Poly(ADP-ribose) synthesis following DNA damage in cells heterozygous or homozygous for the xeroderma pigmentosum genotype.

McCurry, Lynette; Jacobson, Myron K.

doi:10.1016/s0021-9258(19)70002-7

Cited by 62 publications

(7 citation statements)

References 38 publications

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“…3AB had only small effects on the NAD level in undamaged cells. The results in Figure 1 are similar to those obtained with various other cell types (Skidmore et al, 1979;Rankin et al, 1980;Durkacz et al, 1980;McCurry & Jacobson, 1981;Shall et al, 1981).…”

Section: Methodssupporting

confidence: 88%

Role of poly(adenosine diphosphate ribose) in deoxyribonucleic acid repair in human fibroblasts

James¹,

Lehmann²

1982

Biochemistry

143

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We have investigated the role of poly(adenosine diphosphate ribose) in DNA repair in human fibroblasts by observing the effects of 3-aminobenzamide (3AB), a specific inhibitor of poly(ADP-ribose) synthesis, on various aspects of DNA repair. After treatment of human fibroblasts with dimethyl sulfate (DMS), 3AB retarded the joining of strand breaks; unscheduled DNA synthesis was unaffected after low doses of DMS but was stimulated after high doses. 3AB also enhanced the cytotoxicity of DMS. After gamma irradiation there was a slight inhibition by 3AB of the rejoining of single-strand breaks but no effect on the rejoining of double-strand breaks, unscheduled DNA synthesis, DNA replicative synthesis, or cytotoxicity. There were no effects of 3AB on the repair of UV damage. On the basis of the different kinetics of the various steps of excision repair processes after different treatments of fibroblasts, our results are interpreted as evidence that the synthesis of poly(ADP-ribose) is involved in the ligation step of excision repair.

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Section: Methodssupporting

confidence: 88%

Role of poly(adenosine diphosphate ribose) in deoxyribonucleic acid repair in human fibroblasts

James¹,

Lehmann²

1982

Biochemistry

143

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“…Effect of CC-1065 on NAD Content in Xeroderma Pigmentosum Fibroblasts. Previous studies have shown that the occurrence of DNA strand breaks is the common factor of DNA damage that elicits poly(ADP-ribose) synthesis (Jacobson et al, 1983;Berger et al, 1980;McCurry & Jacobson, 1981). Cells homozygous for the XP genotype are grossly defective in the introduction of DNA strand breaks (and thus in the initiation of DNA excision repair) for specific types of DNA damage including pyrimidine dimers and a variety of bulky DNA adducts.…”

Section: Resultsmentioning

confidence: 99%

“…Cells homozygous for the XP genotype are grossly defective in the introduction of DNA strand breaks (and thus in the initiation of DNA excision repair) for specific types of DNA damage including pyrimidine dimers and a variety of bulky DNA adducts. XP cells are also defective in the synthesis of poly(ADP-ribose) for such lesions (Berger et al, 1980;McCurry & Jacobson, 1981). Thus, it was of interest to determine if CC-1065, which results in a bulky but nondistortive DNA adduct, would elicit NAD depletion in these cells.…”

Section: Resultsmentioning

confidence: 99%

“…The results described here show that CC-1065 is a very potent agent for effecting NAD depletion in human cells. Previous studies of the mechanism of NAD depletion using other DNA alkylating agents have provided a likely mechanism of this effect (Smulson et al, 1977;Goodwin et al, 1978; Juarez-Salinas et Jacobson et al, 1980Jacobson et al, , 1984Berger et al, 1980;McCurry & Jacobson, 1981). DNA alkylation results in the appearance of DNA strand breaks either directly or indirectly due to enzymes involved in DNA excision repair.…”

Section: Discussionmentioning

confidence: 99%

“…A common feature of the various complmentation groups within this genotype is the inability to cause DNA incisions prerequisite to subsequent steps of DNA excision repair. It has been previously shown that XP cells are also unable to cause NAD depletion in response to UV light (McCurry & Jacobson, 1981). Since CC-1065 causes a bulky but nondistortive DNA adduct (Reynolds et al, 1985), it was of considerable interest to determine whether XP cells could cause NAD depletion in response to this drug.…”

Section: Discussionmentioning

confidence: 99%

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Depletion of nicotinamide adenine dinucleotide in normal and xeroderma pigmentosum fibroblast cells by the antitumor drug CC-1065

Jacobson¹,

Twehous²,

Hurley³

1986

Biochemistry

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CC-1065 is an extremely potent antitumor antibiotic that forms a well-defined adduct with DNA in which the molecule lies within the minor groove and is covalently attached through N3 of adenine. Addition of CC-1065 to human fibroblast cells produced a prolonged depletion of the nicotinamide adenine dinucleotide (NAD) pool even at extremely low drug concentrations (0.01 microgram/mL). The depletion of NAD by CC-1065 was blocked by 3-aminobenzamide, which is consistent with a NAD depletion mechanism involving poly-(ADP-ribose) synthesis in response to a repair-induced DNA strand breakage event. Significantly, similar extents of NAD depletion were also evident in xeroderma pigmentosum cells of complementation groups A and D following exposure to CC-1065. Since this NAD depletion is presumably associated with repair-induced incision, the repair of CC-1065-DNA adducts can probably take place by a pathway distinct from that involved in repair of more conventional bulky DNA adducts. The prolonged depletion of NAD, even at low doses of drug, suggests that CC-1065 causes DNA damage that results in a delay or block in DNA excision repair between the excision and ligation steps.

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DNA topoisomerases and DNA repair

Downes

Johnson

1988

BioEssays

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Sum ma ryDNA topoisomerases are enzymes that can modify, and may regulate, the topological state of DNA through concerted breaking and rejoining of the DNA strands. They have been believed to be directly involved in DNA excision repair, and perhaps to be required for the control of repair as well. The vicissitudes of this hypothesis provide a noteworthy example of the dangers of interpreting cellular phenomena without genetic informatior and vice versa.

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Poly(ADP-ribose) synthesis following DNA damage in cells heterozygous or homozygous for the xeroderma pigmentosum genotype.

Cited by 62 publications

References 38 publications

Role of poly(adenosine diphosphate ribose) in deoxyribonucleic acid repair in human fibroblasts

Role of poly(adenosine diphosphate ribose) in deoxyribonucleic acid repair in human fibroblasts

Depletion of nicotinamide adenine dinucleotide in normal and xeroderma pigmentosum fibroblast cells by the antitumor drug CC-1065

DNA topoisomerases and DNA repair

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