PMID- 10213452
OWN - NLM
STAT- MEDLINE
DCOM- 19990615
LR  - 20141120
IS  - 0022-3034 (Print)
IS  - 0022-3034 (Linking)
VI  - 39
IP  - 1
DP  - 1999 Apr
TI  - Kainate-elicited seizures induce mRNA encoding a CaMK-related peptide: a putative
      modulator of kinase activity in rat hippocampus.
PG  - 41-50
AB  - By means of differential display techniques, we have previously identified an
      mRNA transcript whose expression is highly induced in the rat hippocampus by
      kainate-elicited seizures. Here, we report the cloning of a corresponding cDNA
      encoding a 55-amino-acid, serine-rich peptide which contains four predicted
      phosphorylation sites. The peptide was designated CaMK-related peptide (CARP) as 
      it shares significant amino acid sequence identity with part of a novel putative 
      calcium/calmodulin-dependent kinase (CaMK-VI) that was also cloned in this study.
      It appears that CARP and CaMK-VI are derived from the same gene through
      differential splicing. Intriguingly, CARP also exhibits 64% amino acid sequence
      identity with the C-terminal part of human doublecortin, encoded by a recently
      identified gene which is mutated in patients with X-linked lissencephaly and the 
      double-cortex syndrome. In addition, the structure of CARP resembles the
      autoinhibitory, serine-rich N-terminal domain of CaMK-IV, suggesting a possible
      modulatory role of CARP with respect to CaMK activity. Northern blot analysis and
      in situ hybridization experiments showed that CARP mRNA is specifically induced
      by kainate-elicited seizures in the dentate gyrus and in the pyramidal layers CA1
      and CA2, but not in CA3. In contrast, kainate-induced seizures did not change the
      level of expression of the CaMK-VI gene. We propose that CARP induction leads to 
      the modulation of kinase activity in specific subregions of the rat hippocampus, 
      providing a negative feedback mechanism for seizure-induced kinases.
FAU - Vreugdenhil, E
AU  - Vreugdenhil E
AD  - Division of Medical Pharmacology, Leiden/Amsterdam Center for Drug Research,
      Leiden University, The Netherlands.
FAU - Datson, N
AU  - Datson N
FAU - Engels, B
AU  - Engels B
FAU - de Jong, J
AU  - de Jong J
FAU - van Koningsbruggen, S
AU  - van Koningsbruggen S
FAU - Schaaf, M
AU  - Schaaf M
FAU - de Kloet, E R
AU  - de Kloet ER
LA  - eng
SI  - GENBANK/AF045469
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - J Neurobiol
JT  - Journal of neurobiology
JID - 0213640
RN  - 0 (Carrier Proteins)
RN  - 0 (DNA, Complementary)
RN  - 0 (Microtubule-Associated Proteins)
RN  - 0 (Neuropeptides)
RN  - 0 (Phosphoproteins)
RN  - 0 (RNF34 protein, human)
RN  - 0 (Recombinant Proteins)
RN  - 0 (doublecortin protein)
RN  - EC 2.7.11.17 (Calcium-Calmodulin-Dependent Protein Kinases)
RN  - SIV03811UC (Kainic Acid)
SB  - IM
MH  - Amino Acid Sequence
MH  - Animals
MH  - Calcium-Calmodulin-Dependent Protein Kinases/chemistry
MH  - Carrier Proteins
MH  - Cloning, Molecular
MH  - Consensus Sequence
MH  - DNA, Complementary
MH  - Gene Expression Regulation/drug effects
MH  - Hippocampus/drug effects/*metabolism/pathology
MH  - Humans
MH  - Kainic Acid/*toxicity
MH  - Male
MH  - *Microtubule-Associated Proteins
MH  - Molecular Sequence Data
MH  - Neuropeptides/chemistry/genetics
MH  - Phosphoproteins/biosynthesis/chemistry/*genetics
MH  - Rats
MH  - Rats, Wistar
MH  - Recombinant Proteins/biosynthesis/chemistry
MH  - Seizures/chemically induced/genetics/*metabolism
MH  - Sequence Alignment
MH  - Sequence Homology, Amino Acid
MH  - Transcription, Genetic/*drug effects
EDAT- 1999/04/23 02:03
MHDA- 2000/06/20 09:00
CRDT- 1999/04/23 02:03
PHST- 1999/04/23 02:03 [pubmed]
PHST- 2000/06/20 09:00 [medline]
PHST- 1999/04/23 02:03 [entrez]
AID - 10.1002/(SICI)1097-4695(199904)39:1<41::AID-NEU4>3.0.CO;2-X [pii]
PST - ppublish
SO  - J Neurobiol. 1999 Apr;39(1):41-50.