The RIO kinases: An atypical protein kinase family required for ribosome biogenesis and cell cycle progression

2005 ◽  
Vol 1754 (1-2) ◽  
pp. 14-24 ◽  
Author(s):  
Nicole LaRonde-LeBlanc ◽  
Alexander Wlodawer
1998 ◽  
Vol 335 (2) ◽  
pp. 417-424 ◽  
Author(s):  
Kazunori AKIMOTO ◽  
Masaaki NAKAYA ◽  
Tomoyuki YAMANAKA ◽  
Junpei TANAKA ◽  
Shin-ichi MATSUDA ◽  
...  

p70 S6 kinase (p70 S6K) has been implicated in the regulation of cell cycle progression. However, the mechanism of its activation is not fully understood. In the present work, evidence is provided that an atypical protein kinase C (PKC) isotype, PKCλ, is indispensable, but not sufficient, for the activation of p70 S6K. Both the regulatory and kinase domains of PKCλ associate directly with p70 S6K. Overexpression of the kinase domain without kinase activity or the regulatory domain of PKCλ results in the suppression of the serum-induced activation of p70 S6K. In addition, two types of dominant-negative mutants of PKCλ, as well as a kinase-deficient mutant of p70 S6K, suppress serum-induced DNA synthesis and E2F activation. The overexpresion of the active form of PKCλ, however, fails to activate p70 S6K. These results suggest that PKCλ is a mediator in the regulation of p70 S6K activity and plays an important role in cell cycle progression.


2003 ◽  
Vol 8 (4) ◽  
pp. 311-324 ◽  
Author(s):  
Koichi Kitamura ◽  
Keiko Mizuno ◽  
Akiko Etoh ◽  
Yoshiko Akita ◽  
Akitomo Miyamoto ◽  
...  

2004 ◽  
Vol 232 (1) ◽  
pp. 98-105 ◽  
Author(s):  
Bingzhi Yu ◽  
Yajie Wang ◽  
Ying Liu ◽  
Yi Liu ◽  
Xinna Li ◽  
...  

2011 ◽  
Vol 286 (14) ◽  
pp. 12796-12802 ◽  
Author(s):  
Kyung-Jong Lee ◽  
Yu-Fen Lin ◽  
Han-Yi Chou ◽  
Hirohiko Yajima ◽  
Kazi R. Fattah ◽  
...  

1999 ◽  
Vol 56 (4) ◽  
pp. 1258-1261 ◽  
Author(s):  
Yoshio Terada ◽  
Seiji Inoshita ◽  
Osamu Nakashima ◽  
Michio Kuwahara ◽  
Sei Sasaki ◽  
...  

Oncogene ◽  
2008 ◽  
Vol 27 (37) ◽  
pp. 4986-4997 ◽  
Author(s):  
C W Yde ◽  
B B Olsen ◽  
D Meek ◽  
N Watanabe ◽  
B Guerra

1999 ◽  
Vol 19 (5) ◽  
pp. 3857-3868 ◽  
Author(s):  
Heidrun Ellinger-Ziegelbauer ◽  
Kathleen Kelly ◽  
Ulrich Siebenlist

ABSTRACT Signal-induced proliferation, differentiation, or stress responses of cells depend on mitogen-activated protein kinase (MAPK) cascades, the core modules of which consist of members of three successively acting kinase families (MAPK kinase kinase [MAP3K], MAPK kinase, and MAPK). It is demonstrated here that the MEKK3 kinase inhibits cell proliferation, a biologic response not commonly associated with members of the MAP3K family of kinases. A conditionally activated form of MEKK3 stably expressed in fibroblasts arrests these cells in early G1. MEKK3 critically blocks mitogen-driven expression of cyclin D1, a cyclin which is essential for progression of fibroblasts through G1. The MEKK3-induced block of cyclin D1 expression and of cell cycle progression may be mediated via p38 MAPK, a downstream effector of MEKK3. The MEKK3-mediated block of proliferation also reverses Ras-induced cellular transformation, suggesting possible tumor-suppressing functions for this kinase. Together, these results suggest an involvement of the MEKK3 kinase in negative regulation of cell cycle progression, and they provide the first insights into biologic activities of this kinase.


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