SKI (SKI Proto-Oncogene)

Furthermore, transduction of SKImut2/3 in preclinical models of both T cell receptor (TCR) and CAR-T cell therapies prolonged survival in mice bearing xenografted liquid or solid tumors. Collectively, these findings establish SKImut2/3 expression as a promising therapeutic strategy to enhance both the durability and effector function of T cell-based cancer immunotherapies.

These data indicate SKI involvement in p21 transcription and that SKI-p21 signaling causes cell cycle arrest in G1, suppressing intrahepatic CC cell growth. Therefore, SKI may be a potential therapeutic target for intrahepatic CC.

Instead we show that it is predominantly activated via Activin A-dependent receptor clustering, which induces its auto-activation, leading to downstream SMAD1/5 phosphorylation. The relevance of this for the pathogenesis of FOP and DIPG will be discussed.

Collectively, the results of the present study demonstrated that miR-195-5p suppressed HA progression and its effects were mediated via SKI. Therefore, the miR-195-5p/SKI axis may represent a novel therapeutic target for HA.

We further revealed that induced SKI expression in already differentiated pathogenic Th17 cells reduced the maintenance of Th17 program and ameliorated EAE in an adoptive T cell transfer model. Therefore, our study provides valuable insights of targeting SKI to modulate pathogenic Th17 cell function and treat Th17-related diseases.