Results 161 to 170 of about 62,945 (257)

Cold adaptation of a thermostable Enzyme, 3-isopropylmalate dehydrogenase

open access: yesCold adaptation of a thermostable Enzyme, 3-isopropylmalate dehydrogenase
2000 【要旨】
openaire  

Mitochondrial Carrier SLC25A13 Drives Ferroptosis Resistance and Immune Evasion via a STAT3–IFI6 Circuit in Breast Cancer

open access: yesAdvanced Science, EarlyView.
SLC25A13 is identified as an immunometabolic driver of triple‐negative breast cancer that sustains ferroptosis resistance and immune evasion through a STAT3–IFI6 circuit. Pharmacologic degradation of SLC25A13 restores ferroptosis sensitivity and enhances anti‐PD‐1 efficacy, highlighting a strategy to convert immune‐cold tumors into immunotherapy ...
Yingze Zhu   +8 more
wiley   +1 more source

How Advanced Artificial Intelligence Technologies Shape Drug–Drug and Drug–Target Interaction Modeling

open access: yesAdvanced Science, EarlyView.
This review explores the convergence of artificial intelligence technologies in modeling drug–drug and drug–target interactions. By evaluating advanced feature engineering, architectural innovations, and learning paradigms reveals shared evolutionary trends and critical challenges, such as cold‐start settings and shortcut learning.
Xin Sun, Tong Wang
wiley   +1 more source

A Non‐Canonical Role of SMAD4 in Regulating 3D Genome Architecture to Inhibit Lung Squamous Cell Carcinoma Development

open access: yesAdvanced Science, EarlyView.
SMAD4 is identified as a guardian of 3D genome architecture in lung squamous cell carcinoma. Loss of SMAD4 unleashes EP300 at chromatin loop anchors, strengthening enhancer–promoter looping and H3K27ac at the SOX2 locus to drive aberrant SOX2 activation and tumor cell proliferation.
Qian Tang   +33 more
wiley   +1 more source

Targeting KDM3B Elicits Anti‐tumor Immunity by Alleviating SHP1–mediated STING Suppression in Triple–Negative Breast Cancer

open access: yesAdvanced Science, EarlyView.
P3FI–90 treatment targets KDM3B, reshapes the epigenetic landscape, and suppresses SHP1 expression, thereby activating STING–TBK1–IRF3–type I IFN signaling pathway. Consequently, CD8+ T cells are recruited to the tumor site and activated to produce IFN–γ and GZMB, leading to the killing of TNBC cells.
Xiaolong Wang   +8 more
wiley   +1 more source

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