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encodes one of the two helicase components of basal transcription/DNA repair factor IIH (TFIIH), a ten-subunit, multifunctional complex that is essential for multiple processes, including basal transcription initiation and DNA damage repair via the nucleotide excision repair (NER) pathway [6,7]. Alterations in XPD resulting in defective TFIIH function are associated with UV-sensitive, multisystem disorders including xeroderma pigmentosum (XP), XP combined with Cockayne syndrome (CS), and trichothiodystrophy (TTD) [8–10]. XP is marked by sun-induced pigmentation anomalies and a greater than 1,000-fold elevation in skin cancer risk. Severe cases can also present with growth retardation and primary neurodegeneration [11]. CS and TTD, on the other hand, are segmental progeroid disorders characterised by progressive post-natal growth failure and primary demyelination resulting in severe neurodysfunction, but without a clear cancer predisposition [12–15]. Patients with TTD additionally display hallmark sulphur-deficient brittle hair and nails and scaling skin [13], resulting from a basal transcription defect in specific cell types [16,17]. A related disorder with the cancer predisposition of XP combined with the neurodevelopmental complications of CS (XPCS), although rare, has also been described [18].\n"}

{"project":"craft-ca-core-dev","denotations":[{"id":"T429","span":{"begin":0,"end":3},"obj":"PR:000007164"},{"id":"T430","span":{"begin":50,"end":91},"obj":"GO:0005675"},{"id":"T431","span":{"begin":70,"end":80},"obj":"GO:0006281"},{"id":"T432","span":{"begin":93,"end":98},"obj":"GO:0005675"},{"id":"T433","span":{"begin":132,"end":139},"obj":"GO:0032991"},{"id":"T434","span":{"begin":227,"end":244},"obj":"GO:0006281"},{"id":"T435","span":{"begin":253,"end":279},"obj":"GO:0006289"},{"id":"T436","span":{"begin":281,"end":284},"obj":"GO:0006289"},{"id":"T437","span":{"begin":316,"end":319},"obj":"PR:000007164"},{"id":"T438","span":{"begin":343,"end":348},"obj":"GO:0005675"},{"id":"T439","span":{"begin":397,"end":403},"obj":"UBERON:0000467"},{"id":"T440","span":{"begin":832,"end":837},"obj":"GO:0007567"},{"id":"T441","span":{"begin":1042,"end":1046},"obj":"UBERON:0001037"},{"id":"T442","span":{"begin":1051,"end":1056},"obj":"UBERON:0001705"},{"id":"T443","span":{"begin":1230,"end":1248},"obj":"GO:0007399"}],"text":"XPD encodes one of the two helicase components of basal transcription/DNA repair factor IIH (TFIIH), a ten-subunit, multifunctional complex that is essential for multiple processes, including basal transcription initiation and DNA damage repair via the nucleotide excision repair (NER) pathway [6,7]. Alterations in XPD resulting in defective TFIIH function are associated with UV-sensitive, multisystem disorders including xeroderma pigmentosum (XP), XP combined with Cockayne syndrome (CS), and trichothiodystrophy (TTD) [8–10]. XP is marked by sun-induced pigmentation anomalies and a greater than 1,000-fold elevation in skin cancer risk. Severe cases can also present with growth retardation and primary neurodegeneration [11]. CS and TTD, on the other hand, are segmental progeroid disorders characterised by progressive post-natal growth failure and primary demyelination resulting in severe neurodysfunction, but without a clear cancer predisposition [12–15]. Patients with TTD additionally display hallmark sulphur-deficient brittle hair and nails and scaling skin [13], resulting from a basal transcription defect in specific cell types [16,17]. A related disorder with the cancer predisposition of XP combined with the neurodevelopmental complications of CS (XPCS), although rare, has also been described [18].\n"}

