Vaccinia-Related Kinase Signaling in Cell Cycle Regulation
Summary
Vaccinia-related kinases (particularly VRK1) are a family of nuclear serine–threonine kinases that integrate proliferative signals with chromatin dynamics to orchestrate cell-cycle progression. VRK1 expression is induced as cells exit quiescence (G0) and enter G1, where it promotes cyclin D1 transcription and aids in early gene expression programmes. Through phosphorylation of histone H3 at Thr3, VRK1 primes chromatin for mitotic entry and collaborates with mitotic kinases to ensure proper chromosome condensation and segregation. Beyond histone marks, VRK1 regulates epigenetic modifiers and nuclear bodies, such as Cajal bodies, influencing RNA–protein complex assembly and DNA repair factor recruitment. Dysregulation of VRK1 signalling has been linked to oncogenic proliferation, resistance to genotoxic stress and neurological disorders, underlining its dual role in normal cell-cycle control and disease pathogenesis.
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Vaccinia-Related Kinase Signaling in Cell Cycle Regulation publication trend
The graph below shows the total number of articles in vaccinia-related kinase signaling in cell cycle regulation across all publications each year (not limited to Nature Index journals).
Technical terms
Vaccinia-related kinase 1 (VRK1): A nuclear serine–threonine kinase that regulates chromatin modifications and cell-cycle transitions.
G0 phase: A quiescent, non-dividing state from which cells re-enter the cycle upon mitogenic stimulation.
Histone H3 Thr3 phosphorylation: Addition of a phosphate to threonine 3 on histone H3, marking chromatin for mitotic entry.
Histone H4 Lys16 acetylation (H4K16ac): Acetylation of lysine 16 on histone H4, associated with open chromatin and active transcription.
Cajal bodies: Nuclear substructures that assemble small nuclear ribonucleoproteins, whose dynamics are influenced by VRK1.
References
- Nuclear functions regulated by the VRK1 kinase. Nucleus (2024).
- VRK1 Kinase Activity Modulating Histone H4K16 Acetylation Inhibited by SIRT2 and VRK-IN-1. International Journal of Molecular Sciences (2023).
- VRK1 and AURKB form a complex that cross inhibit their kinase activity and the phosphorylation of histone H3 in the progression of mitosis. Cellular and Molecular Life Sciences (2018).
- Human VRK1 Is an Early Response Gene and Its Loss Causes a Block in Cell Cycle Progression. PLOS ONE (2008).
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