The role of p38 MAP kinase and c-Jun N-terminal protein kinase signaling in the differentiation and apoptosis of immortalized neural stem cells

Author(s):  
Se-Ran Yang ◽  
Sung-Dae Cho ◽  
Nam-Shik Ahn ◽  
Ji-Won Jung ◽  
Joon-Suk Park ◽  
...  
2003 ◽  
Vol 10 (4-6) ◽  
pp. 437-443 ◽  
Author(s):  
Takashi Kojima ◽  
Toshinobu Yamamoto ◽  
Masaki Murata ◽  
Mengdong Lan ◽  
Ken-ichi Takano ◽  
...  

Oncogene ◽  
2005 ◽  
Vol 25 (20) ◽  
pp. 2909-2919 ◽  
Author(s):  
R M Baldwin ◽  
M Garratt-Lalonde ◽  
D A E Parolin ◽  
P M Krzyzanowski ◽  
M A Andrade ◽  
...  

2005 ◽  
Vol 25 (9) ◽  
pp. 3670-3681 ◽  
Author(s):  
Deborah Brancho ◽  
Juan-Jose Ventura ◽  
Anja Jaeschke ◽  
Beth Doran ◽  
Richard A. Flavell ◽  
...  

ABSTRACT Mixed-lineage protein kinase 3 (MLK3) is a member of the mitogen-activated protein (MAP) kinase kinase kinase group that has been implicated in multiple signaling cascades, including the NF-κB pathway and the extracellular signal-regulated kinase, c-Jun NH2-terminal kinase (JNK), and p38 MAP kinase pathways. Here, we examined the effect of targeted disruption of the murine Mlk3 gene. Mlk3 −/− mice were found to be viable and healthy. Primary embryonic fibroblasts prepared from these mice exhibited no major signaling defects. However, we did find that MLK3 deficiency caused a selective reduction in tumor necrosis factor (TNF)-stimulated JNK activation. Together, these data demonstrate that MLK3 contributes to the TNF signaling pathway that activates JNK.


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