Dataset Information

Molecular characterization of ribosome defective cell lines

ABSTRACT: We generated a unique panel of isogenic cell models with the following genotypes via CRISPR-Cas9 engineering: Rpl5+/-, Rpl10 R98S, Rpl11+/-, Rpl22+/-, Rpl22-/-, Rps15 P131S and Rps15 H137Y. As cellular background, we chose for Ba/F3 cells. These are mouse lymphoid pro-B-cells, offering a relevant cellular background as most of these mutations have been linked to lymphoid malignancies as T-ALL and CLL. Quantitative proteomics profiling of this isogenic cell line panel shed a light on the molecular biology underlying the oncogenic mechanisms of these ribosomal lesions.

INSTRUMENT(S):

ORGANISM(S): Mus Musculus (mouse)

TISSUE(S): Cell Culture, Hematopoietic Cell

SUBMITTER: Delphi Van Haver

LAB HEAD: Kim De Keersmaecker

PROVIDER: PXD051831 | Pride | 2025-11-18

REPOSITORIES: Pride

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Dataset's files

Source:

			Action	DRS
	Experimental_design_SG.xlsx	Xlsx
	F001855_2p_uPAC7_PRC-5065_1_Keersmaecker_WT_Clone_1.raw	Raw
	F001857_2p_uPAC7_PRC-5065_2_Keersmaecker_WT_Clone_2.raw	Raw
	F001859_2p_uPAC7_PRC-5065_3_Keersmaecker_WT_Clone_3.raw	Raw
	F001861_2p_uPAC7_PRC-5065_4_Keersmaecker_WT_Clone_A14.raw	Raw

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Publications

A RiboCancer cell line panel reveals that CLL-associated Rps15 mutations translationally rewire transcription through codon-specific tRNA accommodation defects.

Astier Anaïs A Caruso Marino M Vereecke Stijn S Santo Paulo E PE Capron Coralie C Froment Carine C Rinaldi Dana D Cabrerizo Granados David D Leclercq Marine M Royaert Jonathan J Verbeeck Jelle J Pasau Naomy N Plassart Laura L Pepe Daniele D Verbruggen Steven S Paraqindes Hermes H Lebaron Simon S Marcel Virginie V Durand Sébastien S Chapat Clément C Menschaert Gerben G Close Pierre P Rapino Francesca F Catez Frédéric F Marcoux Julien J Plisson-Chastang Célia C De Keersmaecker Kim K

HemaSphere 20260603 6

Recurrent point mutations in ribosomal proteins (RPs) RPL10 and RPS15 are found in T-cell acute lymphoblastic leukemia (T-ALL) and chronic lymphocytic leukemia (CLL), respectively. Furthermore, deletions of RPL5, RPL11, and RPL22 are frequent in hematologic diseases such as Diamond Blackfan Anemia, T-ALL, multiple myeloma, and in a variety of solid tumors. Yet, the role of these RP defects in dysregulation of the ribosomal translation function remains poorly understood. We engineered an isogenic ...[more]

PMID: 42255948

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