Signaling of Protein Kinases in Development and Disease (2nd Edition)

A special issue of Biomedicines (ISSN 2227-9059). This special issue belongs to the section "Cell Biology and Pathology".

Deadline for manuscript submissions: 30 September 2026 | Viewed by 1477

Editor


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Guest Editor
Department of Pharmacology, University of Virginia, Charlottesville, VA, USA
Interests: cell signaling of protein kinases; mechanism of ciliopathy
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Special Issue Information

Dear Colleagues,

Protein kinases comprise one of the largest and most abundant gene families in humans and play a pivotal role in signal transduction during tissue development, patterning, and homeostasis through the phosphorylation and functional modulation of protein substrates. Both germ-line and somatic mutations in kinase genes have been associated with many human diseases. Protein kinases are the second most targeted group for drug development. Novel therapeutic strategies to target protein kinases and intervene in cell signaling are still limited due to our incomplete understanding of their signaling mechanisms.

This Special Issue welcomes both comprehensive reviews and original articles to highlight the recent progress in the discovery of new mechanisms by which protein kinases function and human mutations disrupt kinase signaling and impact signal transduction.

Dr. John Zheng Fu
Guest Editor

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Keywords

  • kinase
  • phosphorylation
  • signaling
  • mutation
  • mechanism
  • development
  • inhibitor
  • disease

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Published Papers (1 paper)

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Research

15 pages, 1295 KB  
Article
Use of Small-Molecule Inhibitors of CILK1 and AURKA as Cilia-Promoting Drugs to Decelerate Medulloblastoma Cell Replication
by Sean H. Fu, Chelsea Park, Niyathi A. Shah, Ana Limerick, Ethan W. Powers, Cassidy B. Mann, Emily M. Hyun, Ying Zhang, David L. Brautigan, Sijie Hao, Roger Abounader and Zheng Fu
Biomedicines 2026, 14(2), 265; https://doi.org/10.3390/biomedicines14020265 - 24 Jan 2026
Viewed by 1169
Abstract
Background/Objective: The primary cilium is the sensory organelle of a cell and a dynamic membrane protrusion during the cell cycle. It originates from the centriole at G0/G1 and undergoes disassembly to release centrioles for spindle formation before a cell enters [...] Read more.
Background/Objective: The primary cilium is the sensory organelle of a cell and a dynamic membrane protrusion during the cell cycle. It originates from the centriole at G0/G1 and undergoes disassembly to release centrioles for spindle formation before a cell enters mitosis, thereby serving as a cell cycle checkpoint. Cancer cells that undergo rapid cell cycle and replication have a low ciliation rate. In this study, we aimed to identify cilia-promoting drugs that can accelerate ciliation and decelerate replication of cancer cells. Methods: To perform a comprehensive and efficient literature search on drugs that can promote ciliation, we developed an intelligent process that integrates either the GPT 4 Turbo, Gemini 1.5 Pro, or Claude 3.5 Haiku application programming interfaces (APIs) into a PubMed scraper that we coded, enabling the large language models (LLMs) to directly query articles for predefined user questions. We evaluated the performance of this intelligent literature search based on metrics and tested the effect of two candidate drugs on ciliation and proliferation of medulloblastoma cells. Results: Gemini was the best model overall, as it balanced high accuracy with solid precision and recall scores. Among the top candidate drugs identified are Alvocidib and Alisertib, small-molecule inhibitors of CILK1 and AURKA, respectively. Here, we show that both kinase inhibitors can effectively increase cilia frequency and significantly decrease the replication of medulloblastoma cells. Conclusions: The results demonstrated the potential of using cilia-promoting drugs, such as Alvocidib and Alisertib, to suppress cancer cell replication. Additionally, it shows the massive benefits of integrating accessible large language models to conduct sweeping, rapid, and accurate literature searches. Full article
(This article belongs to the Special Issue Signaling of Protein Kinases in Development and Disease (2nd Edition))
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