PuSH - Publication Server of Helmholtz Zentrum München: Quantitative modeling of signaling in aggressive B cell lymphoma unveils conserved core network.

Navigation

Home

Deutsch

Research

Advanced Search

Browse by ...

... Journal

... Publication Type

... Research Data

... Publication Year

Publication overview

Support & Contact

Contact persons

Help

Data protection

Klinger, B.* ; Rausch, I.* ; Sieber, A.* ; Kutz, H. ; Kruse, V.* ; Kirchner, M.* ; Mertins, P.* ; Kieser, A. ; Blüthgen, N.* ; Kube, D.*

Quantitative modeling of signaling in aggressive B cell lymphoma unveils conserved core network.

PLoS Comput. Biol. 20:e1012488 (2024)

Publ. Version/Full Text

DOI

PMC

	Open Access Gold

Abstract
Metrics
Extra information

B cell receptor (BCR) signaling is required for the survival and maturation of B cells and is deregulated in B cell lymphomas. While proximal BCR signaling is well studied, little is known about the crosstalk of downstream effector pathways, and a comprehensive quantitative network analysis of BCR signaling is missing. Here, we semi-quantitatively modelled BCR signaling in Burkitt lymphoma (BL) cells using systematically perturbed phosphorylation data of BL-2 and BL-41 cells. The models unveiled feedback and crosstalk structures in the BCR signaling network, including a negative crosstalk from p38 to MEK/ERK. The relevance of the crosstalk was verified for BCR and CD40 signaling in different BL cells and confirmed by global phosphoproteomics on ERK itself and known ERK target sites. Compared to the starting network, the trained network for BL-2 cells was better transferable to BL-41 cells. Moreover, the BL-2 network was also suited to model BCR signaling in Diffuse large B cell lymphoma cells lines with aberrant BCR signaling (HBL-1, OCI-LY3), indicating that BCR aberration does not cause a major downstream rewiring.

Altmetric

Additional Metrics?

[➜Log in]

Edit extra informations Login

Publication type Article: Journal article

Document type Scientific Article

Corresponding Author

Keywords Colon-cancer; Receptor; Feedback; Kinase; Erk; Pathogenesis; Inhibition; Activation; Mechanisms; Expression

ISSN (print) / ISBN 1553-734X

e-ISSN 1553-7358

Journal PLoS Computational Biology

Quellenangaben Volume: 20, Issue: 10, Article Number: e1012488

Publisher Public Library of Science (PLoS)

Publishing Place 1160 Battery Street, Ste 100, San Francisco, Ca 94111 Usa

Non-patent literature Publications

Reviewing status Peer reviewed

Institute(s) Research Unit Gene Vector (AGV)
Research Unit Signaling and Translation (SAT)

Grants Bundesinstitut fur Risikobewertung
DKFZ (Young Investigator Grant)
Deutsche Krebshilfe
MSTARS-2
Federal Ministry of Education and Research (BMBF)