PMID- 17941051
OWN - NLM
STAT- MEDLINE
DCOM- 20080428
LR  - 20091119
IS  - 1097-4547 (Electronic)
IS  - 0360-4012 (Linking)
VI  - 86
IP  - 3
DP  - 2008 Feb 15
TI  - The MAPK pathway is required for depolarization-induced "promiscuous" 
      immediate-early gene expression but not for depolarization-restricted 
      immediate-early gene expression in neurons.
PG  - 593-602
AB  - Depolarization, growth factors, neurotrophins, and other stimuli induce 
      expression of immediate early genes (IEGs) in neurons. We identified a subset of 
      IEGs, IPD-IEGs, which are induced preferentially by depolarization, but not by 
      neurotrophins or growth factors, in PC12 cells. The "promiscuous" IEGs Egr1 and 
      c-fos, induced by growth factors and neurotrophins, in addition to 
      depolarization, require activation of the MAP kinase signaling pathway for 
      induction in response to KCl depolarization in PC12 cells; MEK1/2 inhibitors 
      block KCl-induced Egr1 and c-fos expression. In contrast, MEK1/2 inhibition has 
      no effect on KCl-induced expression of the known IPD-IEGs in PC12 cells. 
      Additional "candidate" IDP-IEGs were identified by a microarray comparison of 
      genes induced by KCl in the presence vs. the absence of an MEK1/2 inhibitor in 
      PC12 cells. Northern blot analyses demonstrated that representative newly 
      identified candidate IPD-IEGs, as with the known IPD-IEGs, are also induced by a 
      MAP kinase- independent pathway in response to depolarization, both in PC12 cells 
      and in rat primary cortical neurons. Nerve growth factor and epidermal growth 
      factor are unable to induce the expression of the Crem/Icer, Nur77, Nor1, Rgs2, 
      Dusp1 (Mkp1), and Dscr1 genes in PC12 cells, validating their identification as 
      IPD-IEGs. Inhibiting calcium/calmodulin-dependent kinase II (CaMKII), 
      calcineurin, or protein kinase A (PKA) activity prevents KCl-induced IPD-IEG mRNA 
      accumulation, suggesting that the IPD-IEG genes are induced by depolarization in 
      neurons via a combination of calcineurin/PKA- and CaMKII-dependent pathways.
CI  - (c) 2007 Wiley-Liss, Inc.
FAU - Machado, Hidevaldo B
AU  - Machado HB
AD  - Department of Biological Chemistry, University of California, Los Angeles, Los 
      Angeles, California, USA.
FAU - Vician, Linda J
AU  - Vician LJ
FAU - Herschman, Harvey R
AU  - Herschman HR
LA  - eng
GR  - R01 NS28660/NS/NINDS NIH HHS/United States
PT  - Comparative Study
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
PL  - United States
TA  - J Neurosci Res
JT  - Journal of neuroscience research
JID - 7600111
RN  - 0 (Early Growth Response Protein 1)
RN  - 0 (Egr1 protein, rat)
RN  - 0 (Mitogens)
RN  - 0 (Nerve Growth Factors)
RN  - 0 (Proto-Oncogene Proteins c-fos)
RN  - EC 2.7.11.11 (Cyclic AMP-Dependent Protein Kinases)
RN  - EC 2.7.11.17 (Calcium-Calmodulin-Dependent Protein Kinase Type 2)
RN  - EC 2.7.11.24 (Mitogen-Activated Protein Kinases)
RN  - EC 3.1.3.16 (Calcineurin)
SB  - IM
MH  - Animals
MH  - Blotting, Northern
MH  - Calcineurin/metabolism
MH  - Calcium-Calmodulin-Dependent Protein Kinase Type 2/metabolism
MH  - Cerebral Cortex/cytology/drug effects/metabolism/physiology
MH  - Cyclic AMP-Dependent Protein Kinases/metabolism
MH  - Early Growth Response Protein 1/*genetics
MH  - Electrophysiology
MH  - Gene Expression/*physiology
MH  - MAP Kinase Signaling System/*physiology
MH  - Mitogen-Activated Protein Kinases/*metabolism
MH  - Mitogens/pharmacology
MH  - Nerve Growth Factors/pharmacology
MH  - Neurons/drug effects/metabolism/*physiology
MH  - PC12 Cells/drug effects/metabolism
MH  - Proto-Oncogene Proteins c-fos/*genetics
MH  - Rats
MH  - Reproducibility of Results
MH  - Signal Transduction/physiology
EDAT- 2007/10/18 09:00
MHDA- 2008/04/29 09:00
CRDT- 2007/10/18 09:00
PHST- 2007/10/18 09:00 [pubmed]
PHST- 2008/04/29 09:00 [medline]
PHST- 2007/10/18 09:00 [entrez]
AID - 10.1002/jnr.21529 [doi]
PST - ppublish
SO  - J Neurosci Res. 2008 Feb 15;86(3):593-602. doi: 10.1002/jnr.21529.