Results 211 to 220 of about 2,044,691 (300)

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

The Cancer Cell Metabolic Reprogramming Remodels the Tumor Microenvironment: Molecular Mechanisms and Therapeutic Strategies

open access: yesAdvanced Science, EarlyView.
This review elucidates how cancer cell metabolic reprogramming—across glucose, lipid, amino acid, and nucleotide pathways—remodels the tumor microenvironment to suppress anti‐tumor immunity and promote immune escape. Targeting these metabolic axes offers promising strategies to overcome immunotherapy resistance and enhance cancer treatment.
Guoqing Xiang   +5 more
wiley   +1 more source

The Adipose‐Sympathetic Nerve Crosstalk: FSTL1 as an Adipocyte‐Derived Neurotrophic Factor for WAT Browning

open access: yesAdvanced Science, EarlyView.
As a novel adipose‐derived neurotrophic factor, Follistatin‐like 1 is endocytosed by sympathetic neurons primarily via tropomyosin‐related kinase B. This process promotes sympathetic innervation in adipose tissue and norepinephrine release, leading to white adipose tissue browning, enhanced thermogenesis, and anti‐obesity effects in mice.
Xiao‐Wei Jia   +13 more
wiley   +1 more source

AARS1‐Mediated H3K27 Lactylation Rewires Glycolysis to Sustain Aggressive and Recurrent Bladder Cancer

open access: yesAdvanced Science, EarlyView.
AARS1 drives PI3K–AKT–mTOR‐dependent glycolysis in bladder cancer, promoting lactate accumulation, increased lactylation, H3K27la enrichment at the HK2 promoter, and HK2 transcription. HK2 reinforces glycolysis, sustaining a metabolic–epigenetic program associated with tumor progression, recurrence, and metastasis.
Qin Yuan   +13 more
wiley   +1 more source

Cancer‐Associated Fibroblasts Promote Glucose Metabolic Reprogramming and Progression of Triple‐Negative Breast Cancer via Exosomal circFAD104‐Mediated Intercellular Communication

open access: yesAdvanced Science, EarlyView.
CAF‐derived exosomes deliver circFAD104 into TNBC cells, where it acts as a molecular scaffold that bridges the E3 ligase MARCHF8 and PGM1, promoting MARCHF8‐mediated K48‐linked ubiquitination and proteasomal degradation of PGM1. Loss of PGM1 redirects glucose‐phosphate flux from glycogen synthesis toward glycolysis, thereby driving stemness, EMT, and ...
Lei Wang   +16 more
wiley   +1 more source

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