Cyclin-Dependent Kinase Synthetic Lethality Partners in DNA Damage Response

Cyclin-dependent kinases (CDKs) are pivotal mediators and effectors of the DNA damage response (DDR) that regulate both the pathway components and proteins involved in repair processes. Synthetic lethality (SL) describes a situation in which two genes are linked in such a way that the lack of functi...

Full description

Saved in:
Bibliographic Details
Published in:International journal of molecular sciences 2022-03, Vol.23 (7), p.3555
Main Authors: Kciuk, Mateusz, Gielecińska, Adrianna, Mujwar, Somdutt, Mojzych, Mariusz, Kontek, Renata
Format: Article
Language:English
Subjects:
Cancer
Cell cycle
Cell death
Cell division
Cell viability
Cyclin-dependent kinase
cyclin-dependent kinase (CDK)
Cyclin-dependent kinases
Cyclin-Dependent Kinases - genetics
Cyclin-Dependent Kinases - metabolism
Deoxyribonucleic acid
Depletion
DNA
DNA damage
DNA Damage - genetics
DNA damage response (DDR)
DNA Repair
inhibitor
Kinases
Licenses
Metabolism
MYC oncogene
Myc protein
p53 Protein
poly (ADP-ribose) polymerase 1 (PARP-1)
Poly(ADP-ribose) polymerase
Poly(ADP-ribose) Polymerase Inhibitors
Poly(ADP-ribose) Polymerases - metabolism
Proteins
Regulation
Repair
Review
Ribose
Synthetic Lethal Mutations
synthetic lethality
Transcription factors
Tumor cells
Tumors
Citations: Items that this one cites
Items that cite this one
Online Access:Get full text
Tags: Add Tag
No Tags, Be the first to tag this record!
Description
Summary:Cyclin-dependent kinases (CDKs) are pivotal mediators and effectors of the DNA damage response (DDR) that regulate both the pathway components and proteins involved in repair processes. Synthetic lethality (SL) describes a situation in which two genes are linked in such a way that the lack of functioning of just one maintains cell viability, while depletion of both triggers cell death. Synthetic lethal interactions involving CDKs are now emerging, and this can be used to selectively target tumor cells with DNA repair defects. In this review, SL interactions of CDKs with protooncogene products MYC, poly (ADP-ribose) polymerase (PARP-1), and cellular tumor antigen p53 (TP53) are discussed. The individual roles of each of the SL partners in DDR are described.
ISSN:1422-0067
1661-6596
1422-0067
DOI:10.3390/ijms23073555