Molecular mechanisms behind the functional (non)redundancy of CK1 paralogs in the Wnt pathway

Programmable protein degraders enable selective knockdown of pathogenic β-catenin subpopulations in vitro and in vivo

Aberrant activation of Wnt signaling results in unregulated accumulation of cytosolic β-catenin, which subsequently enters the nucleus and promotes transcription of genes that contribute to cellular proliferation and malignancy. Here, we sought to eliminate pathogenic β-catenin from the cytosol using designer ubiquibod...

Differential tyrosine phosphorylation status of the nuclear scaffold Parafibromin/CDC73 determines its role in cancer development.

Parafibromin/CDC73 is a multifunctional nuclear scaffold protein with context-dependent roles in tumorigenesis, functioning as both a tumor suppressor and an oncogenic driver. Originally identified as the product of the HRPT2 tumor suppressor gene, which is mutated in hyperparathyroidism-jaw tumor syndrome, Parafibromi...

Functional divergence of WWC family proteins in human endothelial cells

The Hippo signaling pathway is increasingly recognized as a key regulator of endothelial cell (EC) proliferation, migration and vascular development. However, the roles of its upstream scaffold proteins remain poorly understood. Although WWC family proteins are widely regarded as functionally redundant activators of LA...

Generation and molecular validation of an OsCAF1AΔPXLXP deletion mutant as a resource for future functional studies in rice

In Silico Phosphoproteomic Profiling of the MAP3K3 Signaling Network

Background: Mitogen-activated protein kinase kinase kinase 3 (MAP3K3) is a serine/threonine kinase that exhibits oncogenic activity in various cancers. Despite the established role of MAP3K3 in signal transduction, its phosphosignaling landscape, including the mechanisms underlying its activation and the identification...

Casein Kinase 1 and CK2 as Therapeutic Targets in Cancer: Molecular Pharmacology, Toxicological Considerations, and Clinical Progress.

Novel dual-therapy approaches targeting CK1/CK2-regulated pathways have further improved the therapeutic specificity and efficacy and hold great promise for selectively targeting cancer-causing signaling pathways and advancing cancer precision medicine.