PMID- 26554024
OWN - NLM
STAT- MEDLINE
DCOM- 20160504
LR  - 20160106
IS  - 1470-8728 (Electronic)
IS  - 0264-6021 (Linking)
VI  - 473
IP  - 2
DP  - 2016 Jan 15
TI  - TRPC3 amplifies B-cell receptor-induced ERK signalling via protein kinase 
      D-dependent Rap1 activation.
PG  - 201-10
LID - 10.1042/BJ20150596 [doi]
AB  - Sustained activation of extracellular-signal-regulated kinase (ERK) has an 
      important role in the decision regarding the cell fate of B-lymphocytes. 
      Recently, we demonstrated that the diacylglycerol-activated non-selective cation 
      channel canonical transient receptor potential 3 (TRPC3) is required for the 
      sustained ERK activation induced by the B-cell receptor. However, the signalling 
      mechanism underlying TRPC3-mediated ERK activation remains elusive. In the 
      present study, we have shown that TRPC3 mediates Ca(2+) influx to sustain 
      activation of protein kinase D (PKD) in a protein kinase C-dependent manner in 
      DT40 B-lymphocytes. The later phase of ERK activation depends on the small 
      G-protein Rap1, known as a downstream target of PKD, whereas the earlier phase of 
      ERK activation depends on the Ras protein. It is of interest that sustained ERK 
      phosphorylation is required for the full induction of the immediate early gene 
      Egr-1 (early growth response 1). These results suggest that TRPC3 reorganizes the 
      BCR signalling complex by switching the subtype of small G-proteins to sustain 
      ERK activation in B-lymphocytes.
CI  - (c) 2016 Authors; published by Portland Press Limited.
FAU - Numaga-Tomita, Takuro
AU  - Numaga-Tomita T
AD  - Division of Cardiocirculatory Signaling, Okazaki Institute for Integrative 
      Bioscience (National Institute for Physiological Sciences), National Institutes 
      of Natural Sciences, 5-1 Higashiyama, Myodaiji-cho, Okazaki, Aichi 444-8787, 
      Japan SOKENDAI (School of Life Science, The Graduate University for Advanced 
      Studies), Graduate School of Pharmaceutical Sciences, Kyushu University, Fukuoka 
      812-8582, Japan.
FAU - Nishida, Motohiro
AU  - Nishida M
AD  - Division of Cardiocirculatory Signaling, Okazaki Institute for Integrative 
      Bioscience (National Institute for Physiological Sciences), National Institutes 
      of Natural Sciences, 5-1 Higashiyama, Myodaiji-cho, Okazaki, Aichi 444-8787, 
      Japan SOKENDAI (School of Life Science, The Graduate University for Advanced 
      Studies), Graduate School of Pharmaceutical Sciences, Kyushu University, Fukuoka 
      812-8582, Japan PRESTO, JST, 4-1-8 Honcho, Kawaguchi, Saitama 332-0012, Japan 
      nishida@nips.ac.jp mori@sbchem.kyoto-u.ac.jp.
FAU - Putney, James W Jr
AU  - Putney JW Jr
AD  - National Institute of Environmental Health Sciences, National Institutes of 
      Health (NIH), 2233, Research Triangle Park, NC 27709, U.S.A.
FAU - Mori, Yasuo
AU  - Mori Y
AD  - Laboratory of Molecular Biology, Department of Synthetic and Biological 
      Chemistry, Graduate School of Engineering, Kyoto University, Kyoto University 
      Katsura campus, Nishikyo-ku, Kyoto 615-8510, Japan nishida@nips.ac.jp 
      mori@sbchem.kyoto-u.ac.jp.
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20151109
PL  - England
TA  - Biochem J
JT  - The Biochemical journal
JID - 2984726R
RN  - 0 (TRPC Cation Channels)
RN  - 0 (TRPC3 cation channel)
RN  - EC 2.7.10.- (protein kinase D)
RN  - EC 2.7.11.13 (Protein Kinase C)
RN  - EC 3.6.5.2 (rap1 GTP-Binding Proteins)
SB  - IM
MH  - Animals
MH  - B-Lymphocytes/*metabolism
MH  - Cell Line
MH  - Chickens
MH  - MAP Kinase Signaling System/*physiology
MH  - Protein Kinase C/*metabolism
MH  - TRPC Cation Channels/*biosynthesis
MH  - rap1 GTP-Binding Proteins/*metabolism
OTO - NOTNLM
OT  - B-lymphocytes
OT  - Ca2+ signalling
OT  - ERK
OT  - Egr-1
OT  - Rap1
OT  - TRP channel
EDAT- 2015/11/11 06:00
MHDA- 2016/05/05 06:00
CRDT- 2015/11/11 06:00
PHST- 2015/05/26 00:00 [received]
PHST- 2015/11/09 00:00 [accepted]
PHST- 2015/11/11 06:00 [entrez]
PHST- 2015/11/11 06:00 [pubmed]
PHST- 2016/05/05 06:00 [medline]
AID - BJ20150596 [pii]
AID - 10.1042/BJ20150596 [doi]
PST - ppublish
SO  - Biochem J. 2016 Jan 15;473(2):201-10. doi: 10.1042/BJ20150596. Epub 2015 Nov 9.