Back

THE FAM53C/DYRK1A axis regulates the G1/S transition of the cell cycle

Hammond, T.; Choi, J. B.; Membreno, M. W.; Demeter, J.; Ng, R.; Bhattacharya, D.; Nguyen, T.; Bossard, C.; Hartmann, G. G.; Skotheim, J.; Jackson, P. K.; Pasca, A. M.; Rubin, S.; Sage, J.

2024-12-11 cell biology
10.1101/2024.12.10.627280 bioRxiv
Show abstract

A growing number of therapies are being developed to target the cell cycle machinery for the treatment of cancer and other human diseases. Consequently, a greater understanding of the factors regulating cell cycle progression becomes essential to help enhance the response to these new therapies. Here, using data from the Cancer Dependency Map, we identified FAM53C as a new regulator of cell cycle progression. We found that FAM53C is critical for this cell cycle transition and that it acts upstream of the CyclinD-CDK4/6-RB axis and of p53 in the regulation of the G1/S transition. By mass spectrometry, biochemical, and cellular assays, we identified and validated DYRK1A as a cell cycle kinase that is inhibited by and directly interacts with FAM53C. Consistent with the role for FAM53C identified in cells in culture, FAM53C knockout human cortical organoids display increased cell cycle arrest and growth defects. Fam53C knockout mice show minor behavioral phenotypes. Because DYRK1A dysregulation contributes to developmental disorders such as Down syndrome as well as tumorigenesis, future strategies aiming at regulating FAM53C activity may benefit a broad range of patients.

Published in eLife (predicted rank #1) · training set

Matching journals

The top 11 journals account for 50% of the predicted probability mass.

50% of probability mass above

"Similar papers" are the closest papers from that journal in the model's embedding space. They show what the match is built on, but the ranking comes mostly from a classifier over the whole training set, not from these examples alone.