{"project":"craft-ca-core-ex-dev","denotations":[{"id":"T499","span":{"begin":0,"end":3},"obj":"PR_EXT:000007164"},{"id":"T500","span":{"begin":4,"end":11},"obj":"SO_EXT:sequence_coding_function"},{"id":"T501","span":{"begin":27,"end":35},"obj":"GO_EXT:0004386"},{"id":"T502","span":{"begin":50,"end":91},"obj":"GO:0005675"},{"id":"T503","span":{"begin":56,"end":69},"obj":"GO_EXT:transcription"},{"id":"T504","span":{"begin":56,"end":69},"obj":"_FRAGMENT"},{"id":"T505","span":{"begin":81,"end":87},"obj":"GO_EXT:transcription_factor"},{"id":"T506","span":{"begin":70,"end":73},"obj":"CHEBI_SO_EXT:DNA"},{"id":"T507","span":{"begin":70,"end":80},"obj":"GO:0006281"},{"id":"T508","span":{"begin":93,"end":98},"obj":"GO:0005675"},{"id":"T509","span":{"begin":132,"end":139},"obj":"GO:0032991"},{"id":"T510","span":{"begin":198,"end":211},"obj":"GO_EXT:transcription"},{"id":"T511","span":{"begin":227,"end":230},"obj":"CHEBI_SO_EXT:DNA"},{"id":"T512","span":{"begin":227,"end":244},"obj":"GO:0006281"},{"id":"T513","span":{"begin":253,"end":263},"obj":"CHEBI_SO_EXT:nucleotide"},{"id":"T514","span":{"begin":253,"end":279},"obj":"GO:0006289"},{"id":"T515","span":{"begin":264,"end":272},"obj":"SO_EXT:sequence_deletion_process"},{"id":"T516","span":{"begin":281,"end":284},"obj":"GO:0006289"},{"id":"T517","span":{"begin":301,"end":312},"obj":"SO_EXT:sequence_alteration_entity_or_process"},{"id":"T518","span":{"begin":316,"end":319},"obj":"PR_EXT:000007164"},{"id":"T519","span":{"begin":343,"end":348},"obj":"GO:0005675"},{"id":"T520","span":{"begin":397,"end":403},"obj":"UBERON:0000467"},{"id":"T521","span":{"begin":559,"end":571},"obj":"GO_PATO_EXT:biological_pigmentation_process_or_quality"},{"id":"T522","span":{"begin":625,"end":629},"obj":"UBERON_EXT:zone_of_skin_or_skin_of_body"},{"id":"T523","span":{"begin":678,"end":684},"obj":"GO_EXT:biological_growth_entity_or_process"},{"id":"T524","span":{"begin":832,"end":837},"obj":"GO:0007567"},{"id":"T525","span":{"begin":838,"end":844},"obj":"GO_EXT:biological_growth_entity_or_process"},{"id":"T526","span":{"begin":867,"end":878},"obj":"GO_EXT:myelin_assembly_or_myelination"},{"id":"T527","span":{"begin":1016,"end":1023},"obj":"CHEBI_EXT:sulfur"},{"id":"T528","span":{"begin":1042,"end":1046},"obj":"UBERON:0001037"},{"id":"T529","span":{"begin":1051,"end":1056},"obj":"UBERON:0001705"},{"id":"T530","span":{"begin":1069,"end":1073},"obj":"UBERON_EXT:zone_of_skin_or_skin_of_body"},{"id":"T531","span":{"begin":1103,"end":1116},"obj":"GO_EXT:transcription"},{"id":"T532","span":{"begin":1136,"end":1140},"obj":"CL_GO_EXT:cell"},{"id":"T533","span":{"begin":1230,"end":1248},"obj":"GO:0007399"}],"relations":[{"id":"R245","pred":"_lexicallyChainedTo","subj":"T505","obj":"T504"}],"text":"XPD encodes one of the two helicase components of basal transcription/DNA repair factor IIH (TFIIH), a ten-subunit, multifunctional complex that is essential for multiple processes, including basal transcription initiation and DNA damage repair via the nucleotide excision repair (NER) pathway [6,7]. Alterations in XPD resulting in defective TFIIH function are associated with UV-sensitive, multisystem disorders including xeroderma pigmentosum (XP), XP combined with Cockayne syndrome (CS), and trichothiodystrophy (TTD) [8–10]. XP is marked by sun-induced pigmentation anomalies and a greater than 1,000-fold elevation in skin cancer risk. Severe cases can also present with growth retardation and primary neurodegeneration [11]. CS and TTD, on the other hand, are segmental progeroid disorders characterised by progressive post-natal growth failure and primary demyelination resulting in severe neurodysfunction, but without a clear cancer predisposition [12–15]. Patients with TTD additionally display hallmark sulphur-deficient brittle hair and nails and scaling skin [13], resulting from a basal transcription defect in specific cell types [16,17]. A related disorder with the cancer predisposition of XP combined with the neurodevelopmental complications of CS (XPCS), although rare, has also been described [18].\n"}

