Cyclin-Dependent Kinase Synthetic Lethality Partners in DNA Damage Response

被引：10

作者：

Kciuk, Mateusz ^{[1
,2
]}

Gielecinska, Adrianna ^{[1
]}

Mujwar, Somdutt ^{[3
]}

Mojzych, Mariusz ^{[4
]}

Kontek, Renata ^{[1
]}

机构：

[1] Univ Lodz, Dept Mol Biotechnol & Genet, Banacha 12-16, PL-90237 Lodz, Poland

[2] Univ Lodz, Doctoral Sch Exact & Nat Sci, Banacha St 12-16, PL-90237 Lodz, Poland

[3] Maharishi Markandeshwar Deemed Univ Mullana, MM Coll Pharm, Ambala 133207, India

[4] Siedlce Univ Nat Sci & Humanities, Dept Chem, 3 Maja 54, PL-08110 Siedlce, Poland

来源：

INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES | 2022年 / 23卷 / 07期

关键词：

cyclin-dependent kinase (CDK); DNA damage response (DDR); inhibitor; MYC oncogene; poly (ADP-ribose) polymerase 1 (PARP-1); synthetic lethality; POLY(ADP-RIBOSE) POLYMERASE PARP; C-MYC; GENOMIC INSTABILITY; BREAST-CANCER; CELL LYMPHOMA; P53; REPLICATION; INHIBITION; CDK1; APOPTOSIS;

D O I：

10.3390/ijms23073555

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

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.

引用

页数：16

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