| Id |
Subject |
Object |
Predicate |
Lexical cue |
| T1 |
0-144 |
Sentence |
denotes |
A 3' --> 5' XPB helicase defect in repair/transcription factor TFIIH of xeroderma pigmentosum group B affects both DNA repair and transcription. |
| T1 |
0-144 |
Sentence |
denotes |
A 3' --> 5' XPB helicase defect in repair/transcription factor TFIIH of xeroderma pigmentosum group B affects both DNA repair and transcription. |
| T2 |
145-303 |
Sentence |
denotes |
XPB is a subunit of the basal transcription factor TFIIH, which is also involved in nucleotide excision repair (NER) and potentially in cell cycle regulation. |
| T2 |
145-303 |
Sentence |
denotes |
XPB is a subunit of the basal transcription factor TFIIH, which is also involved in nucleotide excision repair (NER) and potentially in cell cycle regulation. |
| T3 |
304-463 |
Sentence |
denotes |
A frameshift mutation in the 3'-end of the XPB gene is responsible for a concurrence of two disorders: xeroderma pigmentosum (XP) and Cockayne's syndrome (CS). |
| T3 |
304-463 |
Sentence |
denotes |
A frameshift mutation in the 3'-end of the XPB gene is responsible for a concurrence of two disorders: xeroderma pigmentosum (XP) and Cockayne's syndrome (CS). |
| T4 |
464-682 |
Sentence |
denotes |
We have isolated TFIIH from cells derived from a patient (XP11BE) who carries this frameshift mutation (TFIIHmut) and from the mother of this patient (TFIIHwt) to determine the biochemical consequences of the mutation. |
| T4 |
464-682 |
Sentence |
denotes |
We have isolated TFIIH from cells derived from a patient (XP11BE) who carries this frameshift mutation (TFIIHmut) and from the mother of this patient (TFIIHwt) to determine the biochemical consequences of the mutation. |
| T5 |
683-804 |
Sentence |
denotes |
Although identical in composition and stoichiometry to TFIIHwt, TFIIHmut shows a reduced 3' --> 5' XPB helicase activity. |
| T5 |
683-804 |
Sentence |
denotes |
Although identical in composition and stoichiometry to TFIIHwt, TFIIHmut shows a reduced 3' --> 5' XPB helicase activity. |
| T6 |
805-923 |
Sentence |
denotes |
A decrease in helicase and DNA-dependent ATPase activities was also observed with the mutated recombinant XPB protein. |
| T6 |
805-923 |
Sentence |
denotes |
A decrease in helicase and DNA-dependent ATPase activities was also observed with the mutated recombinant XPB protein. |
| T7 |
924-968 |
Sentence |
denotes |
The XPB mutation causes a severe NER defect. |
| T7 |
924-968 |
Sentence |
denotes |
The XPB mutation causes a severe NER defect. |
| T8 |
969-1058 |
Sentence |
denotes |
In addition, we provide evidence for a decrease in basal transcription activity in vitro. |
| T8 |
969-1058 |
Sentence |
denotes |
In addition, we provide evidence for a decrease in basal transcription activity in vitro. |
| T9 |
1059-1203 |
Sentence |
denotes |
The latter defect may provide an explanation for many of the XP and CS symptoms that are difficult to rationalize based solely on an NER defect. |
| T9 |
1059-1203 |
Sentence |
denotes |
The latter defect may provide an explanation for many of the XP and CS symptoms that are difficult to rationalize based solely on an NER defect. |
| T10 |
1204-1457 |
Sentence |
denotes |
Thus, this work presents the first detailed analysis of a naturally occurring mutation in a basal transcription factor and supports the concept that the combined XP/CS clinical entity is actually the result of a combined transcription/repair deficiency. |
| T10 |
1204-1457 |
Sentence |
denotes |
Thus, this work presents the first detailed analysis of a naturally occurring mutation in a basal transcription factor and supports the concept that the combined XP/CS clinical entity is actually the result of a combined transcription/repair deficiency. |