ArticleBiochemical pharmacology2014
BAFF activates Erk1/2 promoting cell proliferation and survival by Ca2+-CaMKII-dependent inhibition of PP2A in normal and neoplastic B-lymphoid cells.
Article in Biochemical pharmacology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 24 citations in OpenAlex.
- Design and development of a bispecific antibody targeting BAFF and IL-17 for systemic lupus erythematosus treatment.BMC biology · 2025Article
- Mechanical stress facilitates calcium influx and growth of alveolar epithelial cells via activation of the BDKRB1/CaRespiratory research · 2025Article
- B cell immunometabolism in health and disease.Nature immunology · 2025Review
- The function of serine/threonine-specific protein kinases in B cells.Frontiers in immunology · 2024Review
- ICAM-1 mediated cell-cell adhesion exerts dual roles on human B cell differentiation and IgG production.iScience · 2023Article
- Metformin prevents BAFF activation of Erk1/2 from B-cell proliferation and survival by impeding mTOR-PTEN/Akt signaling pathway.International immunopharmacology · 2021Article
- Rapamycin inhibits B-cell activating factor (BAFF)-stimulated cell proliferation and survival by suppressing CaCell calcium · 2020Article
- Wnt5a/CaMKII/ERK/CCL2 axis is required for tumor-associated macrophages to promote colorectal cancer progression.International journal of biological sciences · 2020Article
- BAFF inhibits autophagy promoting cell proliferation and survival by activating CaCellular signalling · 2019Article
- Profiling the interactome of protein kinase C ζ by proteomics and bioinformatics.Proteome science · 2018Article
- Rapamycin attenuates BAFF-extended proliferation and survival via disruption of mTORC1/2 signaling in normal and neoplastic B-lymphoid cells.Journal of cellular physiology · 2018Article
- Article
- Rapamycin inhibits BAFF-stimulated cell proliferation and survival by suppressing mTOR-mediated PP2A-Erk1/2 signaling pathway in normal and neoplastic B-lymphoid cells.Cellular and molecular life sciences : CMLS · 2015Article
- The emerging role of CaMKII in cancer.Oncotarget · 2015Review
- Effects of B-lymphocyte dysfunction on the serum copper, selenium and zinc levels of rheumatoid arthritis patients.Pakistan journal of medical sciences · 2014Article
Corrections and comments
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Authors and funding
10 authors at 2 institutions in 2 countries.
Funding
Abstract
B-cell activating factor (BAFF) is involved in not only the physiology of normal B cells, but also the pathophysiology of aggressive B cells related to malignant and autoimmune diseases. However, how excessive BAFF promotes aggressive B-cell proliferation and survival is not well understood. Here we show that excessive human soluble BAFF (hsBAFF) enhanced cell proliferation and survival in normal and B-lymphoid (Raji) cells, which was associated with suppression of PP2A, resulting in activation of Erk1/2. This is supported by the findings that pretreatment with U0126 or PD98059, expression of dominant negative MKK1, or overexpression of PP2A prevented hsBAFF-induced activation of Erk1/2 and cell proliferation/viability in the cells. It appears that hsBAFF-mediated PP2A-Erk1/2 pathway and B-cell proliferation/viability was Ca(2+)-dependent, as pretreatment with BAPTA/AM, EGTA or 2-APB significantly attenuated these events. Furthermore, we found that inhibiting CaMKII with KN93 or silencing CaMKII also attenuated hsBAFF-mediated PP2A-Erk1/2 signaling and B-cell proliferation/viability. The results indicate that BAFF activates Erk1/2, in part through Ca(2+)-CaMKII-dependent inhibition of PP2A, increasing cell proliferation/viability in normal and neoplastic B-lymphoid cells. Our data suggest that inhibitors of CaMKII and Erk1/2, activator of PP2A or manipulation of intracellular Ca(2+) may be exploited for prevention of excessive BAFF-induced aggressive B-cell malignancies and autoimmune diseases.
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