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Laboratory of Mitochondrial Biology and Metabolism, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, MD, USA.

Although lipid-derived acetyl-coenzyme A (CoA) is a major carbon source for histone acetylation, the contribution of fatty acid β-oxidation (FAO) to this process remains poorly characterized. To investigate this, we generated mitochondrial acetyl-CoA acetyltransferase 1 (ACAT1, distal FAO enzyme) knockout macrophages. C-carbon tracing confirmed reduced FA-derived carbon incorporation into histone H3, and RNA sequencing identified diminished interferon-stimulated gene expression in the absence of ACAT1.

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Background: We developed a prognostic model to evaluate the overall survival (OS) and progression-free survival (PFS) of patients with unresectable hepatocellular carcinoma (u-HCC) treated with Hepatic arterial infusion chemotherapy of infusion oxaliplatin, fluorouracil and leucovorin (FOLFOX-HAIC).

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School of Environment and Energy, Peking University Shenzhen Graduate School, University Town, Xili, Nanshan District, 518055, Shenzhen, China.

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Programmed neurite degeneration in human central nervous system neurons driven by changes in NAD metabolism.

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In vitro Toxicology and Biomedicine, Dept. inaugurated by the Doerenkamp-Zbinden foundation, University of Konstanz, 78457, Konstanz, Germany.

Neurite degeneration (ND) precedes cell death in many neurodegenerative diseases. However, it remains unclear how this compartmentalized cell death process is orchestrated in the central nervous system (CNS). The establishment of a CNS axotomy model (using modified 3D LUHMES cultures) allowed us to study metabolic control of ND in human midbrain-derived neurons without the use of toxicants or other direct disturbance of cellular metabolism.

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Targeting the mevalonate pathway potentiates NUAK1 inhibition-induced immunogenic cell death and antitumor immunity.

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The induction of immunogenic cell death (ICD) impedes tumor progression via both tumor cell-intrinsic and -extrinsic mechanisms, representing a robust therapeutic strategy. However, ICD-targeted therapy remains to be explored and optimized. Through kinome-wide CRISPR-Cas9 screen, NUAK family SNF1-like kinase 1 (NUAK1) is identified as a potential target.

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