MYB (MYB Proto-Oncogene, Transcription Factor)

Based on multi-omics analysis, our findings indicate that the PI3K/AKT pathway is a key factor contributing to the significant prognostic disparity between TNBC and Non-TNBC. Within this pathway, the MYB gene emerges as a potential therapeutic target. This discovery provides a potential basis for future research exploring MYB as a therapeutic target for TNBC patients.

Combined use of LEF1 and β-catenin improved sensitivity (90%) but resulted in a medium specificity (93%). In conclusion, the proposed immunohistochemical panel can improve diagnostic accuracy in basaloid tumors of the salivary glands.

In summary, this study found that under the regulation of CMCS, AeMYB6, AeMYB315-1, and AeMYB35-2 cooperatively regulate the expression of multiple genes in the phenylpropanoid pathway, jointly regulating lignin accumulation. This result provides important scientific basis for revealing the mechanism of CMCS delaying postharvest lignification of okra.

A 264-gene signature from HPVon HMSC cells correlated with worse prognosis in HPV + OPSCC (p < 0.003), suggesting an alternate role for HPV. Further validation of the HPV-MYB association and gene signature may improve therapeutic strategies in HPV-related malignancies.

In conclusion, we characterize the breadth of angiocentric glioma patterns in terms of demographics, anatomic location, and MYB fusion patterns. The updated molecular diagnosis of angiocentric glioma as of 2021 warrants continued exploration of the scope of MYB oncogene fusions as drivers of prognosis and targets for future therapies.

While other clinical factors (e.g., T stage) contribute to prognosis, these alterations identify patients who may benefit from dual-pathway inhibitors. Prospective validation is needed to confirm clinical utility.

Rescue experiments indicated that MYB upregulation counteracted the tumor-suppressive effects of miRNA-195-5p and reactivated PI3K/AKT/mTOR signaling. miRNA-195-5p suppresses proliferation and metastasis in TNBC by targeting MYB and inhibiting the PI3K/AKT/mTOR pathway.

This study demonstrates that soybean resistance to Pm involves multiple TF families and diverse metabolic pathways. These findings provide novel insights into the molecular regulatory network governing soybean resistance to Pm and lay the groundwork for further investigation of the molecular mechanisms underlying SDM resistance.

This opposing effect could provide a good opportunity for specific gene regulation, with great potential for further development of a precise therapeutic agent. This study provides a novel example for a practical therapeutic approach through coordinated gene quadruplex modulations, which sets up a good foundation for developing high-efficacy anti-tumor drugs without significant side effects.

Pathway analysis revealed that mutations in the spatial query sample prominently affect the PI3K-AKT and IL-17 signaling pathways, together with a downregulation of canonical Wnt signaling in some regions of the tissue architecture adjacent to immune cells. Collectively, these results underscore the complex regulatory landscape of SGACC and offer insights into its cellular dynamics and possible therapeutic vulnerabilities.

These findings indicate that PsnMYB30 significantly enhances the salt tolerance and drought resistance of transgenic tobacco. These results indicate that PsnMYB30 is a key target gene for studying salt-tolerant and drought-resistant plants in genetic breeding.

Rescue experiments using the hedgehog signaling inhibitor GANT58 attenuated the suppressive effect of MYB overexpression on NK cytotoxicity. In summary, MYB inhibited NK cell cytotoxicity by activating the hedgehog signaling pathway in cervical cancer, suggesting its potential as a novel diagnostic marker and immunotherapeutic target.