Structural impact of 8-oxoguanine on human topoisomerase I

Lesher, D.; Pommier, ﻿Yves; Stewart, Lance; Redinbo, Matthew R.

doi:10.1107/s0108767302089869

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Tdp1 and Scan11

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2007

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“…Trapping is caused by displacement of the 5′hydroxyl terminus, which becomes unavailable for attack on the TopoI cleavage complex. Similarly, TopoI cleavage complexes can become unduly long lived due to the enhanced binding of TopoI to oxidative base lesions, as demonstrated for 8 oxoguanine (Lesher et al, 2002). Dead-end or long-lived TopoI cleavage complexes serve as the substrate for TDP1, following the proteolytic degradation of the topoisomerase (Debéthune et al, 2002;Interthal et al, 2001).…”

Section: Tdp1 and Scan1mentioning

confidence: 99%

Defective DNA Repair and Neurodegenerative Disease

Rass

Ahel

West

2007

Cell

307

254

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Defects in cellular DNA repair processes have been linked to genome instability, heritable cancers, and premature aging syndromes. Yet defects in some repair processes manifest themselves primarily in neuronal tissues. This review focuses on studies defining the molecular defects associated with several human neurological disorders, particularly ataxia with oculomotor apraxia 1 (AOA1) and spinocerebellar ataxia with axonal neuropathy 1 (SCAN1). A picture is emerging to suggest that brain cells, due to their nonproliferative nature, may be particularly prone to the progressive accumulation of unrepaired DNA lesions.

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Section: Tdp1 and Scan1mentioning

confidence: 99%