본문으로 건너뛰기
← 뒤로

RHOA controls oncogenic B cell receptor signaling in aggressive lymphoma.

1/5 보강
Proceedings of the National Academy of Sciences of the United States of America 📖 저널 OA 100% 2022: 2/2 OA 2023: 1/1 OA 2024: 8/8 OA 2025: 44/44 OA 2026: 58/58 OA 2022~2026 2026 Vol.123(5) p. e2534531123 OA
Retraction 확인
출처

Jacobs AN, Jahn D, Beringer T, Wolf S, Krishnan RK, Engelke M

📝 환자 설명용 한 줄

Diffuse large B cell lymphoma (DLBCL) is characterized by a variety of specific genetic alterations that impact signaling pathway dependencies and therapeutic outcomes.

이 논문을 인용하기

↓ .bib ↓ .ris
APA Jacobs AN, Jahn D, et al. (2026). RHOA controls oncogenic B cell receptor signaling in aggressive lymphoma.. Proceedings of the National Academy of Sciences of the United States of America, 123(5), e2534531123. https://doi.org/10.1073/pnas.2534531123
MLA Jacobs AN, et al.. "RHOA controls oncogenic B cell receptor signaling in aggressive lymphoma.." Proceedings of the National Academy of Sciences of the United States of America, vol. 123, no. 5, 2026, pp. e2534531123.
PMID 41591906 ↗

Abstract

Diffuse large B cell lymphoma (DLBCL) is characterized by a variety of specific genetic alterations that impact signaling pathway dependencies and therapeutic outcomes. Among the recurrently mutated genes, we identified , a member of the small GTPase family, as a selective dependency in DLBCL. Here, we show that RHOA function is essential for the survival of ABC DLBCL cells because it sustains oncogenic B cell receptor (BCR) signaling through maintaining a signaling-permissive conformation of the cortical actin network. This enables the formation of active BCR microclusters at the cell surface, ultimately resulting in constitutive, BCR-driven NF-κB survival signaling. Moreover, we found that RHOA controlled endocytosis of the BCR and thereby the assembly of the endolysosomal My-T-BCR multiprotein complex, a central activator of NF-κB consisting of MYD88, Toll-like receptor 9, and the internalized BCR. The recurrent DLBCL-associated R5W mutation rendered RHOA constitutively active in its GTP-bound state and changed the conformation of the actin network from primarily filamentous actin to globular actin. This altered actin state led to an increase in BCR microcluster formation, amplification of NF-κB signaling, and resistance to inhibitors targeting chronic active BCR signaling. Hence, our study establishes RHOA and its mutant isoforms as critical regulators of oncogenic BCR signaling in DLBCL.

🏷️ 키워드 / MeSH 📖 같은 키워드 OA만

🏷️ 같은 키워드 · 무료전문 — 이 논문 MeSH/keyword 기반

🟢 PMC 전문 열기