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Deletion of epithelial HKDC1 decelerates cellular proliferation and impairs mitochondrial function of tumorous epithelial cells thereby protecting from intestinal carcinogenesis
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作者 Lea Järke Saskia Weber-Stiehl +13 位作者 Kensuke Shima Karlis Arturs Moors Jerome Genth Fenja Amrei Schuran Lena Best Markus Tschurtschenthaler Burkhardt Flemer Silke Lüschen Christoph Röcken andreas tholey Christoph Kaleta Jan Rupp Philip Rosenstiel Felix Sommer 《Cancer Communications》 2025年第7期722-727,共6页
A metabolic switch favoring glycolysis over aerobic oxidative phosphorylation,termed the“Warburg effect”,is a hallmark of cancer cells[1].Hexokinase(HK)catalyzes the first and irreversible step of glycolysis,thereby... A metabolic switch favoring glycolysis over aerobic oxidative phosphorylation,termed the“Warburg effect”,is a hallmark of cancer cells[1].Hexokinase(HK)catalyzes the first and irreversible step of glycolysis,thereby limiting overall glycolytic activity.Mammals encode five HK family members:HK1-4 and HKDC1(HK domain containing 1).HKDC1 has an exceptionally low glucose affinity and,therefore,low hexokinase activity under physiological conditions[2],raising questions about its function.A recent study indicated that HKDC1 functions as a glucose sensor within the tumor microenvironment[3],and its dysregulated expression has been associated with chronic inflammation[4]and various cancers[5]. 展开更多
关键词 metabolic switch aerobic oxidative phosphorylationtermed mitochondrial function HKDC intestinal carcinogenesis epithelial cells cellular proliferation Warburg effect
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