Ontology highlight
ABSTRACT:
INSTRUMENT(S):
ORGANISM(S): Homo Sapiens (human)
TISSUE(S): Kidney Epithelial Cell
DISEASE(S): Lung Cancer
SUBMITTER:
AUDEBERT Stephane
LAB HEAD: Luca Lignitto, PhD
PROVIDER: PXD062976 | Pride | 2026-06-11
REPOSITORIES: Pride
| Action | DRS | |||
|---|---|---|---|---|
| ElonC_HeCe_Rep1.raw | Raw | |||
| ElonC_HeCe_Rep1_20240322170829.raw | Raw | |||
| ElonC_HeCe_Rep2.raw | Raw | |||
| ElonC_HeCe_Rep2_20240322215621.raw | Raw | |||
| ElonC_HeCe_Rep3.raw | Raw |
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Ahmed Bashir B Salaun Daniele D Jordan Jack B JB Daulat Avais A Pastorello Chiara C Brito Tarcísio T Yang Yuying Y Josselin Emmanuelle E Byrne Deborah D Betzi Stephane S Pelletier Amandine A Vernerey Julien J Ferreira Lorene L Castellano Remy R Audebert Stephane S Camoin Luc L Pane Attilio A Bechara Cherine C Borg Jean-Paul JP Modesti Mauro M Lignitto Luca L
Molecular cell 20260504 10
Lung cancers frequently increase iron demand to sustain growth, which makes them vulnerable to ferroptosis. While Cullin 2-RING ubiquitin ligases (CRL2s) are critical regulators of stress responses and redox balance, their role in ferroptosis mechanisms remains largely unknown. Here, we identify the E3 ligase CRL2<sup>FEM1B</sup> as a key regulator of the ferroptotic response. CRL2<sup>FEM1B</sup> recruits BTB and CNC homolog 1 (BACH1), a transcriptional regulator of ferroptosis, for degradation ...[more]