{"project":"2_test","denotations":[{"id":"17020410-15220921-84795124","span":{"begin":295,"end":296},"obj":"15220921"},{"id":"17020410-8465201-84795125","span":{"begin":297,"end":298},"obj":"8465201"},{"id":"17020410-11709541-84795126","span":{"begin":524,"end":525},"obj":"11709541"},{"id":"17020410-11443545-84795126","span":{"begin":524,"end":525},"obj":"11443545"},{"id":"17020410-11185579-84795127","span":{"begin":728,"end":730},"obj":"11185579"},{"id":"17020410-1308368-84795128","span":{"begin":960,"end":962},"obj":"1308368"},{"id":"17020410-11369901-84795128","span":{"begin":960,"end":962},"obj":"11369901"},{"id":"17020410-10892338-84795128","span":{"begin":960,"end":962},"obj":"10892338"},{"id":"17020410-11950998-84795128","span":{"begin":960,"end":962},"obj":"11950998"},{"id":"17020410-11369901-84795129","span":{"begin":1075,"end":1077},"obj":"11369901"},{"id":"17020410-11242112-84795130","span":{"begin":1148,"end":1150},"obj":"11242112"},{"id":"17020410-12393803-84795131","span":{"begin":1151,"end":1153},"obj":"12393803"},{"id":"17020410-15226750-84795132","span":{"begin":1317,"end":1319},"obj":"15226750"},{"id":"T92258","span":{"begin":295,"end":296},"obj":"15220921"},{"id":"T31924","span":{"begin":297,"end":298},"obj":"8465201"},{"id":"T49919","span":{"begin":524,"end":525},"obj":"11709541"},{"id":"T59412","span":{"begin":524,"end":525},"obj":"11443545"},{"id":"T88110","span":{"begin":728,"end":730},"obj":"11185579"},{"id":"T43502","span":{"begin":960,"end":962},"obj":"1308368"},{"id":"T79694","span":{"begin":960,"end":962},"obj":"11369901"},{"id":"T70430","span":{"begin":960,"end":962},"obj":"10892338"},{"id":"T83742","span":{"begin":960,"end":962},"obj":"11950998"},{"id":"T54985","span":{"begin":1075,"end":1077},"obj":"11369901"},{"id":"T87059","span":{"begin":1148,"end":1150},"obj":"11242112"},{"id":"T94780","span":{"begin":1151,"end":1153},"obj":"12393803"},{"id":"T90963","span":{"begin":1317,"end":1319},"obj":"15226750"}],"text":"XPD encodes one of the two helicase components of basal transcription/DNA repair factor IIH (TFIIH), a ten-subunit, multifunctional complex that is essential for multiple processes, including basal transcription initiation and DNA damage repair via the nucleotide excision repair (NER) pathway [6,7]. Alterations in XPD resulting in defective TFIIH function are associated with UV-sensitive, multisystem disorders including xeroderma pigmentosum (XP), XP combined with Cockayne syndrome (CS), and trichothiodystrophy (TTD) [8–10]. XP is marked by sun-induced pigmentation anomalies and a greater than 1,000-fold elevation in skin cancer risk. Severe cases can also present with growth retardation and primary neurodegeneration [11]. CS and TTD, on the other hand, are segmental progeroid disorders characterised by progressive post-natal growth failure and primary demyelination resulting in severe neurodysfunction, but without a clear cancer predisposition [12–15]. Patients with TTD additionally display hallmark sulphur-deficient brittle hair and nails and scaling skin [13], resulting from a basal transcription defect in specific cell types [16,17]. A related disorder with the cancer predisposition of XP combined with the neurodevelopmental complications of CS (XPCS), although rare, has also been described [18].\n"}