PMID- 11948429
OWN - NLM
STAT- MEDLINE
DCOM- 20020429
LR  - 20230531
IS  - 0950-9232 (Print)
IS  - 0950-9232 (Linking)
VI  - 21
IP  - 15
DP  - 2002 Apr 4
TI  - Differential effects of JNK1 and JNK2 on signal specific induction of apoptosis.
PG  - 2441-5
AB  - The c-Jun N-terminal kinases (JNKs) are activated by a variety of stress inducing 
      agents and are thought to regulate apoptosis in a cell type and signal-specific 
      manner. We have used fibroblasts lacking JNK1 or JNK2 to define their roles in 
      response to different stress signals. Lack of JNK1 results in reduced c-Jun 
      phosphorylation and resistance to UV-induced cell death. JNK2 deficient cells 
      show increased sensitivity to UV irradiation which correlates with elevated and 
      sustained phosphorylation of JNK1 and c-Jun. On the contrary, both Jnk1-/- and 
      Jnk2-/- cells were more sensitive to tumor necrosis factor - alpha (TNF-alpha) 
      and sorbitol-induced cell death. Treatment of Jnk1-/- cells with these reagents 
      resulted in reduced JNK activity and a concomitant reduction of c-Jun 
      phosphorylation, suggesting that phosphorylation of c-Jun does not influence 
      TNF-alpha and sorbitol-induced apoptosis in fibroblasts. Moreover, both JNK1 and 
      JNK2 appear to negatively regulate apoptosis independent of c-Jun 
      phosphorylation. These data provide genetic evidence that although the JNK 
      pathway is activated by a plethora of signals, it is required only for the 
      induction of UV-induced cell death in a c-Jun phosphorylation-dependent manner, 
      but not for TNF-alpha and sorbitol-induced apoptosis.
FAU - Hochedlinger, Konrad
AU  - Hochedlinger K
AD  - Research Institute of Molecular Pathology (IMP), Dr. Bohrgasse 7, A-1030 Vienna, 
      Austria.
FAU - Wagner, Erwin F
AU  - Wagner EF
FAU - Sabapathy, Kanaga
AU  - Sabapathy K
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - England
TA  - Oncogene
JT  - Oncogene
JID - 8711562
RN  - 0 (Proto-Oncogene Proteins c-jun)
RN  - 0 (Tumor Necrosis Factor-alpha)
RN  - 506T60A25R (Sorbitol)
RN  - EC 2.7.1.24 (Mitogen-Activated Protein Kinase 9)
RN  - EC 2.7.11.24 (Mitogen-Activated Protein Kinase 8)
RN  - EC 2.7.11.24 (Mitogen-Activated Protein Kinases)
SB  - IM
EIN - Oncogene. 2023 Jun;42(25):2099-2100. PMID: 37258744
MH  - Animals
MH  - *Apoptosis
MH  - Cell Line, Transformed
MH  - Cells, Cultured
MH  - Fibroblasts/cytology/metabolism/radiation effects
MH  - Gene Deletion
MH  - *MAP Kinase Signaling System
MH  - Mitogen-Activated Protein Kinase 8
MH  - Mitogen-Activated Protein Kinase 9
MH  - Mitogen-Activated Protein Kinases/genetics/*physiology
MH  - Models, Biological
MH  - Phosphorylation
MH  - Proto-Oncogene Proteins c-jun/metabolism
MH  - Sorbitol/pharmacology
MH  - Tumor Necrosis Factor-alpha/pharmacology
MH  - Ultraviolet Rays
EDAT- 2002/04/12 10:00
MHDA- 2002/05/01 10:01
CRDT- 2002/04/12 10:00
PHST- 2001/09/10 00:00 [received]
PHST- 2002/01/14 00:00 [revised]
PHST- 2002/01/18 00:00 [accepted]
PHST- 2002/04/12 10:00 [pubmed]
PHST- 2002/05/01 10:01 [medline]
PHST- 2002/04/12 10:00 [entrez]
AID - 10.1038/sj.onc.1205348 [doi]
PST - ppublish
SO  - Oncogene. 2002 Apr 4;21(15):2441-5. doi: 10.1038/sj.onc.1205348.