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Related Concept Videos

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Induced Pluripotent Stem Cells

Stem cells are undifferentiated cells that divide and produce different cell types. Ordinarily, cells that have differentiated into a specific cell type are terminally differentiated; however, scientists have found a way to reprogram these mature cells so that they dedifferentiate and return to an unspecialized, proliferative state. These cells are pluripotent like embryonic stem cells—able to produce all cell types—and are called induced pluripotent stem cells (iPSCs).
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The stepwise destruction of specific proteins is necessary for the progression and completion of the cell cycle. Such proteins are ubiquitinated by ubiquitin ligases and then subsequently destroyed by the proteasome. The SCF (Skp1/Cullin/F-box) and the anaphase-promoting complex (APC) are two important ubiquitin ligases involved in cell cycle progression. While SCF is active throughout the cell cycle, APC gets activated during metaphase to anaphase transition. Cdc20 or Cdh1 binds to APC and...
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Related Experiment Video

Updated: Jun 3, 2026

Chemical Inactivation of the E3 Ubiquitin Ligase Cereblon by Pomalidomide-based Homo-PROTACs
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Crotonylation impedes c-Myc oncogenic activity.

Nicholas J Wallbillich1,2, Peng Liao1,2, Rashmi Srivastava1,2

  • 1Department of Biochemistry and Molecular Biology, Tulane University School of Medicine, 1430 Tulane Avenue, New Orleans, LA 70112.

Proceedings of the National Academy of Sciences of the United States of America
|June 1, 2026
PubMed
Summary

Crotonylation, a modification of the oncoprotein c-Myc, impairs its cancer-driving activity. Specific mutations in c-Myc enhance its oncogenic functions by altering interactions with its regulator Skp2.

Keywords:
Skp2c-Myccrotonylationoncogenesisposttranslational modification

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Area of Science:

  • Biochemistry
  • Molecular Biology
  • Oncology

Background:

  • c-Myc is a crucial oncoprotein regulated by posttranslational modifications.
  • Understanding these modifications is key to comprehending c-Myc's role in cancer.

Purpose of the Study:

  • To investigate c-Myc crotonylation, a novel posttranslational modification.
  • To determine the functional impact of c-Myc crotonylation on its oncogenic activity.

Main Methods:

  • Biochemical analyses and high-resolution mass spectrometry were employed.
  • Site-directed mutagenesis of identified crotonylation sites was performed.
  • Interactions between c-Myc and Skp2 were assessed.

Main Results:

  • c-Myc was found to be crotonylated at multiple lysine residues.
  • Mutations at K289 and K298 enhanced cell proliferation and c-Myc binding to Skp2.
  • The K298N mutation, found in human tumors, exhibited increased oncogenic activity.
  • Crotonylation impairs c-Myc's oncogenic activity by modulating Skp2 interaction.

Conclusions:

  • Crotonylation is a regulatory mechanism for c-Myc.
  • This modification can attenuate c-Myc's oncogenic potential.
  • Targeting c-Myc crotonylation may offer therapeutic strategies in cancer treatment.