PMID- 10098834
OWN - NLM
STAT- MEDLINE
DCOM- 19990413
LR  - 20190630
IS  - 0022-3042 (Print)
IS  - 0022-3042 (Linking)
VI  - 72
IP  - 4
DP  - 1999 Apr
TI  - Molecular cloning of multiple splicing variants of JIP-1 preferentially expressed
      in brain.
PG  - 1335-43
AB  - Stress-activated protein kinase/c-Jun N-terminal kinase (SAPK/JNK) is activated
      by a variety of cellular or environmental stresses. Proper regulation of the
      SAPK/JNK pathway may be critical for cell survival or death under various
      conditions. In this study, we report the molecular cloning of novel isoforms of
      JIP-1, which harbor a putative phosphotyrosine interaction domain and a
      helix-loop-helix domain, as well as an SH3 homologous region in the C terminus.
      Northern analysis indicates that transcription variant jip-1 is expressed in
      brain and kidney and transcription variants jip-2 and jip-3 are specifically
      expressed in brain. In situ hybridization data showed that the hybridized jip
      messages were heavily concentrated in adult brain, and were particularly enriched
      in the cerebral cortex and hippocampus, the brain regions vulnerable to
      pathological states such as hypoxia-ischemia, epilepsy, and Alzheimer's disease. 
      All the deduced protein products of the jip transcription variants appear to have
      a similar property in that they inhibit the SAPK/JNK stimulation when
      overexpressed. Inhibition of SAPK activation by overexpression of the novel
      isoform JIP-2a resulted in suppression of etoposide-induced cell death in a
      neuroglioma cell line, N18TG. These findings suggest that JIP may play an
      important role in regulation of the SAPK pathway that is involved in
      stress-induced cellular responses.
FAU - Kim, I J
AU  - Kim IJ
AD  - Laboratory for Basic Research, Hanhyo Institutes of Technology, Taejon, Korea.
FAU - Lee, K W
AU  - Lee KW
FAU - Park, B Y
AU  - Park BY
FAU - Lee, J K
AU  - Lee JK
FAU - Park, J
AU  - Park J
FAU - Choi, I Y
AU  - Choi IY
FAU - Eom, S J
AU  - Eom SJ
FAU - Chang, T S
AU  - Chang TS
FAU - Kim, M J
AU  - Kim MJ
FAU - Yeom, Y I
AU  - Yeom YI
FAU - Chang, S K
AU  - Chang SK
FAU - Lee, Y D
AU  - Lee YD
FAU - Choi, E J
AU  - Choi EJ
FAU - Han, P L
AU  - Han PL
LA  - eng
SI  - GENBANK/AF109768
SI  - GENBANK/AF109769
SI  - GENBANK/AF109770
SI  - GENBANK/AF109771
SI  - GENBANK/AF109772
SI  - GENBANK/AF109773
SI  - GENBANK/AF109774
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - England
TA  - J Neurochem
JT  - Journal of neurochemistry
JID - 2985190R
RN  - 0 (Adaptor Proteins, Signal Transducing)
RN  - 0 (Carrier Proteins)
RN  - 0 (DNA, Complementary)
RN  - 0 (Mapk8ip protein, mouse)
RN  - EC 2.7.- (Protein Kinases)
RN  - EC 2.7.11.24 (JNK Mitogen-Activated Protein Kinases)
RN  - EC 2.7.12.2 (MAP Kinase Kinase 4)
RN  - EC 2.7.12.2 (Mitogen-Activated Protein Kinase Kinases)
SB  - IM
MH  - *Adaptor Proteins, Signal Transducing
MH  - Alternative Splicing/*physiology
MH  - Animals
MH  - Apoptosis/genetics
MH  - Brain/cytology/enzymology
MH  - Brain Chemistry/*physiology
MH  - Carrier Proteins/*genetics
MH  - Cloning, Molecular
MH  - DNA, Complementary/isolation & purification
MH  - Gene Expression Regulation, Enzymologic
MH  - Gene Library
MH  - *JNK Mitogen-Activated Protein Kinases
MH  - MAP Kinase Kinase 4
MH  - Mice
MH  - Mice, Inbred BALB C
MH  - *Mitogen-Activated Protein Kinase Kinases
MH  - Molecular Sequence Data
MH  - Neurons/cytology/enzymology
MH  - Protein Kinases/metabolism
MH  - Sequence Homology, Amino Acid
MH  - Signal Transduction/physiology
MH  - Transcription, Genetic/physiology
EDAT- 1999/03/31 00:00
MHDA- 1999/03/31 00:01
CRDT- 1999/03/31 00:00
PHST- 1999/03/31 00:00 [pubmed]
PHST- 1999/03/31 00:01 [medline]
PHST- 1999/03/31 00:00 [entrez]
AID - 10.1046/j.1471-4159.1999.721335.x [doi]
PST - ppublish
SO  - J Neurochem. 1999 Apr;72(4):1335-43. doi: 10.1046/j.1471-4159.1999.721335.x.