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Updated: Jan 7, 2026

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ジネセノシド派生体AD-1は,AMPK/mTOR-グリコリシス経路経由で腫瘍関連マクロファージの分極化を再プログラムすることによって,大腸炎に関連した大腸癌の進行を抑制する

Yuan Fu1, Jinfang Zhang1, Xizhu Fang2

  • 1Immunology Biology Key Laboratory, Yanbian University, Yanji 133002, China; Key Laboratory of Natural Medicines of the Changbai Mountain, Ministry of Education, Yanbian University, Yanji 133002, China; Department of Immunology and Pathogenic Biology, College of Medicine, Yanbian University, Yanji 133002, China.

Bioorganic chemistry
|January 3, 2026
PubMed
まとめ

No abstract available in PubMed .

キーワード:
AMPK/mTORシグナリング経路大腸炎に関連した結腸直腸がんジンゼノシド誘導体AD-1グライコリシス腫瘍に関連したマクロファージの偏化

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The mammalian target of rapamycin or mTOR protein was discovered in 1994 due to its direct interaction with rapamycin. The protein gets its name from a yeast homolog called TOR. The mTOR protein complex in mammalian cells plays a major role in balancing anabolic processes such as the synthesis of proteins, lipids, and nucleotides and catabolic processes, such as autophagy in response to environmental cues, such as availability of nutrients and growth factors.
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