Proteomics

Dataset Information

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THE FAM53C/DYRK1A AXIS REGULATES THE G1/S TRANSITION OF THE CELL CYCLE


ABSTRACT: A growing number of small molecules are becoming available 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 to response of patients to these drugs. Here we identified the poorly-studied factor FAM53C as a new regulator of the G1/S transition. We first used data from the Cancer Dependency Map to identify new candidate regulators of the G1/S transition, and validated FAM53C as necessary and sufficient for this cell cycle transition. Genetic approaches showed that FAM53C acts upstream of the RB tumor suppressor. By mass spectrometry, we identified and validated DYRK1A as a kinase normally inhibited by FAM53C. DYRK1A is an upstream negative regulator of Cyclin D, which also negatively regulates RB. Fam53C knockout mice are viable but show defects in growth. Together, these experiments identify FAM53C as a regulator of DYRK1A and of cell cycle progression in G1.

INSTRUMENT(S):

ORGANISM(S): Homo Sapiens (human)

TISSUE(S): Kidney

SUBMITTER: Janos Demeter  

LAB HEAD: Peter Kent Jackson

PROVIDER: PXD055829 | Pride | 2026-04-23

REPOSITORIES: Pride

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