Results 201 to 210 of about 660,583 (250)

A Single‐Amino‐Acid Ligand for LAT1: A Minimalist and Modular Platform for Lysosome‐Targeted Degradation of Membrane Proteins

open access: yesAdvanced Science, EarlyView.
LA‐LYTAC repurposes the cancer‐enriched amino acid transporter LAT1 as a lysosomal trafficking receptor for targeted membrane‐protein degradation. A single phenylalanine‐derived ligand, modularly linked to antibodies or small‐molecule binders, recruits PD‐L1, EGFR, or integrins to LAT1, triggering transporter‐mediated internalization, lysosomal ...
Liquan Zhu   +12 more
wiley   +1 more source

Precise individual measures of inhibitory control. [PDF]

open access: yesNat Hum Behav
Lee HJ   +7 more
europepmc   +1 more source

BCG HSP70 Reprograms Macrophages via Central Trained Immunity to Suppress Prostate Cancer

open access: yesAdvanced Science, EarlyView.
BCG‐derived HSP70 (Dnak) safely induces central trained immunity via epigenetic, metabolic, and O‐GlcNAcylation reprogramming of bone marrow progenitors, driving tumor‐associated macrophages toward an M1‐like phenotype to suppress prostate cancer. ABSTRACT Trained immunity offers a promising yet clinically challenging strategy for cancer immunotherapy,
Peng Liu   +12 more
wiley   +1 more source

Tumor‐Derived Exosomal circAP2B1 Induces M2 Macrophage Polarization by Enhancing Mitochondrial Homeostasis to Promote Esophageal Squamous Cell Carcinoma Progression

open access: yesAdvanced Science, EarlyView.
ESCC‐derived exosomal circAP2B1 promotes tumor progression by reprogramming mitochondrial metabolism via the ESRRA/KPNA1/MFN2 axis to induce M2 polarization of macrophages. ABSTRACT Esophageal squamous cell carcinoma (ESCC) remodels the immunosuppressive tumor microenvironment via exosome‐mediated intercellular communication.
Yiru Wang   +5 more
wiley   +1 more source

Crosstalk Between CTSB+ Glioblastoma Cells and S100A10+ Macrophages: A Self‐Reinforcing Circuit Promotes Immune Evasion and Limits Response to Immunotherapy

open access: yesAdvanced Science, EarlyView.
In glioblastoma, M2‐polarized macrophages secrete IL‐6, which activates STAT3 signaling in tumor cells to upregulate CTSB. Tumor‐derived CTSB binds the C‐terminus of macrophage S100A10, reinforcing M2 polarization and further IL‐6 secretion, thereby establishing a feedforward IL‐6/STAT3/CTSB/S100A10 loop. This cascade drives tumor growth, invasion, and
Hao Zhang   +11 more
wiley   +1 more source

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