scholarly journals Cell Cycle Regulation by Chlamydomonas Cyclin-Dependent Protein Kinases

2018 ◽  
Vol 30 (2) ◽  
pp. 271-271
Author(s):  
Gregory Bertoni
2019 ◽  
Vol 19 (12) ◽  
pp. 1051-1058 ◽  
Author(s):  
Ting Wang ◽  
Zhuyu Xu ◽  
Yongping Lu ◽  
Jianyou Shi ◽  
Wenbo Liu ◽  
...  

Sirtuins family is a class of NDA+ dependent protein deacetylases that play a key role in the regulation of several aspects of biological processes, such as cell cycle regulation, autophagy, immune and inflammatory response. Many studies have shown that sirtuins2 as a key player in the cancer pathway is of great significance in tumorigenesis. This review summarizes the newly discovered, in recent years, some SIRT2 inhibitors for cancer target structure, action mechanism, biological activity, substrate specificity, and signaling pathways.


2009 ◽  
Vol 17 (2) ◽  
pp. 244-256 ◽  
Author(s):  
Anton Khmelinskii ◽  
Johanna Roostalu ◽  
Helio Roque ◽  
Claude Antony ◽  
Elmar Schiebel

1996 ◽  
Vol 317 (3) ◽  
pp. 633-641 ◽  
Author(s):  
Stephen A. OSMANI ◽  
Xiang S. YE

Great progress has recently been made in our understanding of the regulation of the eukaryotic cell cycle, and the central role of cyclin-dependent kinases is now clear. In Aspergillus nidulans it has been established that a second class of cell-cycle-regulated protein kinases, typified by NIMA (encoded by the nimA gene), is also required for cell cycle progression into mitosis. Indeed, both p34cdc2/cyclin B and NIMA have to be correctly activated before mitosis can be initiated in this species, and p34cdc2/cyclin B plays a role in the mitosis-specific activation of NIMA. In addition, both kinases have to be proteolytically destroyed before mitosis can be completed. NIMA-related kinases may also regulate the cell cycle in other eukaryotes, as expression of NIMA can promote mitotic events in yeast, frog or human cells. Moreover, dominant-negative versions of NIMA can adversely affect the progression of human cells into mitosis, as they do in A. nidulans. The ability of NIMA to influence mitotic regulation in human and frog cells strongly suggests the existence of a NIMA pathway of mitotic regulation in higher eukaryotes. A growing number of NIMA-related kinases have been isolated from organisms ranging from fungi to humans, and some of these kinases are also cell-cycle-regulated. How NIMA-related kinases and cyclin-dependent kinases act in concert to promote cell cycle transitions is just beginning to be understood. This understanding is the key to a full knowledge of cell cycle regulation.


Blood ◽  
2007 ◽  
Vol 109 (10) ◽  
pp. 4351-4359 ◽  
Author(s):  
Henric S. Adler ◽  
Sebastian Kubsch ◽  
Edith Graulich ◽  
Stephan Ludwig ◽  
Juergen Knop ◽  
...  

Abstract Regulatory T cells play an essential role in the control of self-tolerance and processes of adaptive immunity. Tolerogenic IL-10–modulated human dendritic cells (IL-10DCs) induce anergic T cells with strong suppressive properties (iTregs) that inhibit the activation of effector T cells. In this study, we evaluated the interaction between cell-cycle regulation and intracellular signaling in these iTregs. Analysis of signal transduction events revealed a down-regulation of the mitogen-activated protein kinases (MAPKs) Jun N-terminal kinase (JNK) and a nonactivation of extracellular-signal–regulated kinase (ERK) in contrast to a marked activation of p38 MAPK and the p38 effector MAPK-activated protein kinases 2/3 (MAPKAP2/3). The elevated activation of p38 is critical for the induction and maintenance of anergy controlled by an increased expression of the cell-cycle inhibitor p27Kip1. Moreover, blocking experiments with the specific inhibitor SB203580 demonstrated that the regulatory function of iTregs is associated with an enhanced p38 MAPK activity. In contrast to other Treg populations, the suppressor function of iTregs is independent of IL-10. In conclusion, our data indicate that a cross-talk of cell-cycle regulation and p38-dependent signal transduction is required for the suppressor function of iTregs.


2012 ◽  
Vol 125 (19) ◽  
pp. 4423-4433 ◽  
Author(s):  
A. M. Fry ◽  
L. O'Regan ◽  
S. R. Sabir ◽  
R. Bayliss

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