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1                                    The three xeroderma pigmentosum group A and the xeroderma pigmento
2 ome sample showed the high susceptibility of xeroderma pigmentosum groups A and D only at a higher fl
3 istently, RecQ4 could directly interact with xeroderma pigmentosum group A, and this interaction was
4 plex-induced mutagenesis was not detected in xeroderma pigmentosum group A cells nor in Cockayne's sy
5  is activated in Cockayne's syndrome but not Xeroderma pigmentosum group A cells providing evidence t
6                                          The xeroderma pigmentosum group A complementing protein (XPA
7                                          The xeroderma pigmentosum group A complementing protein (XPA
8 p70) and 34-kDa (p34) subunits interact with Xeroderma pigmentosum group A complementing protein (XPA
9 um group A mutant cells, suggesting that the xeroderma pigmentosum group A damage recognition protein
10 JW cells and cells with defective Artemis or xeroderma pigmentosum group A genes.
11 on of the nuclear foci formed with RecQ4 and xeroderma pigmentosum group A in human cells.
12                  Bioassays were conducted in xeroderma pigmentosum group A knockout mice and diethyln
13 eased gamma-OHPdG levels in the liver DNA of xeroderma pigmentosum group A knockout mice and remarkab
14 randed breaks were not made by extracts from xeroderma pigmentosum group A mutant cells, suggesting t
15 asts deficient in DNA repair (derived from a xeroderma pigmentosum group A patient) failed to augment
16                                Two proteins, xeroderma pigmentosum group A protein (XPA) and replicat
17  of most NER proteins, but low levels of the xeroderma pigmentosum group A protein (XPA) and the ERCC
18     A direct interaction between RPA and the xeroderma pigmentosum group A protein (XPA) facilitates
19 ing protein that can form a complex with the xeroderma pigmentosum group A protein (XPA).
20  that of the damage recognition protein XPA (xeroderma pigmentosum group A protein).
21 omparable decreases in zinc content for XPA (xeroderma pigmentosum group A) protein (CCCC zinc finger
22 we showed that the essential NER factor XPA (xeroderma pigmentosum group A) underwent nuclear accumul
23 l mutant cell lines defective in DNA repair: xeroderma pigmentosum group A (XP-A) and Cockayne syndro
24 ed the repair of these lesions in normal and xeroderma pigmentosum group A (XP-A) cells.
25 that extracts from cells of individuals with xeroderma pigmentosum group A (XP-A) do not repair some
26 Here, we report that TC-NER-deficient cells [xeroderma pigmentosum group A (XP-A), XP-D, XP-F, XP-G,
27 pair (GM637) and repair-deficient cells from xeroderma pigmentosum groups A (XP12RO) and E (XP2RO).
28                                              Xeroderma pigmentosum group A (XPA) is a core nucleotide
29                                              Xeroderma pigmentosum Group A (XPA) is a crucial factor
30                                        Human xeroderma pigmentosum group A (XPA) is an essential prot
31 ate-limiting subunit of excision repair, the xeroderma pigmentosum group A (XPA) protein, and the exc
32 idence showing that the cellular function of xeroderma pigmentosum group A (XPA), a major nucleotide
33     We identify mitochondrial dysfunction in xeroderma pigmentosum group A (XPA), a nucleotide excisi
34 se progeroid cells exhibited nuclear foci of xeroderma pigmentosum group A (XPA), a unique nucleotide
35 um variant (XPV) cells compared with normal, xeroderma pigmentosum group A (XPA), and Fanconi anemia
36 ncluding TFIID, TFIIH, RNA polymerase II and xeroderma pigmentosum group A (XPA), in the triplex-medi
37 te cyclase activity, which in turn activated Xeroderma pigmentosum group A (XPA)-binding protein 1 an
38 ATR physically interacts with the NER factor Xeroderma pigmentosum group A (XPA).
39 o recessive cancer-predisposition syndromes, xeroderma pigmentosum group A (XPAC) and Fanconi anemia

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