MYLK (Myosin Light Chain Kinase)

Mechanistically, AGTPBP1 activated the MAPK/ERK pathway through elevated ERK1/2 phosphorylation, and pharmacological inhibition of ERK phosphorylation using PD98059 abrogated both ERK phosphorylation and AGTPBP1-driven phenotypes, establishing ERK as an essential mediator...Notably, ERK signaling modulated MYLK activity (phosphorylated MYLK) without altering MYLK expression, indicating that AGTPBP1 regulates MYLK at the transcriptional level, whereas ERK controls its post-translational activity. Collectively, AGTPBP1 promotes PDAC progression through a dual mechanism involving ERK-dependent proliferative signaling and ERK-independent MYLK upregulation, positioning both molecules as potential therapeutic targets.

Furthermore, RBA significantly inhibited the redistribution of tight junctions by activating the nuclear factor-kappa B (NF-κB)-myosin light-chain kinase signaling pathway. This study indicates that RBA regulates tight junction protein localization and intestinal permeability by modulating the NF-κB pathway, thereby suggesting its potential as a nutraceutical for treating IBD.

This dual-model approach improved the reliability of biomarker identification while reducing model-specific biases. These results set the stage for early identification, more accurate subtype classification, and possible therapeutic targeting in breast cancer.

SBH may mediate the cytostatic and anti-metastatic effects by targeting the JAK2/STAT3 and FAK/MYLK signaling axes.

Elevated SCD1 levels correlate with increased MYLK4 levels, and their concurrent expression forecasts regorafenib resistance and poor prognosis in colorectal cancer...Patients with colorectal cancer exhibiting elevated MYLK4 activity and wild-type p53 may derive clinical benefits from this combination therapy. These results suggest that MYLK4 may serve as a promising therapeutic target for the treatment of colorectal cancer.

Activation of Jag1/Notch1/Hes1 signaling pathway protects the intestinal mucosal barrier from inflammatory injury by abrogating MLCK-dependent TJ dysregulation.

These findings suggest that MLCK1-dependent tight junction regulation is essential for ICIs colitis, positioning barrier restoration as a potential therapeutic strategy.

This study elucidates the critical biological functions of MYLK2 in breast cancer, suggesting that it may serve as a promising prognostic biomarker. These findings provide new insights for early diagnosis and treatment strategies in breast cancer management.

Our integrated analysis suggests that DEP may promote prostate carcinogenesis via a multidimensional network centered on calcium signaling perturbation, neuroendocrine dysregulation, and tumor microenvironment acidification, potentially illustrating a genome-exposome interaction mechanism beyond endocrine disruption. We propose that our analytical framework could serve as a reproducible approach for translational exposomics.

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.