MYLK (Myosin Light Chain Kinase)

These findings provide concrete molecular targets for antiangiogenic therapy and establish clinically actionable biomarkers for glioma patient stratification in the 3PM framework. The online version contains supplementary material available at 10.1007/s13167-025-00428-1.

In conclusion, TLS had a protective effect on human GBC, and its related genes, played a potential role in diagnosis, prognosis, immune infiltration, and metastasis of GBC. Our findings provided a new insight for the research on clinical biomarkers of GBC and development of its therapeutic targets.

We identified some differentially expressed genes relevant to oncogenic signaling and immunosuppressive tumor-associated macrophages. These findings provide novel insights into factors affecting prognosis in patients with residual disease after NAC for early-stage TNBC.

Binding efficiency of repurposed drugs was evaluated using molecular docking, molecular dynamics (MD) simulations, and MM-GBSA analysis. Our findings provide the potential therapeutic drugs and targets of prostate adenocarcinoma metastasis with possibilities for follow-up in vitro and in vivo validation.

Additionally, two benign variants in the FBN1 and MYLK genes, associated with thoracic aortic disease, were found. These findings emphasis the importance of genetic counseling and further research into genotype-phenotype correlations.

We successfully constructed MDPC with validated prognostic prediction value. This classification system provided clinicians with an effective tool to stratify PRAD patients, identifying high-risk individuals, recognizing patients prone to develop bone metastasis, and offering opportunities for early intervention to improve patients' prognosis.

Sunitinib is a receptor tyrosine kinase inhibitor used for the treatment of renal cell carcinoma and imatinib-resistant gastrointestinal stromal tumors...Moreover, pharmacological intervention of the cardiac myosin activator omecamtiv mecarbil (OM) or overexpression of MYLK3 significantly restored the expression of MYLK3 and reversed pathogenic phenotypes in sunitinib-treated iPSC-CMs. Nanoparticle delivery of OM effectively prevented sunitinib-induced cardiac dysfunction in mice. Our findings suggest that sunitinib-induced MYLK3 degradation causes the inhibition of the CAMK2-PLN-ATP2A2a signaling pathway and leads to sunitinib-induced arrhythmogenesis, and that MYLK3 can act as a novel cardioprotective target for sunitinib-induced cardiotoxicity.

The addition of the MYLK-specific inhibitor ML-7 reversed the effect of FOXP2 overexpression on the invasion and migration of EC cells. FOXP2 suppresses the proliferation, invasion, and migration of EC cells through the activation of MYLK.

Our results show that phosphorylation of CARMIL1 in the C-terminal domain highly influences actin cytoskeletal organization. It offers new insights on CARMIL1-mediated cellular functions, deepening our comprehension of its involvement in cytoskeletal dynamics.

These findings indicated that dietary FB1 negatively impacts the growth performance of juvenile grass carp, likely due to reduced digestive and absorptive capacities, elevated intestinal Sa and So levels, and disruption of intestinal structure integrity. This study filled the study gap on the toxicity of FB1 to the intestines of aquatic animals.

Importantly, we identified that cancer cell-derived MAMDC2 promotes MYLK expression in cancer-associated fibroblasts (CAFs) through paracrine signaling. Our findings suggest MAMDC2 may function as a stromal-associated regulator in MSS colorectal cancer with a high tumor stromal ratio (TSR).

MLCK inhibition disrupts myosin II activity, leading to unresolved replication stress, DNA damage, and activation of the p53-mediated apoptosis pathway. Our findings suggest that targeting MLCK offers a promising therapeutic strategy for MYC-driven cancers.