Results 221 to 230 of about 14,389,011 (296)

An Aggregation‐Induced Polymerization Poly(Disulfide)‐Drug Nanoplatform for Autoimmune Uveitis Therapy via Inhibiting the cGAS‐STING Pathway

open access: yesAdvanced Science, EarlyView.
A cationic poly(disulfide)‐drug nanoplatform (LA/DexP) was developed to treat experimental autoimmune uveitis (EAU). With potent blood‐retinal barrier penetrability, LA/DexP releases DSP in response to high ROS and scavenges cfDNA to inhibit the cGAS‐STING signaling pathway.
Yuelan Wu   +12 more
wiley   +1 more source

AI Designed Conformation Locking Peptides Target STING to Restore Diabetic Wound Healing

open access: yesAdvanced Science, EarlyView.
A generative AI pipeline identifies SCP‐1, a conformation‐locking peptide that stabilizes inactive STING. Incorporated into a dual‐responsive hydrogel for localized, MMP‐9‐triggered release, SCP‐1 suppresses inflammation, promotes reparative macrophage polarization, and accelerates diabetic wound healing.
Xinyu Li   +8 more
wiley   +1 more source

Whole-body irradiation causes long-term impairments in the maintenance and function of naïve CD4 T cells specific for self- and non-self-antigens. [PDF]

open access: yesJ Immunol
Kannan SK   +12 more
europepmc   +1 more source

A Personalized Haplotype‐Resolved Near‐Gapless Genome Framework for Somatic Variant Discovery in Hepatocellular Carcinoma

open access: yesAdvanced Science, EarlyView.
A patient‐specific, haplotype‐resolved genome framework improves detection and interpretation of somatic variants in hepatocellular carcinoma. Using multi‐platform sequencing, the personalized assembly resolves complex regions including centromeres and MHC/HLA loci, enhances structural variant discovery, and links regulatory alterations to allele ...
Jiazheng Lin   +17 more
wiley   +1 more source

CD4+ T Cells Mediate MHC-Deficient Tumor Rejection and Endothelial Cell Reprogramming. [PDF]

open access: yesCancer Immunol Res
Kim SI   +12 more
europepmc   +1 more source

UFL1‐Mediated UFMylation of ENO1 Restrains Aerobic Glycolysis and Colorectal Cancer Progression

open access: yesAdvanced Science, EarlyView.
UFMylation restrains aerobic glycolysis and colorectal cancer progression by modifying the glycolytic enzyme ENO1. Pharmacological enhancement of the UFL1–ENO1 interaction by the FDA‐approved antibiotic torezolid promotes ENO1 UFMylation, suppresses tumor metabolism, and sensitizes colorectal cancer to chemotherapy, revealing an actionable metabolic ...
Xiuqing Ma   +14 more
wiley   +1 more source

Fingolimod increases cellular resistance to HIV-1 infection and limits viral reservoir size in peripheral CD4+ T-cells. [PDF]

open access: yesPLoS Pathog
Moraga E   +12 more
europepmc   +1 more source

Targeting Tex10 Overcomes Oxaliplatin Resistance by Competitively Disrupting the Non‐Canonical BAF Complex in Colorectal Cancer

open access: yesAdvanced Science, EarlyView.
This study reveals that Tex10 drives oxaliplatin resistance in colorectal cancer by competitively binding BRD9 to disrupt the ncBAF complex, thereby suppressing AMBRA1 transcription and ULK1‐mediated autophagy. Gemcitabine is identified as a direct Tex10 inhibitor that restores autophagy and overcomes resistance.
Ping Xu   +9 more
wiley   +1 more source

CD4+ T Cells Sensitize Quasimesenchymal Breast Tumors Lacking CD73 to Anti-CTLA4 Immune Checkpoint Blockade Therapy. [PDF]

open access: yesCancer Res Commun
Chandraganti S   +16 more
europepmc   +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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