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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 anion exchanger that can transport Cl-, I-, HCO3 - and formate [6,7]. Expression has been found in the inner ear and thyroid gland consistent with the clinical signs of deafness and goiter [2,3,8]. In addition, pendrin expression has been found in the kidney [9], mammary gland [10], uterus [11], testes [12] and placenta [13]. No expression was found in fetal or adult brain, consistent with a peripheral cause of deafness [2,11].\nExpression of pendrin mRNA in the inner ear has been found in several places including the cochlea, the vestibular labyrinth and the endolymphatic sac [8]. The precise location of pendrin protein expression, however, has not yet been determined. The variability of deafness in Pendred syndrome and the observation that deafness is sometimes late in onset suggest that pendrin dysfunction may not be the direct cause of deafness. It is conceivable that pendrin dysfunction favors changes in the expression levels of proteins that are critical for the maintenance of the hearing function. Detailed studies aimed at identifying the direct cause of deafness in Pendred syndrome have recently become possible due to the generation of a pendrin-specific polyclonal antibody [9] and the development of Slc26a4-/- mice, which bear a targeted disruption of the mouse Slc26a4 gene [14]. The aim in the present study was to determine the location of pendrin and the cause of deafness in Slc26a4-/- mice."}

{"project":"craft-ca-core-ex-dev","denotations":[{"id":"T696","span":{"begin":51,"end":60},"obj":"GO:0030849"},{"id":"T697","span":{"begin":148,"end":157},"obj":"SO_EXT:sequence_alteration_entity_or_process"},{"id":"T698","span":{"begin":169,"end":173},"obj":"SO_EXT:0000704"},{"id":"T699","span":{"begin":174,"end":181},"obj":"PR_EXT:000015039"},{"id":"T700","span":{"begin":189,"end":194},"obj":"SO_EXT:sequence_coding_function"},{"id":"T701","span":{"begin":203,"end":210},"obj":"CHEBI_PR_EXT:protein"},{"id":"T702","span":{"begin":211,"end":218},"obj":"PR_EXT:000015039"},{"id":"T703","span":{"begin":325,"end":329},"obj":"UBERON:0000033"},{"id":"T704","span":{"begin":338,"end":348},"obj":"UBERON_EXT:vestibule_or_vestibular_system"},{"id":"T705","span":{"begin":487,"end":493},"obj":"CHEBI:16382"},{"id":"T706","span":{"begin":510,"end":526},"obj":"UBERON:0012246"},{"id":"T707","span":{"begin":521,"end":526},"obj":"GO_UBERON_EXT:lumen"},{"id":"T708","span":{"begin":552,"end":558},"obj":"CHEBI:16382"},{"id":"T709","span":{"begin":552,"end":575},"obj":"_FRAGMENT"},{"id":"T710","span":{"begin":587,"end":595},"obj":"GO:1904200"},{"id":"T711","span":{"begin":580,"end":598},"obj":"_FRAGMENT"},{"id":"T712","span":{"begin":624,"end":629},"obj":"GO:0016324"},{"id":"T713","span":{"begin":599,"end":612},"obj":"UBERON:0002046"},{"id":"T714","span":{"begin":599,"end":629},"obj":"CL:0002257"},{"id":"T715","span":{"begin":613,"end":623},"obj":"UBERON:0000483"},{"id":"T716","span":{"begin":646,"end":657},"obj":"CHEBI:49706"},{"id":"T717","span":{"begin":689,"end":708},"obj":"UBERON:0002279"},{"id":"T718","span":{"begin":780,"end":787},"obj":"PR_EXT:000015039"},{"id":"T719","span":{"begin":794,"end":799},"obj":"CHEBI:22563"},{"id":"T720","span":{"begin":794,"end":809},"obj":"GO_EXT:0015301"},{"id":"T721","span":{"begin":819,"end":828},"obj":"GO_EXT:biological_routing_or_transport"},{"id":"T722","span":{"begin":829,"end":832},"obj":"CHEBI:17996"},{"id":"T723","span":{"begin":834,"end":836},"obj":"CHEBI:16382"},{"id":"T724","span":{"begin":838,"end":844},"obj":"CHEBI:17544"},{"id":"T725","span":{"begin":849,"end":856},"obj":"CHEBI:15740"},{"id":"T726","span":{"begin":864,"end":874},"obj":"GO:0010467"},{"id":"T727","span":{"begin":897,"end":906},"obj":"UBERON:0001846"},{"id":"T728","span":{"begin":911,"end":924},"obj":"UBERON:0002046"},{"id":"T729","span":{"begin":1005,"end":1012},"obj":"PR_EXT:000015039"},{"id":"T730","span":{"begin":1013,"end":