Cited by 199Protein Kinase Regulation and GTPase SignalingProtein Tyrosine PhosphatasesNF-κB Signaling Pathways

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Involvement of Guanosine Triphosphatases and Phospholipase C-γ2 in Extracellular Signal–regulated Kinase, c-Jun NH2-terminal Kinase, and p38 Mitogen-activated Protein Kinase Activation by the B Cell Antigen Receptor

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Hashimoto, Ari, Okada, Hidetaka, Jiang, Aimin, Kurosaki, Mari, Greenberg, Steven, Clark, Edward A., Kurosaki, Tomohiro·1998·The Journal of Experimental Medicine

DOI 10.1084/jem.188.7.1287PMC PMC2212492

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Abstract

Mitogen-activated protein (MAP) kinase family members, including extracellular signal–regulated kinase (ERK), c-Jun NH2-terminal kinase ( JNK), and p38 MAP kinase, have been implicated in coupling the B cell antigen receptor (BCR) to transcriptional responses. However, the mechanisms that lead to the activation of these MAP kinase family members have been poorly elucidated. Here we demonstrate that the BCR-induced ERK activation is reduced by loss of Grb2 or expression of a dominant-negative form of Ras, RasN17, whereas this response is not affected by loss of Shc. The inhibition of the ERK response was also observed in phospholipase C (PLC)-γ2–deficient DT40 B cells, and expression of RasN17 in the PLC-γ2–deficient cells completely abrogated the ERK activation. The PLC-γ2 dependency of ERK activation was most likely due to protein kinase C (PKC) activation rather than calcium mobilization, since loss of inositol 1,4,5-trisphosphate receptors did not affect ERK activation. Similar to cooperation of Ras with PKC activation in ERK response, both PLC-γ2–dependent signal and GTPase are required for BCR-induced JNK and p38 responses. JNK response is dependent on Rac1 and calcium mobilization, whereas p38 response requires Rac1 and PKC activation.

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Authors: Hashimoto, A., Okada, H., Jiang, A., Kurosaki, M., Greenberg, S., Clark, E. A., & Kurosaki, T.
Affiliations: Kansai Medical University (JP)
Corresponding author: Kurosaki, Tomohiro
ORCID: Hashimoto, Ari
Okada, Hidetaka
Jiang, Aimin
Clark, Edward A.
Kurosaki, Tomohiro
Venue: The Journal of Experimental Medicine
Publisher: Rockefeller University Press
Published: 1998-10-05
Volume: 188
Issue: 7
Pages: 1287-1295
ISSN: 0022-1007 (ISSN-L)
1540-9538
DOI: 10.1084/jem.188.7.1287
PMC: PMC2212492
OpenAlex: W1965678722
Cited by: 199
References: 68
Citations by year: 2026: 1 · 2025: 2 · 2024: 1 · 2021: 4 · 2020: 7 · 2019: 3 · 2018: 8 · 2017: 4 · 2016: 4 · 2015: 8 · 2014: 6 · 2013: 5 · 2012: 2
FWCI: 5.59
Type: journal article
Language: en
Open access: green
www.ncbi.nlm.nih.gov
Licence: cc-by-nc-sa
Locations: The Journal of Experimental Medicine (publishedVersion)
PubMed Central (publishedVersion, cc-by-nc-sa)
PubMed (publishedVersion)
Funders: National Institutes of Health (5p01gm042508-09)
National Institute of General Medical Sciences (GM42508, GM-37905, R01GM037905)
Topics: Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Protein Kinase Regulation and GTPase Signaling
Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Protein Tyrosine Phosphatases
Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › NF-κB Signaling Pathways
Keywords: B cell receptor, extracellular signal-regulated kinase, c-Jun NH2-terminal kinase, p38 MAPK, PLCγ2, Ras, Grb2, Shc, protein kinase C, Rac1, calcium mobilization, IP3 receptor, MAPK activation, signal transduction, B cell signaling
MeSH terms: Animals, Cell Line, Chickens, Enzyme Activation, Isoenzymes, Type C Phospholipases, Protein Kinase C, Proteins, Receptors, Antigen, B-Cell, Signal Transduction, Calcium-Calmodulin-Dependent Protein Kinases, GTP-Binding Proteins, Mitogen-Activated Protein Kinase 1, GTP Phosphohydrolases, rac GTP-Binding Proteins, Mitogen-Activated Protein Kinases, JNK Mitogen-Activated Protein Kinases, p38 Mitogen-Activated Protein Kinases, Adaptor Proteins, Signal Transducing, GRB2 Adaptor Protein, Phospholipase C gamma

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Involvement of Guanosine Triphosphatases and Phospholipase C-γ2 in Extracellular Signal–regulated Kinase, c-Jun NH2-terminal Kinase, and p38 Mitogen-activated Protein Kinase Activation by the B Cell Antigen Receptor

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