Cell cycle regulation of DNA repair in normal and repair deficient human cells

1981 ◽  
Vol 36 (1) ◽  
pp. 19-31 ◽  
Author(s):  
Pawan K. Gupta ◽  
Michael A. Sirover
Keyword(s):  
Cell Cycle ◽  
Dna Repair ◽  
Cell Cycle Regulation ◽  
Human Cells ◽  
Cycle Regulation

scholarly journals Genetic variants and cognitive functions in patients with brain tumors

2019 ◽  
Vol 21 (10) ◽  
pp. 1297-1309 ◽  
Author(s):  
Denise D Correa ◽  
Jaya Satagopan ◽  
Axel Martin ◽  
Erica Braun ◽  
Maria Kryza-Lacombe ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Cell Cycle ◽  
Dna Repair ◽  
Brain Tumor ◽  
Brain Tumors ◽  
Cell Cycle Regulation ◽  
Cognitive Outcome ◽  
Cholesterol Transport ◽  
Tumor Patients ◽  
Cycle Regulation

AbstractBackgroundPatients with brain tumors treated with radiotherapy (RT) and chemotherapy (CT) often experience cognitive dysfunction. We reported that single nucleotide polymorphisms (SNPs) in the APOE, COMT, and BDNF genes may influence cognition in brain tumor patients. In this study, we assessed whether genes associated with late-onset Alzheimer’s disease (LOAD), inflammation, cholesterol transport, dopamine and myelin regulation, and DNA repair may influence cognitive outcome in this population.MethodsOne hundred and fifty brain tumor patients treated with RT ± CT or CT alone completed a neurocognitive assessment and provided a blood sample for genotyping. We genotyped genes/SNPs in these pathways: (i) LOAD risk/inflammation/cholesterol transport, (ii) dopamine regulation, (iii) myelin regulation, (iv) DNA repair, (v) blood–brain barrier disruption, (vi) cell cycle regulation, and (vii) response to oxidative stress. White matter (WM) abnormalities were rated on brain MRIs.ResultsMultivariable linear regression analysis with Bayesian shrinkage estimation of SNP effects, adjusting for relevant demographic, disease, and treatment variables, indicated strong associations (posterior association summary [PAS] ≥ 0.95) among tests of attention, executive functions, and memory and 33 SNPs in genes involved in: LOAD/inflammation/cholesterol transport (eg, PDE7A, IL-6), dopamine regulation (eg, DRD1, COMT), myelin repair (eg, TCF4), DNA repair (eg, RAD51), cell cycle regulation (eg, SESN1), and response to oxidative stress (eg, GSTP1). The SNPs were not significantly associated with WM abnormalities.ConclusionThis novel study suggests that polymorphisms in genes involved in aging and inflammation, dopamine, myelin and cell cycle regulation, and DNA repair and response to oxidative stress may be associated with cognitive outcome in patients with brain tumors.

scholarly journals Focus-ING on DNA Integrity: Implication of ING Proteins in Cell Cycle Regulation and DNA Repair Modulation

Cancers ◽  
2019 ◽  
Vol 12 (1) ◽  
pp. 58
Author(s):  
Jérôme Archambeau ◽  
Alice Blondel ◽  
Rémy Pedeux
Keyword(s):  
Cell Cycle ◽  
Dna Repair ◽  
Chromatin Remodeling ◽  
Tumor Suppressor Genes ◽  
Cell Cycle Regulation ◽  
Genomic Stability ◽  
Dna Integrity ◽  
Damage Response ◽  
The Stability ◽  
Cycle Regulation

The ING family of tumor suppressor genes is composed of five members (ING1-5) involved in cell cycle regulation, DNA damage response, apoptosis and senescence. All ING proteins belong to various HAT or HDAC complexes and participate in chromatin remodeling that is essential for genomic stability and signaling pathways. The gatekeeper functions of the INGs are well described by their role in the negative regulation of the cell cycle, notably by modulating the stability of p53 or the p300 HAT activity. However, the caretaker functions are described only for ING1, ING2 and ING3. This is due to their involvement in DNA repair such as ING1 that participates not only in NERs after UV-induced damage, but also in DSB repair in which ING2 and ING3 are required for accumulation of ATM, 53BP1 and BRCA1 near the lesion and for the subsequent repair. This review summarizes evidence of the critical roles of ING proteins in cell cycle regulation and DNA repair to maintain genomic stability.

scholarly journals Lack of cell cycle regulation of telomerase activity in human cells

1997 ◽  
Vol 94 (20) ◽  
pp. 10687-10692 ◽  
Author(s):  
S. E. Holt ◽  
D. L. Aisner ◽  
J. W. Shay ◽  
W. E. Wright
Keyword(s):  
Cell Cycle ◽  
Cell Cycle Regulation ◽  
Telomerase Activity ◽  
Human Cells ◽  
Cycle Regulation

scholarly journals Cell cycle regulation of human DNA repair and chromatin remodeling genes

DNA Repair ◽  
2015 ◽  
Vol 30 ◽  
pp. 53-67 ◽  
Author(s):  
Robin Mjelle ◽  
Siv Anita Hegre ◽  
Per Arne Aas ◽  
Geir Slupphaug ◽  
Finn Drabløs ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Dna Repair ◽  
Chromatin Remodeling ◽  
Cell Cycle Regulation ◽  
Human Dna ◽  
Cycle Regulation

SP-02: Cell Cycle Regulation of the DNA Damage Response: Targeting WEE1 Kinase to Impair DNA Repair.

2012 ◽  
Vol 104 ◽  
pp. 21
Author(s):  
M.A.T.M. Van Vugt ◽  
M. Krajewska ◽  
H. Sillje ◽  
A.M. Heijink ◽  
Y. Bisselink ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Dna Damage ◽  
Dna Repair ◽  
Dna Damage Response ◽  
Cell Cycle Regulation ◽  
Damage Response ◽  
Wee1 Kinase ◽  
Cycle Regulation

scholarly journals Cell cycle regulation in Aspergillus by two protein kinases

1996 ◽  
Vol 317 (3) ◽  
pp. 633-641 ◽  
Author(s):  
Stephen A. OSMANI ◽  
Xiang S. YE
Keyword(s):  
Cell Cycle ◽  
Protein Kinases ◽  
Cell Cycle Regulation ◽  
Cell Cycle Progression ◽  
Human Cells ◽  
Dominant Negative ◽  
Cyclin B ◽  
Cyclin Dependent Kinases ◽  
Cycle Regulation ◽  
Mitotic Regulation

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.

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