B4GALNT1 (Beta-1,4-N-Acetyl-Galactosaminyltransferase 1)

Furthermore, SP1 degradation, SMAD activation, and their DNA binding patterns show the reciprocal role of p300 on SP1 and SMAD complexes. Altogether we have identified SMAD2/4 as an activator complex, p300 as a positive regulator, and uncovered a critical p300-SMAD-SP1 regulatory axis in GM2-synthase transcriptional regulation.

In vitro, within lung adenocarcinoma cell lines, B4GALNT1 knockdown and CERS4 overexpression suppressed cell proliferation, migration, and epithelial-to-mesenchymal transition, supporting their roles in lung adenocarcinoma progression. These findings highlight B4GALNT1 and CERS4 as potential prognostic biomarkers and therapeutic targets in lung adenocarcinoma, warranting further clinical investigation.

Our computational framework provides a robust, interpretable, biologically grounded predictor of GD2 expression, offering greater consistency and clinical interpretability over existing gene-based signatures. Importantly, with over 20 GD2-directed trials ongoing, our approach may help prioritize tumor entities with high GD2 levels, delineate candidate patient subgroups, and generate testable hypotheses in underexplored cancers, thereby supporting patient stratification and eligibility screening for clinical trials.

The four identified SRGs were significantly associated with clinical outcomes and immunological features in HCC. These findings provide a foundation for advancing early diagnostic strategies, refining prognostic assessments, and guiding personalized therapeutic approaches for patients with HCC.

This activity involves governing inflammatory responses alongside cellular proliferation, migration, and differentiation processes. These findings offer a theoretical foundation supporting paeonol's potential clinical utility in cervical cancer management.

This study is the first to establish a sphingolipid metabolism-based five-gene signature in HNSCC. Its superior reliability and accuracy in predicting prognosis and immune response offer new clinical perspectives.

Profile C was found only in cell lines of the mesenchymal subtype. These findings support further investigation of GG composition and associated enzyme expression as potential biomarkers for risk stratification and treatment response in NBL.

Molecular dynamics simulations support that these loops can insert into the lipid bilayer explaining how B4GALNT1 accesses and processes lipid substrates. By combining structure prediction and molecular simulations we propose that this mechanism of dynamic membrane insertion is exploited by other, structurally distinct GSL synthesising enzymes.

These findings lend further support to the growing evidence that GD2 is a potential biomarker of CSCs and epithelial-mesenchymal transition (EMT) in human breast cancer that can be amenable to therapeutic targeting.

The utilization of GARGs in our constructed model exhibits a high level of accuracy in prognosticating glioma and offers promising avenues for the development of therapeutic interventions targeting glioma.

B4GALNT1 is a strong regulator of HCC progression and holds promise as a marker for prognosis and a hallmark for therapy in HCC.

In addition, silencing B4GALNT1 was proved to enhance the tumor-killing efficiency of the programmed cell death protein 1 (PD-1)-targeting strategy in mouse model. In conclusion, this study evaluated B4GALNT1 as a prognostic predictor for HCC patients and revealed the mechanism of B4GALNT1 in microenvironmental remodeling, which extends the understanding of HCC progression and provides a novel auxiliary strategy for HCC immunotherapy.