Macrophage SUCLA2 coupled glutaminolysis manipulates obesity through AMPK

NIAID Data Ecosystem2026-05-02 收录

数据链接：

https://figshare.com/articles/dataset/Macrophage_SUCLA2_coupled_glutaminolysis_manipulates_obesity_through_AMPK/28303577 数据链接链接失效反馈

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The data contains all raw data, images and blots.

创建时间：

2025-02-19

FMDV activated glycolysis and hijacked HK2 to inhibit innate immunity and promote viral replication

病毒学

免疫代谢

FMD seriously restricts the healthy development of global animal husbandry, and the unclear pathogenic mechanism of FMDV leads to the difficulty of FMD prevention and purification. Glycolytic remodeli

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免疫代谢

免疫逃逸机制

Immunoediting sculpts immunogenicity and thwarts host anti-tumor responses in tumor cells during tumorigenesis; however, it remains unknown whether metabolic programming of tumor cells can be guided b

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免疫代谢

胰岛素抵抗机制

Chronic Inflammation is a key link between obesity and insulin resistance. We previously showed that two nutrient sensors AMP-activated protein kinase (AMPK) and SIRT1 interact to regulate macrophage

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DataSheet_1_Low-density lipoprotein balances T cell metabolism and enhances response to anti-PD-1 blockade in a HCT116 spheroid model.zip

免疫代谢

PD-1联合治疗

IntroductionThe discovery of immune checkpoints and the development of their specific inhibitors was acclaimed as a major breakthrough in cancer therapy. However, only a limited patient cohort shows s

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CD1d-restricted NKT cell function prevents insulin resistance in lean mice, and is regulated by adipocytes and is regulated by adipocytes

免疫代谢

胰岛素抵抗机制

CD1d-restricted NKT cell function prevents insulin resistance in lean mice, and is regulated by adipocytes and is regulated by adipocytes

ChEBI2012-08-06 更新20