Evidence that xeroderma pigmentosum cells from complementation group E are deficient in a homolog of yeast photolyase.

Patterson, P. Daniel; Chu, Gilbert

doi:10.1128/mcb.9.11.5105

Cited by 57 publications

(38 citation statements)

References 33 publications

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“…There is a rough correlation between the level of UVDRP and nucleotide excision repair [8]. Furthermore, it has been demonstrated that nuclear extracts isolated from some mammalian and yeast repair mutants fail to interact with damaged DNA [3,9,10]. These results strongly suggest the important role of cellular DRP in assisting in DNA repair.…”

Section: Introductionmentioning

confidence: 49%

“…The amount of WDRP from yeast and HeLa crude nuclear extracts is 0.55 and 0.077 molecules per megabase of genomic DNA, respectively. The human UVDRP binding increased by at least 30-fold using nuclear extracts partially purified from the HA column (data not shown), which resulted in an estimated value of more than 2.2 molecules per megabase reported by Patterson and Chu [9]. The yeast UVDRP from crude nuclear extracts is about 0.55 molecules per megabase of genomic DNA.…”

Section: Discussionmentioning

confidence: 81%

“…A DRP, which can complement in vitro repair synthesis of extracts from xeroderma pigmentosum group A (XPA) cells, has been identified in calf thymus [18]. Recently, a photolyase-binding activity was also detected in yeast and Drosophila [9,19]. In this report, we identified a UVDRP from the budding yeast, Saccharomyces cerevisiue, which also exhibits a photolyase activity.…”

Section: Introductionmentioning

confidence: 76%

“…Two recent studies suggest that yeast [9] and Drosophila [19] photolyase constitute the majority of WDRP binding activities. Here, we show that the yeast WDRP binding activity can be reduced by exposure immediately after the binding reaction to PRL (Fig.…”

Section: Yeast Uvdrp Also Exhibits Photolyase Activitymentioning

confidence: 99%

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Lack of DNA enzymatic photoreactivation in HeLa cell‐free extracts

Chao

1993

FEBS Letters

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Using a DNA-protein binding assay, we have previously identitkd and characterized a UV-damaged DNA recognition protein (UVDRP) from HeLa cells [(1991) Nucleic Acids Res. 19, 64134181. In this report, the photoreactivating activity of UVDRP from the yeast, Saccharomyces cerevisiae, and HeLa cells was investigated. Although yeast and human cells are evolutionarily different from each other, both UVDRPs were conserved in the sense of their biochemical characteristics except that the yeast UVDRP also exhibited an enzymatic photoreactivating activity. A mammalian expression vector plasmid DNA carrying the bacterial chloramphenicol acetyltransferase (CAT) gene was UV irradiated in vitro followed immediately by exposure to photoreactivating light, and its transient expression in repair-deficient xeroderma pigmentosum (XP) cells was investigated. More than 80% of the CAT activity was inhibited by UV irradiation, which was partially restored (> 60%) by a partially purified yeast photolyase. In contrast, HeLa cell extracts did not express a photoreactivatable recovery from UV-induced inhibition of the CAT activity tested in the same system. This study has demonstrated the potential use of the DNA-mobility shift assay to investigate enzymatic photoreactivation, and has indicated the absence of the repair mechanism in human cells.

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Section: Introductionmentioning

confidence: 49%

Section: Discussionmentioning

confidence: 81%

Section: Introductionmentioning

confidence: 76%

Section: Yeast Uvdrp Also Exhibits Photolyase Activitymentioning

confidence: 99%

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Lack of DNA enzymatic photoreactivation in HeLa cell‐free extracts

Chao

1993

FEBS Letters

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“…XPE interacts with DDB-2, a 178kDa protein, to form the UV-DDB damage recognition complex that stimulates the damage recognition step in GG-NER. 16 XPE interacts with a variety of proteins to modulate cellular responses to DNA damage. Interactions between XPE and the CBP/p300 17,18 and STAGA 18,19 chromatin remodeling complexes also are critical for the efficient removal of damage by the GG-NER pathway.…”

Section: Finding Dna Damage: Xpa Xpc and Xpementioning

confidence: 99%

Other Proteins Interacting with XP Proteins

Shell

Zou

Molecular Mechanisms of Xeroderma Pigmentosum

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Massive cisplatin overdose by accidental substitution for carboplatin. Toxicity and management

Chu

Mantin

Shen

et al. 1993

Cancer

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Background. Unlike the related drug carboplatin, cisplatin is highly nephrotoxic and must be given with vigorous intravenous hydration at a much lower dose. As the result of an accidental substitution of cisplatin for carboplatin, a 68‐year‐old woman received a massive overdose of cisplatin without intravenous hydration. Methods. Laboratory documentation included measurements of platinum concentrations by atomic absorption spectroscopy and of xeroderma pigmentosum group E (XPE) binding factor, a protein that is involved in the recognition step of DNA repair. Results. Toxicities included severe emesis, myelosuppression, renal failure, and deafness, which are well known. Other toxicities were seizures, hallucinations, loss of vision, and hepatic toxicity, which were unusual and may have been caused by the magnitude of the overdose. As late as day 19, there was a continued cellular response from cisplatin, as evidenced by decreased levels of XPE binding factor in extracts from the patient's peripheral blood lymphocytes. Plasmapheresis was effective in lowering the platinum concentration from greater than 2900 ng/ml to 200 ng/ml and appeared to be of clinical benefit. Even after the onset of renal failure, hydration to increase urine volume resulted in increased urinary excretion of platinum. Granulocyte‐macrophage colony‐stimulating factor (GM‐CSF) was used to ameliorate myelosuppression. The patient received a transplanted kidney from her monozygotic twin sister and survived with no clinically significant deficit except for deafness. Conclusions. No previous reports exist of survival after such a high dose of cisplatin without intravenous hydration. In the future, patients may benefit from similar management and heightened awareness of the possibility of accidental substitution.

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Evidence that xeroderma pigmentosum cells from complementation group E are deficient in a homolog of yeast photolyase.

Cited by 57 publications

References 33 publications

Lack of DNA enzymatic photoreactivation in HeLa cell‐free extracts

Lack of DNA enzymatic photoreactivation in HeLa cell‐free extracts

Other Proteins Interacting with XP Proteins

Massive cisplatin overdose by accidental substitution for carboplatin. Toxicity and management

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