Proteomics

Dataset Information

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Title Heme acts as a molecular degrader linking CRL2-FEM1B to substrate proteolysis and ferroptosis regulation in lung cancer

ABSTRACT: In this project, we attempted to explore the differential proteins profile of lung cancer cells in which the BACH1-CRL2 pathway was manipulated. To this end, we performed DIA-based quantitative proteomics in mouse lung adenocarcinoma KP cells. Control cells and BACH1 null cells were used. Additionally, the expression of CRL2 was silenced using siRNA. A cell line transfected with an siCTRL was used as negative control. 3 biological replicates were used for each sample group.

INSTRUMENT(S):

ORGANISM(S): Mus Musculus (mouse)

TISSUE(S): Malignant Cell

DISEASE(S): Lung Adenocarcinoma

SUBMITTER: AUDEBERT Stephane  

LAB HEAD: Dr Luca Lignitto

PROVIDER: PXD062953 | Pride | 2026-06-11

REPOSITORIES: Pride

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Dataset's files

Source:
Action DRS
KP_sgBach1_siCtrl_Rep1.raw Raw
KP_sgBach1_siCtrl_Rep1_20231117095106.raw Raw
KP_sgBach1_siCtrl_Rep1_20231119180037.raw Raw
KP_sgBach1_siCtrl_Rep2.raw Raw
KP_sgBach1_siCtrl_Rep2_20231118043413.raw Raw
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Publications

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]

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