Note to users. If you're seeing this message, it means that your browser cannot find this page's style/presentation instructions -- or possibly that you are using a browser that does not support current Web standards. Find out more about why this message is appearing, and what you can do to make your experience of our site the best it can be.


Sci. Signal., 19 April 2011
Vol. 4, Issue 169, p. ra25
[DOI: 10.1126/scisignal.2001592]


Editor's Summary

Differential Role for ERKs
Given that cellular differentiation is associated with cell cycle arrest, the processes of differentiation and proliferation are thought to be mutually exclusive, and the transcriptional programs underlying these events are frequently stimulated by distinct extracellular cues. The extracellular signal–regulated kinase (ERK) signaling pathway is responsible for driving proliferation in many cell types, including immune cells, and thus is thought to be involved only in dividing cells (see the Perspective by Allman and Cancro). In B cells, the transcriptional program of proliferating cells is suppressed by the transcriptional repressor Blimp-1, which is required for the differentiation of B cells into antibody-presenting plasma cells, a terminally differentiated cell type. Through experiments with mice deficient in both ERK1 and ERK2 in B cells, Yasuda et al. provide evidence of a critical role for the ERKs in driving the differentiation of plasma cells and show that ERK signaling is required for the expression of Blimp-1. Together, these data expand the role of ERK signaling in B cells and should prompt investigation of the potential involvement of ERK proteins in the differentiation of other cell types.

Citation: T. Yasuda, K. Kometani, N. Takahashi, Y. Imai, Y. Aiba, T. Kurosaki, ERKs Induce Expression of the Transcriptional Repressor Blimp-1 and Subsequent Plasma Cell Differentiation. Sci. Signal. 4, ra25 (2011).

Read the Full Text

Diacylglycerol Kinase {zeta} Limits B Cell Antigen Receptor-Dependent Activation of ERK Signaling to Inhibit Early Antibody Responses.
M. L. Wheeler, M. B. Dong, R. Brink, X.-P. Zhong, and A. L. DeFranco (2013)
Science Signaling 6, ra91
   Abstract »    Full Text »    PDF »
Ezrin Tunes the Magnitude of Humoral Immunity.
D. Pore, N. Parameswaran, K. Matsui, M. B. Stone, I. Saotome, A. I. McClatchey, S. L. Veatch, and N. Gupta (2013)
J. Immunol. 191, 4048-4058
   Abstract »    Full Text »    PDF »
Receptor Cross-Talk Spatially Restricts p-ERK during TLR4 Stimulation of Autoreactive B Cells.
S.-R. Lee, J. A. Rutan, A. J. Monteith, S. Z. Jones, S. A. Kang, K. N. Krum, M. A. Kilmon, J. R. Roques, N. J. Wagner, S. H. Clarke, et al. (2012)
J. Immunol. 189, 3859-3868
   Abstract »    Full Text »    PDF »
IL-2 Requirement for Human Plasma Cell Generation: Coupling Differentiation and Proliferation by Enhancing MAPK-ERK Signaling.
S. Le Gallou, G. Caron, C. Delaloy, D. Rossille, K. Tarte, and T. Fest (2012)
J. Immunol. 189, 161-173
   Abstract »    Full Text »    PDF »
B Cell Receptor-ERK1/2 Signal Cancels PAX5-Dependent Repression of BLIMP1 through PAX5 Phosphorylation: A Mechanism of Antigen-Triggering Plasma Cell Differentiation.
T. Yasuda, F. Hayakawa, S. Kurahashi, K. Sugimoto, Y. Minami, A. Tomita, and T. Naoe (2012)
J. Immunol. 188, 6127-6134
   Abstract »    Full Text »    PDF »
Antigen Feast or Famine.
M. L. Dustin and M. Meyer-Hermann (2012)
Science 335, 408-409
   Abstract »    Full Text »    PDF »
pERKing Up the BLIMP in Plasma Cell Differentiation.
D. M. Allman and M. P. Cancro (2011)
Science Signaling 4, pe21
   Abstract »    Full Text »    PDF »

To Advertise     Find Products

Science Signaling. ISSN 1937-9145 (online), 1945-0877 (print). Pre-2008: Science's STKE. ISSN 1525-8882