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The syndrome is caused by mutations of the PDS gene SLC26A4, which codes for the protein pendrin [2]. Deafness is congenital and generally profound although sometimes late in onset and provoked by light head injury. Vestibular dysfunction is uncommon. Goiter is variable and generally develops around puberty [3]. The cause of goiter appears to be an impairment of iodide fixation in the follicular lumen due to a reduced rate of iodide transport across the apical membrane of thyroid gland epithelial cells [4]. A positive perchlorate discharge test and an enlarged vestibular aqueduct appear to be the most reliable clinical signs of Pendred syndrome [5].\nPendrin is an anio"}

{"project":"craft-ca-core-ex-dev","denotations":[{"id":"T696","span":{"begin":91,"end":100},"obj":"GO:0030849"},{"id":"T697","span":{"begin":188,"end":197},"obj":"SO_EXT:sequence_alteration_entity_or_process"},{"id":"T698","span":{"begin":209,"end":213},"obj":"SO_EXT:0000704"},{"id":"T699","span":{"begin":214,"end":221},"obj":"PR_EXT:000015039"},{"id":"T700","span":{"begin":229,"end":234},"obj":"SO_EXT:sequence_coding_function"},{"id":"T701","span":{"begin":243,"end":250},"obj":"CHEBI_PR_EXT:protein"},{"id":"T702","span":{"begin":251,"end":258},"obj":"PR_EXT:000015039"},{"id":"T703","span":{"begin":365,"end":369},"obj":"UBERON:0000033"},{"id":"T704","span":{"begin":378,"end":388},"obj":"UBERON_EXT:vestibule_or_vestibular_system"},{"id":"T705","span":{"begin":527,"end":533},"obj":"CHEBI:16382"},{"id":"T706","span":{"begin":550,"end":566},"obj":"UBERON:0012246"},{"id":"T707","span":{"begin":561,"end":566},"obj":"GO_UBERON_EXT:lumen"},{"id":"T708","span":{"begin":592,"end":598},"obj":"CHEBI:16382"},{"id":"T709","span":{"begin":592,"end":615},"obj":"_FRAGMENT"},{"id":"T710","span":{"begin":627,"end":635},"obj":"GO:1904200"},{"id":"T711","span":{"begin":620,"end":638},"obj":"_FRAGMENT"},{"id":"T712","span":{"begin":664,"end":669},"obj":"GO:0016324"},{"id":"T713","span":{"begin":639,"end":652},"obj":"UBERON:0002046"},{"id":"T714","span":{"begin":639,"end":669},"obj":"CL:0002257"},{"id":"T715","span":{"begin":653,"end":663},"obj":"UBERON:0000483"},{"id":"T716","span":{"begin":686,"end":697},"obj":"CHEBI:49706"},{"id":"T717","span":{"begin":729,"end":748},"obj":"UBERON:0002279"},{"id":"T718","span":{"begin":820,"end":827},"obj":"PR_EXT:000015039"}],"relations":[{"id":"R329","pred":"_lexicallyChainedTo","subj":"T710","obj":"T709"},{"id":"R330","pred":"_lexicallyChainedTo","subj":"T712","obj":"T711"}],"text":"cause of deafness in Pendred syndrome.\n\nBackground\nPendred syndrome is a relatively common autosomal-recessive disorder characterized by deafness and goiter [1]. The syndrome is caused by mutations of the PDS gene SLC26A4, which codes for the protein pendrin [2]. Deafness is congenital and generally profound although sometimes late in onset and provoked by light head injury. Vestibular dysfunction is uncommon. Goiter is variable and generally develops around puberty [3]. The cause of goiter appears to be an impairment of iodide fixation in the follicular lumen due to a reduced rate of iodide transport across the apical membrane of thyroid gland epithelial cells [4]. A positive perchlorate discharge test and an enlarged vestibular aqueduct appear to be the most reliable clinical signs of Pendred syndrome [5].\nPendrin is an anio"}

