Role of Cell Cycle Proteins in CNS Injury

2007 ◽  
Vol 32 (10) ◽  
pp. 1799-1807 ◽  
Author(s):  
Kimberly R. Byrnes ◽  
Alan I. Faden
2003 ◽  
Vol 23 (6) ◽  
pp. 569-582 ◽  
Author(s):  
Siân V Griffin ◽  
Raimund Pichler ◽  
Takehiko Wada ◽  
Michael Vaughan ◽  
Raghu Durvasula ◽  
...  

2013 ◽  
Vol 270 (12) ◽  
pp. 3153-3162 ◽  
Author(s):  
Fernando López ◽  
César Álvarez-Marcos ◽  
Marta Alonso-Guervós ◽  
Francisco Domínguez ◽  
Carlos Suárez ◽  
...  

2003 ◽  
Vol 18 (1) ◽  
pp. 3-8 ◽  
Author(s):  
Michio Nagata ◽  
Shinsuke Tomari ◽  
Katsuyoshi Kanemoto ◽  
Joichi Usui ◽  
Kevin Lemley

2011 ◽  
Author(s):  
M. Carla Cabrera ◽  
Edgar S. Diaz-Cruz ◽  
Michael J. Pishvaian ◽  
Donald Muccio ◽  
Clinton Grubbs ◽  
...  

10.2741/a501 ◽  
2000 ◽  
Vol 5 (3) ◽  
pp. d121-137 ◽  
Author(s):  
John W Ludlow

Author(s):  
Shamim Mushtaq

Uninhibited proliferation and abnormal cell cycle regulation are the hallmarks of cancer. The main role of cyclin dependent kinases is to regulate the cell cycle and cell proliferation. These protein kinases are frequently down regulated or up regulated in various cancers. Two CDK family members, CDK 11 and 12, have contradicting views about their roles in different cancers. For example, one study suggests that the CDK 11 isoforms, p58, inhibits growth of breast cancer whereas, the CDK 11 isoform, p110, is highly expressed in breast tumor. Studies regarding CDK 12 show variation of opinion towards different parts of the body, however there is a consensus that upregulation of cdk12 increases the risk of breast cancer. Hence, CDK 11 and CDK 12 need to be analyzed to confirm their mechanism and their role regarding therapeutics, prognostic value, and ethnicity in cancer. This article gives an outline on both CDKs of information known up to date from Medline, PubMed, Google Scholar and Web of Science search engines, which were explored and thirty relevant researches were finalized.


2019 ◽  
Vol 26 (11) ◽  
pp. 800-818
Author(s):  
Zujian Xiong ◽  
Xuejun Li ◽  
Qi Yang

Pituitary Tumor Transforming Gene (PTTG) of human is known as a checkpoint gene in the middle and late stages of mitosis, and is also a proto-oncogene that promotes cell cycle progression. In the nucleus, PTTG works as securin in controlling the mid-term segregation of sister chromatids. Overexpression of PTTG, entering the nucleus with the help of PBF in pituitary adenomas, participates in the regulation of cell cycle, interferes with DNA repair, induces genetic instability, transactivates FGF-2 and VEGF and promotes angiogenesis and tumor invasion. Simultaneously, overexpression of PTTG induces tumor cell senescence through the DNA damage pathway, making pituitary adenoma possessing the potential self-limiting ability. To elucidate the mechanism of PTTG in the regulation of pituitary adenomas, we focus on both the positive and negative function of PTTG and find out key factors interacted with PTTG in pituitary adenomas. Furthermore, we discuss other possible mechanisms correlate with PTTG in pituitary adenoma initiation and development and the potential value of PTTG in clinical treatment.


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