Cdk5 links with DNA damage response and cancer

As an atypical member of cyclin dependent kinase family, Cyclin dependent kinase 5 (Cdk5) is considered as a neuron-specific kinase in the past decade due to the abundant existence of its activator p35 in post-mitotic neurons. Recent studies show that Cdk5 participates in a series of biological and...

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Bibliographic Details
Published in:Molecular cancer 2017-03, Vol.16 (1), p.60-60, Article 60
Main Authors: Liu, Wan, Li, Jun, Song, Yu-Shu, Li, Yue, Jia, Yu-Hong, Zhao, Hai-Dong
Format: Article
Language:English
Subjects:
Animals
Apoptosis
Cancer
Cell cycle
Cell Cycle Checkpoints
Cyclin-Dependent Kinase 5 - antagonists & inhibitors
Cyclin-Dependent Kinase 5 - genetics
Cyclin-Dependent Kinase 5 - metabolism
Cyclin-dependent kinases
DNA Damage
DNA Replication
Gene Expression Regulation, Neoplastic
Humans
Kinases
Molecular Targeted Therapy
Neoplasms - drug therapy
Neoplasms - genetics
Neoplasms - metabolism
Neoplasms - pathology
Ovarian cancer
Protein Binding
Review
Signal Transduction - drug effects
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Summary:As an atypical member of cyclin dependent kinase family, Cyclin dependent kinase 5 (Cdk5) is considered as a neuron-specific kinase in the past decade due to the abundant existence of its activator p35 in post-mitotic neurons. Recent studies show that Cdk5 participates in a series of biological and pathological processes in non-neuronal cells, and is generally dysregulated in various cancer cells. The inhibition or knockdown of Cdk5 has been proven to play an anti-cancer role through various mechanisms, and can synergize the killing effect of chemotherapeutics. DNA damage response (DDR) is a series of regulatory events including DNA damage, cell-cycle arrest, regulation of DNA replication, and repair or bypass of DNA damage to ensure the maintenance of genomic stability and cell viability. Here we describe the regulatory mechanisms of Cdk5, its controversial roles in apoptosis and focus on its links to DDR and cancer.
ISSN:1476-4598
1476-4598
DOI:10.1186/s12943-017-0611-1