{"project":"craft-ca-core-dev","denotations":[{"id":"T638","span":{"begin":91,"end":100},"obj":"GO:0030849"},{"id":"T639","span":{"begin":209,"end":213},"obj":"SO:0000704"},{"id":"T640","span":{"begin":214,"end":221},"obj":"PR:000015039"},{"id":"T641","span":{"begin":251,"end":258},"obj":"PR:000015039"},{"id":"T642","span":{"begin":365,"end":369},"obj":"UBERON:0000033"},{"id":"T643","span":{"begin":527,"end":533},"obj":"CHEBI:16382"},{"id":"T644","span":{"begin":550,"end":566},"obj":"UBERON:0012246"},{"id":"T645","span":{"begin":592,"end":598},"obj":"CHEBI:16382"},{"id":"T646","span":{"begin":592,"end":615},"obj":"_FRAGMENT"},{"id":"T647","span":{"begin":627,"end":635},"obj":"GO:1904200"},{"id":"T648","span":{"begin":620,"end":638},"obj":"_FRAGMENT"},{"id":"T649","span":{"begin":664,"end":669},"obj":"GO:0016324"},{"id":"T650","span":{"begin":639,"end":652},"obj":"UBERON:0002046"},{"id":"T651","span":{"begin":639,"end":669},"obj":"CL:0002257"},{"id":"T652","span":{"begin":653,"end":663},"obj":"UBERON:0000483"},{"id":"T653","span":{"begin":686,"end":697},"obj":"CHEBI:49706"},{"id":"T654","span":{"begin":729,"end":748},"obj":"UBERON:0002279"},{"id":"T655","span":{"begin":820,"end":827},"obj":"PR:000015039"}],"relations":[{"id":"R327","pred":"_lexicallyChainedTo","subj":"T647","obj":"T646"},{"id":"R328","pred":"_lexicallyChainedTo","subj":"T649","obj":"T648"}],"text":"cause of deafness in Pendred syndrome.\n\nBackground\nPendred syndrome is a relatively common autosomal-recessive disorder characterized by deafness and goiter [1]. The syndrome is caused by mutations of the PDS gene SLC26A4, which codes for the protein pendrin [2]. Deafness is congenital and generally profound although sometimes late in onset and provoked by light head injury. Vestibular dysfunction is uncommon. Goiter is variable and generally develops around puberty [3]. The cause of goiter appears to be an impairment of iodide fixation in the follicular lumen due to a reduced rate of iodide transport across the apical membrane of thyroid gland epithelial cells [4]. A positive perchlorate discharge test and an enlarged vestibular aqueduct appear to be the most reliable clinical signs of Pendred syndrome [5].\nPendrin is an anio"}

{"project":"2_test","denotations":[{"id":"15320950-9398842-12070934","span":{"begin":260,"end":261},"obj":"9398842"},{"id":"15320950-10650967-12070935","span":{"begin":472,"end":473},"obj":"10650967"},{"id":"15320950-10843192-12070936","span":{"begin":671,"end":672},"obj":"10843192"},{"id":"15320950-10700480-12070937","span":{"begin":816,"end":817},"obj":"10700480"}],"text":"cause of deafness in Pendred syndrome.\n\nBackground\nPendred syndrome is a relatively common autosomal-recessive disorder characterized by deafness and goiter [1]. The syndrome is caused by mutations of the PDS gene SLC26A4, which codes for the protein pendrin [2]. Deafness is congenital and generally profound although sometimes late in onset and provoked by light head injury. Vestibular dysfunction is uncommon. Goiter is variable and generally develops around puberty [3]. The cause of goiter appears to be an impairment of iodide fixation in the follicular lumen due to a reduced rate of iodide transport across the apical membrane of thyroid gland epithelial cells [4]. A positive perchlorate discharge test and an enlarged vestibular aqueduct appear to be the most reliable clinical signs of Pendred syndrome [5].\nPendrin is an anio"}