Results 241 to 250 of about 30,081,745 (303)

Uhrf1‐Mediated PKM2 Degradation via Ubiquitination Alleviates Inflammation and Pyroptosis in Inflammatory Bowel Disease

open access: yesAdvanced Science, EarlyView.
Uhrf1‐mediated PKM2 ubiquitination and degradation repressed the nuclear translocation of PKM2, and EPT served as a molecular glue capable of targeting the Uhrf1–PKM2 complex to alleviate the IBD course, suggesting that the Uhrf1–PKM2 axis was a previously unrecognized strategy for treating IBD.
Juan Zhang   +9 more
wiley   +1 more source

Macrophage RSAD2 Couples mtDNA Synthesis With a Self‐Amplifying Inflammatory Circuit to Orchestrate Tissue Repair

open access: yesAdvanced Science, EarlyView.
Macrophage RSAD2 dually regulates CMPK2—the rate‐limiting enzyme for mitochondrial DNA synthesis—by suppressing its ubiquitination and promoting its phosphorylation via Csnk2a2 recruitment. This amplifies mtDNA production, which simultaneously activates a cGAS‐STING‐IRF3‐RSAD2 feedforward loop and the NLRP3 inflammasome, driving a self‐sustaining ...
Haomiao Yuan   +16 more
wiley   +1 more source

Discovery and Optimization of AMT‐676, a CDH17‐Targeting ADC for the Treatment of Advanced Gastrointestinal Cancers

open access: yesAdvanced Science, EarlyView.
AMT‐676 is a novel antibody‐drug conjugate targeting CDH17, an adhesion molecule uniquely exposed on gastrointestinal tumor surfaces. Engineered with an optimized exatecan payload, it demonstrates profound tumor regression and a robust bystander effect across diverse preclinical models.
Ying‐nan Wang   +21 more
wiley   +1 more source

Epigenetic Reactivation of TNFRSF19 Suppresses Mitophagy and Sensitizes Triple‐Negative Breast Cancer to Doxorubicin

open access: yesAdvanced Science, EarlyView.
TNFRSF19 is an epigenetically silenced regulator of mitophagy in triple‐negative breast cancer. TNFRSF19 deficiency activates the TGFBR1–SMAD3–PINK1 axis to promote mitophagy and confer doxorubicin resistance, whereas decitabine‐mediated restoration of TNFRSF19 suppresses mitophagy and enhances doxorubicin sensitivity, revealing a targetable epigenetic–
Shiyang Liu   +7 more
wiley   +1 more source

Interleukin‐1α Mediates Pancreatic Fibroblast Activation, Regulates Immune Cell Recruitment and Fibrosis in Acute and Chronic Pancreatitis

open access: yesAdvanced Science, EarlyView.
During pancreatitis, IL‐1α is released from necrotic acinar cells. In response to IL‐1α, pancreatic fibroblasts release chemokines and cytokines that regulate the recruitment of immune cells to the damaged organ. Furthermore, IL‐1α primes fibroblasts, resulting in increased tissue fibrosis during chronic pancreatitis.
Hala Mazloum   +13 more
wiley   +1 more source

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