Results 151 to 160 of about 882,801 (245)

Tumor‐Derived Exosomes Deliver Membrane‐Bound Fgl2 to Activate FcγRIIB‐Mediated Immunosuppression in Myeloid‐Derived Suppressor Cells

open access: yesAdvanced Science, EarlyView.
This study reveals that the Fgl2‐FcγRIIB signaling axis is a key mechanism by which MDSCs mediate tumor immune evasion. Tumor‐derived exosomes systemically activate MDSCs via this pathway, positioning this axis as a promising broad‐spectrum target for cancer immunotherapy.
Fenglin Lin   +12 more
wiley   +1 more source

Leveraging Artificial Intelligence and Large Language Models for Cancer Immunotherapy

open access: yesAdvanced Science, EarlyView.
Cancer immunotherapy faces challenges in predicting treatment responses and understanding resistance mechanisms. Artificial intelligence (AI) and machine learning (ML) offer powerful solutions for cancer immunotherapy in patient stratification, biomarker discovery, treatment strategy optimization, and foundation model development.
Xinchao Wu   +4 more
wiley   +1 more source

Selective Inhibition of Integrin β3 Topology Provides a Safer Antithrombotic Strategy

open access: yesAdvanced Science, EarlyView.
Current integrin αIIbβ3 inhibitors effectively reduce thrombosis but also increase bleeding risk. During thrombosis, high shear blood flow can directly activate the integrin αIIbβ3 via a distinct topological change in the β3 transmembrane domain, independent of hemostatic platelet signaling.
Joonha Lee   +11 more
wiley   +1 more source

Cars2‐Mediated Cysteine Catabolism Drives Brown Fat Development and Thermogenesis Through Persulfidating EBF2

open access: yesAdvanced Science, EarlyView.
We demonstrate that Cars2, a cysteine catabolic enzyme in mouse iBAT, is critical for cold tolerance and brown adipocyte differentiation. Through its CPERS activity, Cars2 produces CysSSH/H2S to induce EBF2 persulfidation, promoting its interaction with PPARγ and BRG1 to enhance thermogenic gene expression.
Xin Peng   +8 more
wiley   +1 more source

Disruption of the SNRPF–DDX24–E2F4 Feedback Loop Uncouples Splicing and Transcriptional Regulation to Suppress Ovarian Cancer Progression

open access: yesAdvanced Science, EarlyView.
This study identifies SNRPF as a critical oncogenic driver in ovarian cancer. By regulating a self‐sustaining SNRPF–DDX24–E2F4 feedback loop through intron retention and nonsense‐mediated decay, SNRPF couples RNA splicing with transcriptional regulation to promote tumor progression.
Yingwei Li   +4 more
wiley   +1 more source

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