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Label-free differential proteomics analysis of Ba/F3 expressing WT and mutant R98S RPL10

ABSTRACT: We recently identified a recurrent mutation in the ribosomal gene RPL10 that results in substitution of residue arginine 98 by a serine (R98S) of the ribosomal protein L10 (RPL10) in the contest of T-cell acute lymphoblastic leukemia (T-ALL). To gain insights into the mechanisms by which the RPL10 R98S mutation contributes to T-ALL development, we screened for proteins that are differentially expressed between RPL10 wild type (WT) and RPL10 R98S (R98S) expressing cells. These experiments were conducted in the mouse pro-B Ba/F3 cell line, a well-established hematopoietic model for oncogenic studies.

INSTRUMENT(S): Q Exactive

ORGANISM(S): Mus Musculus (mouse)

TISSUE(S): B Cell, Cell Culture

SUBMITTER: Laura Fancello

LAB HEAD: Kim de Keersmaecker

PROVIDER: PXD005995 | Pride | 2017-11-28

REPOSITORIES: Pride

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The T-cell leukemia-associated ribosomal RPL10 R98S mutation enhances JAK-STAT signaling.

Girardi T T Vereecke S S Sulima S O SO Khan Y Y Fancello L L Briggs J W JW Schwab C C de Beeck J Op JO Verbeeck J J Royaert J J Geerdens E E Vicente C C Bornschein S S Harrison C J CJ Meijerink J P JP Cools J J Dinman J D JD Kampen K R KR De Keersmaecker K K

Leukemia 20170724 3

Several somatic ribosome defects have recently been discovered in cancer, yet their oncogenic mechanisms remain poorly understood. Here we investigated the pathogenic role of the recurrent R98S mutation in ribosomal protein L10 (RPL10 R98S) found in T-cell acute lymphoblastic leukemia (T-ALL). The JAK-STAT signaling pathway is a critical controller of cellular proliferation and survival. A proteome screen revealed overexpression of several Jak-Stat signaling proteins in engineered RPL10 R98S mou ...[more]

PMID: 28744013

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