated with sensory variants of CIDP. Antimitochondrial antibodies are important for the diagnosis of primary biliary cholangitis, but insofar, only 2 studies have reported an association with CIDP.
View Article and Find Full Text PDFAdv Healthc Mater
November 2024
Department of Radiology, Beijing Friendship Hospital, Capital Medical University, 95 Yong'an Rd., Xicheng District, Beijing, 100050, China.
The co-loading of radionuclides and small-molecule chemotherapeutic drugs as nanotheranostic platforms using nanozymes holds tremendous potential for imaging-guided synergistic therapy. This study presents such nanotheranostic platform (Lu-MFeCu@Tan) via co-assembling Lu radionuclide and tanshinone (Tan) into Fe/Cu dual-metal nanozyme (MFeCu). This platform simultaneously enables single-photon emission computed tomography (SPECT) imaging and a quadruple-synergistic tumor therapy approach, including internal radioisotope therapy (RIT), catalysis therapy, chemotherapy, and MFeCu-mediated ferroptosis and cuproptosis therapy.
View Article and Find Full Text PDFInt J Mol Sci
October 2024
Department of Cell and Cancer Biology, College of Medicine and Life Sciences, The University of Toledo, Toledo, OH 43614, USA.
Copper is crucial for many physiological processes across mammalian cells, including energy metabolism, neurotransmitter synthesis, and antioxidant defense mechanisms. However, excessive copper levels can lead to cellular toxicity and "cuproptosis", a form of programmed cell death characterized by the accumulation of copper within mitochondria. Tumor cells are less sensitive to this toxicity than normal cells, the mechanism for which remains unclear.
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