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XPD mutations are associated with an exclusive disease phenotype (e.g., XPDR722W with TTD and XPDR683W with XP) and are thus viewed as causative of the corresponding syndromes. Alleles not associated exclusively with one disorder are considered “likely null” alleles [19,20]. Some of these alleles fail to support viability in a haploid Schizosaccharomyces pombe yeast strain with a null mutation in the XPD homologue rad15 and are thus considered devoid of significant biological activity [19]. This classification of alleles as either causative or null currently defines what we refer to as a “monoallelic” paradigm of XPD disease. However, the identification in recent years of XP complementation group D patients with atypical disease presentation, including symptoms of both XP and TTD [8], casts doubt on the ability of such a monoallelic paradigm to explain clinical heterogeneity in compound heterozygotes."}

{"project":"craft-ca-core-dev","denotations":[{"id":"T444","span":{"begin":5,"end":8},"obj":"PR:000007164"},{"id":"T445","span":{"begin":77,"end":80},"obj":"PR:000007164"},{"id":"T446","span":{"begin":99,"end":102},"obj":"PR:000007164"},{"id":"T447","span":{"begin":182,"end":189},"obj":"SO:0001023"},{"id":"T448","span":{"begin":264,"end":271},"obj":"SO:0001023"},{"id":"T449","span":{"begin":295,"end":302},"obj":"SO:0001023"},{"id":"T450","span":{"begin":342,"end":373},"obj":"NCBITaxon:4896"},{"id":"T451","span":{"begin":409,"end":412},"obj":"PR:000007164"},{"id":"T452","span":{"begin":413,"end":422},"obj":"SO:0000853"},{"id":"T453","span":{"begin":423,"end":428},"obj":"PR:P26659"},{"id":"T454","span":{"begin":524,"end":531},"obj":"SO:0001023"},{"id":"T455","span":{"begin":605,"end":612},"obj":"SO:0001023"},{"id":"T456","span":{"begin":626,"end":629},"obj":"PR:000007164"},{"id":"T457","span":{"begin":842,"end":849},"obj":"SO:0001023"}],"text":"Many XPD mutations are associated with an exclusive disease phenotype (e.g., XPDR722W with TTD and XPDR683W with XP) and are thus viewed as causative of the corresponding syndromes. Alleles not associated exclusively with one disorder are considered “likely null” alleles [19,20]. Some of these alleles fail to support viability in a haploid Schizosaccharomyces pombe yeast strain with a null mutation in the XPD homologue rad15 and are thus considered devoid of significant biological activity [19]. This classification of alleles as either causative or null currently defines what we refer to as a “monoallelic” paradigm of XPD disease. However, the identification in recent years of XP complementation group D patients with atypical disease presentation, including symptoms of both XP and TTD [8], casts doubt on the ability of such a monoallelic paradigm to explain clinical heterogeneity in compound heterozygotes."}

{"project":"craft-ca-core-ex-dev","denotations":[{"id":"T534","span":{"begin":5,"end":8},"obj":"PR_EXT:000007164"},{"id":"T535","span":{"begin":9,"end":18},"obj":"SO_EXT:sequence_alteration_entity_or_process"},{"id":"T536","span":{"begin":77,"end":80},"obj":"PR_EXT:000007164"},{"id":"T537","span":{"begin":99,"end":102},"obj":"PR_EXT:000007164"},{"id":"T538","span":{"begin":182,"end":189},"obj":"SO_EXT:0001023"},{"id":"T539","span":{"begin":258,"end":262},"obj":"SO_EXT:sequence_nullness"},{"id":"T540","span":{"begin":264,"end":271},"obj":"SO_EXT:0001023"},{"id":"T541","span":{"begin":295,"end":302},"obj":"SO_EXT:0001023"},{"id":"T542","span":{"begin":342,"end":373},"obj":"NCBITaxon:4896"},{"id":"T543","span":{"begin":388,"end":392},"obj":"SO_EXT:sequence_nullness"},{"id":"T544","span":{"begin":393,"end":401},"obj":"SO_EXT:sequence_alteration_entity_or_process"},{"id":"T545","span":{"begin":409,"end":412},"obj":"PR_EXT:000007164"},{"id":"T546","span":{"begin":413,"end":422},"obj":"SO_EXT:0000853"},{"id":"T547","span":{"begin":423,"end":428},"obj":"PR_EXT:P26659"},{"id":"T548","span":{"begin":475,"end":485},"obj":"CHEBI_GO_EXT:biological_process_or_quality_or_role"},{"id":"T549","span":{"begin":524,"end":531},"obj":"SO_EXT:0001023"},{"id":"T550","span":{"begin":555,"end":559},"obj":"SO_EXT:sequence_nullness"},{"id":"T551","span":{"begin":605,"end":612},"obj":"SO_EXT:0001023"},{"id":"T552","span":{"begin":626,"end":629},"obj":"PR_EXT:000007164"},{"id":"T553","span":{"begin":842,"end":849},"obj":"SO_EXT:0001023"}],"text":"Many XPD mutations are associated with an exclusive disease phenotype (e.g., XPDR722W with TTD and XPDR683W with XP) and are thus viewed as causative of the corresponding syndromes. Alleles not associated exclusively with one disorder are considered “likely null” alleles [19,20]. Some of these alleles fail to support viability in a haploid Schizosaccharomyces pombe yeast strain with a null mutation in the XPD homologue rad15 and are thus considered devoid of significant biological activity [19]. This classification of alleles as either causative or null currently defines what we refer to as a “monoallelic” paradigm of XPD disease. However, the identification in recent years of XP complementation group D patients with atypical disease presentation, including symptoms of both XP and TTD [8], casts doubt on the ability of such a monoallelic paradigm to explain clinical heterogeneity in compound heterozygotes."}

{"project":"2_test","denotations":[{"id":"17020410-9238033-84795133","span":{"begin":273,"end":275},"obj":"9238033"},{"id":"17020410-10447254-84795134","span":{"begin":276,"end":278},"obj":"10447254"},{"id":"17020410-9238033-84795135","span":{"begin":496,"end":498},"obj":"9238033"},{"id":"17020410-11709541-84795136","span":{"begin":797,"end":798},"obj":"11709541"},{"id":"T56327","span":{"begin":273,"end":275},"obj":"9238033"},{"id":"T63905","span":{"begin":276,"end":278},"obj":"10447254"},{"id":"T81319","span":{"begin":496,"end":498},"obj":"9238033"},{"id":"T90035","span":{"begin":797,"end":798},"obj":"11709541"}],"text":"Many XPD mutations are associated with an exclusive disease phenotype (e.g., XPDR722W with TTD and XPDR683W with XP) and are thus viewed as causative of the corresponding syndromes. Alleles not associated exclusively with one disorder are considered “likely null” alleles [19,20]. Some of these alleles fail to support viability in a haploid Schizosaccharomyces pombe yeast strain with a null mutation in the XPD homologue rad15 and are thus considered devoid of significant biological activity [19]. This classification of alleles as either causative or null currently defines what we refer to as a “monoallelic” paradigm of XPD disease. However, the identification in recent years of XP complementation group D patients with atypical disease presentation, including symptoms of both XP and TTD [8], casts doubt on the ability of such a monoallelic paradigm to explain clinical heterogeneity in compound heterozygotes."}