DOK1 (Docking Protein 1)

The reciprocal regulation between TNF-α and autophagy may contribute to tumor progression in OSCC.

Using proteomics approaches, we uncovered Cofilin as a component of the phosphorylated integrin-Dok1 complex and linked this axis to effective invadopodia formation, a process supporting breast cancer invasion. These data further implicate dynamic modulation of integrin β1 phosphorylation at NPxY sites at different stages of metastatic dissemination.

Through PI3K (phosphatidylin-ositol-3-kinase)/AKT (protein kinase B)/GSK3β (glycogen synthase kinase 3 beta) signaling, DOK1 may control the progression of ccRCC. DOK1 has the potential to serve as a valuable biomarker and target for treatment in ccRCC through its regulation of PI3K/AKT/GSK3β signaling to promote ccRCC progression.

Altogether we demonstrate here a novel aspect of the negative regulation by DOK1 and DOK2 proteins in CD8+ T cells. Indeed, our results allow us to conclude that DOK1 and DOK2 have an inhibitory role following long term T cell stimulations.

Background: Mosunetuzumab (Mosun) is a CD20xCD3 T-cell engaging bispecific monoclonal antibody that redirects T cells to eliminate malignant B cells... Baseline biomarker data reveal an important role for CD4 T cells in Mosun response and suggest that higher prevalence of CD4s may be a factor in the improved response to Mosun in indolent NHL. Our data specifically point to Tfh cells as potential drivers of response, although the mechanisms by which Tfh contributes to response, as well as the implications for other bispecifics, requires more exploration.

We proposed a prediction mode which can effectively identify high-risk LUAD patients and found three novel genes closely correlated with PC tumor infiltration.

Recent studies have also demonstrated the potential role of the kinase in various cancers, including gastric and colorectal cancers and platinum resistance in ovarian cancer. This review discusses the advancements made in SRMS-related biology to date and the path to understanding the cellular and physiological significance of the kinase.

DOK1, in turn, induced the inactivation of MEK/ERK signaling, forming the lncRNA-NEF/DOK1/MEK/ERK regulatory axis to mediate oxaliplatin resistance in CRC. Collectively, our work reveals the critical function of lncRNA-NEF in mediating the oxaliplatin chemotherapy resistance in CRC, and provides a promising therapeutic strategy for CRC patients with oxaliplatin resistance.