Results 201 to 210 of about 114,506,481 (291)

MAM‐Localized MANF Counteracts Microinflammatory Stress to Attenuate Mitochondrial Dysfunction and Cataractogenesis in High Myopia

open access: yesAdvanced Science, EarlyView.
Chronic microinflammation in high myopia suppresses MANF in lens epithelial cells. MANF normally resides within MAMs and promotes ubiquitin‐mediated degradation of the ER Ca2+ pump SERCA2. MANF loss causes pathological SERCA2 accumulation, MAM hyperassembly, and disrupted ER‐to‐mitochondria Ca2+ transfer, leading to mitochondrial failure, oxidative ...
Xin Liu   +8 more
wiley   +1 more source

PRMT5‐Dependent Stabilization of VPS34 Orchestrates Copper Trafficking to Shield Cancer Cells from Cuproptosis and Radiotherapy

open access: yesAdvanced Science, EarlyView.
Radioresistance arises partly from tumor cells evading cuproptosis via unknown defenses. This study reveals that the PRMT5‐VPS34 axis acts as a radiation‐activated anticuproptotic mechanism: PRMT5 methylates VPS34 at Arg174, recruiting USP10 to remove K48‐linked ubiquitination and prevent degradation.
Wei Chen   +17 more
wiley   +1 more source

Targeting the ATX‐LPA Axis Overcomes TKI Resistance and Immunosuppression in Renal Cell Carcinoma via Dual Inhibition of AKT/mTOR and TBK1/IRF3 Pathways

open access: yesAdvanced Science, EarlyView.
ABSTRACT Background Therapeutic resistance limits durable survival in advanced/metastatic renal cell carcinoma (RCC) treated with first‐line tyrosine kinase inhibitor (TKI) plus immune checkpoint inhibitor (ICI). We sought to define key resistance drivers and actionable targets.
Jinchen Luo   +16 more
wiley   +1 more source

S100A8/A9‐High Macrophages Activate Intestinal Fibroblasts via mCCL6/hCCL15‐CCR1 Axis to Drive Intestinal Fibrosis in Crohn's Disease

open access: yesAdvanced Science, EarlyView.
S100A8/A9‐high macrophages are markedly enriched in the stenotic intestinal tissue of patients with Crohn's disease. These profibrotic macrophages secrete mCCL6 in a STAT3‐dependent manner. mCCL6 and its human ortholog hCCL15 activate fibroblasts via the CCR1 receptor, thereby driving excessive collagen deposition.
Shu Wang   +12 more
wiley   +1 more source

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