Related Experiment Video

Updated: Jun 4, 2025

Studying Cell Cycle-regulated Gene Expression by Two Complementary Cell Synchronization Protocols
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Studying Cell Cycle-regulated Gene Expression by Two Complementary Cell Synchronization Protocols

Published on: June 6, 2017

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

Taylar Hammond, Jong Bin Choi, Miles W Membreño

    Biorxiv : the Preprint Server for Biology
    |December 23, 2024
    PubMed

    Insights

    Researchers discovered FAM53C regulates cell cycle progression, acting upstream of the CyclinD-CDK4/6-RB pathway. FAM53C interacts with and inhibits DYRK1A kinase, impacting cell cycle control and organismal growth.

    Area of Science:

    • Cell Biology
    • Molecular Oncology
    • Developmental Biology

    Background:

    • Targeting cell cycle machinery is crucial for cancer therapy.
    • Understanding cell cycle regulators enhances therapeutic responses.
    • FAM53C was a poorly-studied factor with unknown function.

    Purpose of the Study:

    • Identify novel regulators of cell cycle progression.
    • Investigate the role of FAM53C in cell cycle control.
    • Elucidate the molecular mechanism of FAM53C action.

    Main Methods:

    • Utilized Cancer Dependency Map data.
    • Performed mass spectrometry, biochemical, and cellular assays.
    • Generated FAM53C knockout organoid and mouse models.

    Main Results:

    • Identified FAM53C as a novel cell cycle regulator.
    • FAM53C acts upstream of the CyclinD-CDK4/6-RB axis.
    • Discovered DYRK1A kinase is inhibited by FAM53C, rescuing G1 arrest.
    • FAM53C knockout models exhibit growth defects and behavioral phenotypes.

    Conclusions:

    • FAM53C is a critical regulator of the G1/S cell cycle transition.
    • FAM53C directly interacts with and inhibits DYRK1A kinase.
    • Dysregulation of FAM53C impacts organismal development and growth.
    • Targeting FAM53C may offer therapeutic potential for cancer and developmental disorders.

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