2013
DOI: 10.1002/med.21298
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Human DNA Ligases: A Comprehensive New Look for Cancer Therapy

Abstract: Living organisms belonging to all three domains of life, viz., eubacteria, archaeabacteria, and eukaryotes encode one or more DNA ligases. DNA ligases are indispensable in various DNA repair and replication processes and a deficiency or an inhibition of their activity can lead to accumulation of DNA damage and strand breaks. DNA damage, specially strand breaks at unsustainable levels can lead to replication block and/or cell death. DNA ligases as potential anticancer targets have been realized only recently. T… Show more

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Cited by 33 publications
(19 citation statements)
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References 65 publications
(129 reference statements)
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“…32 It is also known that mutations in the Lig4 gene are a cause of severe immunodeficiency. 33 It should be noted that one of the DE genes in the retina of 3-month-old OXYS rats, Ripk3, is among key regulators of programmed necrosis. Mice homozygous for knockout alleles of Ripk3 show resistance to induced inflammatory responses.…”
Section: Discussionmentioning
confidence: 99%
“…32 It is also known that mutations in the Lig4 gene are a cause of severe immunodeficiency. 33 It should be noted that one of the DE genes in the retina of 3-month-old OXYS rats, Ripk3, is among key regulators of programmed necrosis. Mice homozygous for knockout alleles of Ripk3 show resistance to induced inflammatory responses.…”
Section: Discussionmentioning
confidence: 99%
“…Small molecule inhibitors that predominantly target leading or lagging strand synthesis, such as topoisomerases [1], DNA polymerases [2], DNA ligase [3], proliferating cell nuclear antigen (PCNA) [4], ribonucleotide reductase [5], and telomerase [6], have been developed to clinically block uncontrolled cancer proliferation. Although proven chemotherapeutic agents, these compounds target both normal and malignant DNA replication and as such often exhibit deleterious side effects [710].…”
Section: Introductionmentioning
confidence: 99%
“…This may be discouraging from the 805 clinical perspective, as these data indicate that attempts to inhibit human translocations 806 using small molecule inhibitors to LIGIII and LIGIV (Singh et al 2014) are destined to 807 fail due to the robust ability of LIGI to compensate for their absence. That said, any 808 intervention that can skew the fusion spectrum towards inter-chromosomal events, 809 creating a larger mutational burden on cells and influencing their ability to escape a 810…”
Section: Translocations Involving Telomeres Are Mechanistically Distimentioning
confidence: 99%