BACH1 meets its match: Heme licenses BACH1 destruction to tune ferroptosis

Dylan Calhoon1, Javier Garcia-Bermudez1

  • 1Children's Medical Center Research Institute, University of Texas Southwestern Medical Center, Dallas, TX, USA.

Cell Chemical Biology
|July 16, 2026
PubMed

In a recent issue of Molecular Cell, Ahmed and colleagues1 show that heme enables CRL2-FEM1B to recognize and degrade BACH1, linking metabolite-assisted substrate recruitment to ferroptosis regulation. This mechanism connects heme sensing, ubiquitin-mediated proteolysis, and transcriptional control of ferroptosis-protective genes, revealing a potential vulnerability in lung cancer.

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