Nikolaos Patsoukis

RIAM regulates the cytoskeletal distribution and activation of PLC-gamma1 in T cells.

Selective effects of PD-1 on Akt and Ras pathways regulate molecular components of the cell cycle and inhibit T cell proliferation.

Runx1 and Runx3 are involved in the generation and function of highly suppressive IL-17-producing T regulatory cells.

PD-1 inhibits T cell proliferation by upregulating p27 and p15 and suppressing Cdc25A.

Rap1-interacting adapter molecule (RIAM) associates with the plasma membrane via a proximity detector.

PD-1 increases PTEN phosphatase activity while decreasing PTEN protein stability by inhibiting casein kinase 2.

The cyclin dependent kinase inhibitor (R)-roscovitine mediates selective suppression of alloreactive human T cells but preserves pathogen-specific and leukemia-specific effectors.

PD-1 alters T-cell metabolic reprogramming by inhibiting glycolysis and promoting lipolysis and fatty acid oxidation.

Clinical significance of T cell metabolic reprogramming in cancer.

The role of metabolic reprogramming in T cell fate and function.

Immunometabolic Regulations Mediated by Coinhibitory Receptors and Their Impact on T Cell Immune Responses.

The adaptor molecule RIAM integrates signaling events critical for integrin-mediated control of immune function and cancer progression.

Feeling stressed? It might be your T cells.

Publisher Correction: Feeling stressed? It might be your T cells.

Targeting T Cell Metabolism for Improvement of Cancer Immunotherapy.