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Our results indicate that VRK2 phosphorylates COPII component Sec24C and promotes its interaction with SLC7A11, thus facilitating ER-to-Golgi transport and membrane expression of SLC7A11

VRK2 expression stratifies the response of PC to GSH-targeted treatment To further investigate the differential sensitivity to GSH inhibitors between VRK2-expressing and VRK2-deficient pancreatic tumors in vivo, we developed orthotopic pancreatic cancer models using Pan02 cells (Fig

Most adverse reactions resolve within two to four weeks of discontinuation

This approach recognizes that simply identifying the presence of autoimmunity provides insufficient information for developing personalized treatment plans aimed at addressing root causes