Results 181 to 190 of about 5,491 (298)

LMO7 Suppresses Tumor‐Associated Macrophage Phagocytosis of Tumor Cells Through Degradation of LRP1

open access: yesAdvanced Science, EarlyView.
LMO7 in tumor‐associated macrophages suppresses phagocytosis of tumor cells and limits cytotoxic T lymphocytes infiltration, fostering tumor progression. Mechanistically, LMO7 mediates the ubiquitination and degradation of the phagocytic receptor LRP1, impairing its ability to engulf tumor cells and driving macrophages toward an antitumor phenotype ...
Mengkai Li   +12 more
wiley   +1 more source

CDK4/6 Inhibition Induces CD8+ T Cell Antitumor Immunity via MIF‐Induced Functional Orchestration of Tumor‐Associated Macrophages

open access: yesAdvanced Science, EarlyView.
CDK4/6 inhibition promotes CD8+ T cell expansion through tumor‐macrophage crosstalk by activating HIF‐1α and enhancing MIF‐CD44/CD74 signaling. This reprograms TAMs to boost MHC‐I antigen presentation, and CDK4/6 inhibitor‐trained M1 TAM supernatant therapy synergizes with low‐dose PD‐1 blockade to restore antitumor immunity.
Lin He   +17 more
wiley   +1 more source

Hedge Fund Performance Persistence: A Multinomial Approach Application to Asian Hedge Funds

open access: green, 2007
Malick O. Sy   +3 more
openalex   +1 more source

Aberrant SUMOylation Restricts the Targetable Cancer Immunopeptidome

open access: yesAdvanced Science, EarlyView.
Pharmacological SUMOylation inhibition (SUMOi) counteracts tumor immune evasion by unmasking an immunogenic HLA‐I peptide and neoepitope repertoire. By restoring HLA‐I ligand availability through increased antigen processing and presentation, enhanced proteasomal cleavage, and modulated TAP1 peptide affinity, SUMOi boosts tumor immunogenicity ...
Uta M. Demel   +19 more
wiley   +1 more source

Precision Editing of NLRS Improves Effector Recognition for Enhanced Disease Resistance

open access: yesAdvanced Science, EarlyView.
Precision engineering of plant NLR immune receptors enables rational design of enhanced pathogen resistance through mismatched pairing, domain swapping, and targeted mutagenesis. These approaches achieve multi‐fold expansion in recognition breadth while minimizing autoimmunity risks and fitness penalties.
Vinit Kumar   +7 more
wiley   +1 more source

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