1023},"obj":"GO:0010467"},{"id":"T731","span":{"begin":1046,"end":1052},"obj":"UBERON:0002113"},{"id":"T732","span":{"begin":1058,"end":1071},"obj":"UBERON:0001911"},{"id":"T733","span":{"begin":1078,"end":1084},"obj":"UBERON:0000995"},{"id":"T734","span":{"begin":1091,"end":1097},"obj":"UBERON:0000473"},{"id":"T735","span":{"begin":1107,"end":1115},"obj":"UBERON:0001987"},{"id":"T736","span":{"begin":1125,"end":1135},"obj":"GO:0010467"},{"id":"T737","span":{"begin":1158,"end":1163},"obj":"UBERON:0007023"},{"id":"T738","span":{"begin":1164,"end":1169},"obj":"UBERON:0000955"},{"id":"T739","span":{"begin":1226,"end":1236},"obj":"GO:0010467"},{"id":"T740","span":{"begin":1240,"end":1247},"obj":"PR_EXT:000015039"},{"id":"T741","span":{"begin":1248,"end":1252},"obj":"CHEBI_SO_EXT:mRNA"},{"id":"T742","span":{"begin":1260,"end":1269},"obj":"UBERON:0001846"},{"id":"T743","span":{"begin":1317,"end":1324},"obj":"UBERON:0001844"},{"id":"T744","span":{"begin":1330,"end":1350},"obj":"UBERON:0001862"},{"id":"T745","span":{"begin":1359,"end":1376},"obj":"UBERON:0002223"},{"id":"T746","span":{"begin":1406,"end":1413},"obj":"PR_EXT:000015039"},{"id":"T747","span":{"begin":1414,"end":1421},"obj":"CHEBI_PR_EXT:protein"},{"id":"T748","span":{"begin":1422,"end":1432},"obj":"GO:0010467"},{"id":"T749","span":{"begin":1594,"end":1601},"obj":"PR_EXT:000015039"},{"id":"T750","span":{"begin":1678,"end":1685},"obj":"PR_EXT:000015039"},{"id":"T751","span":{"begin":1720,"end":1730},"obj":"GO:0010467"},{"id":"T752","span":{"begin":1741,"end":1749},"obj":"CHEBI_PR_EXT:protein"},{"id":"T753","span":{"begin":1795,"end":1802},"obj":"GO:0007605"},{"id":"T754","span":{"begin":1941,"end":1954},"obj":"_FRAGMENT"},{"id":"T755","span":{"begin":1985,"end":1993},"obj":"GO_EXT:antibody_or_immunoglobulin_biosynthesis_or_production"},{"id":"T756","span":{"begin":1957,"end":1964},"obj":"PR_EXT:000015039"},{"id":"T757","span":{"begin":1985,"end":1993},"obj":"GO:0042571"},{"id":"T758","span":{"begin":2021,"end":2028},"obj":"PR_EXT:000015039"},{"id":"T759","span":{"begin":2028,"end":2029},"obj":"SO_EXT:sequence_nullness_or_absence"},{"id":"T760","span":{"begin":2030,"end":2031},"obj":"SO_EXT:sequence_nullness_or_absence"},{"id":"T761","span":{"begin":2032,"end":2036},"obj":"NCBITaxon:10088"},{"id":"T762","span":{"begin":2078,"end":2083},"obj":"NCBITaxon:10088"},{"id":"T763","span":{"begin":2084,"end":2091},"obj":"PR_EXT:000015039"},{"id":"T764","span":{"begin":2092,"end":2096},"obj":"SO_EXT:0000704"},{"id":"T765","span":{"begin":2165,"end":2172},"obj":"PR_EXT:000015039"},{"id":"T766","span":{"begin":2202,"end":2209},"obj":"PR_EXT:000015039"},{"id":"T767","span":{"begin":2209,"end":2210},"obj":"SO_EXT:sequence_nullness_or_absence"},{"id":"T768","span":{"begin":2211,"end":2212},"obj":"SO_EXT:sequence_nullness_or_absence"},{"id":"T769","span":{"begin":2213,"end":2217},"obj":"NCBITaxon:10088"}],"relations":[{"id":"R329","pred":"_lexicallyChainedTo","subj":"T710","obj":"T709"},{"id":"R330","pred":"_lexicallyChainedTo","subj":"T712","obj":"T711"},{"id":"R331","pred":"_lexicallyChainedTo","subj":"T755","obj":"T754"}],"text":"Background\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 anion exchanger that can transport Cl-, I-, HCO3 - and formate [6,7]. Expression has been found in the inner ear and thyroid gland consistent with the clinical signs of deafness and goiter [2,3,8]. In addition, pendrin expression has been found in the kidney [9], mammary gland [10], uterus [11], testes [12] and placenta [13]. No expression was found in fetal or adult brain, consistent with a peripheral cause of deafness [2,11].\nExpression of pendrin mRNA in the inner ear has been found in several places including the cochlea, the vestibular labyrinth and the endolymphatic sac [8]. The precise location of pendrin protein expression, however, has not yet been determined. The variability of deafness in Pendred syndrome and the observation that deafness is sometimes late in onset suggest that pendrin dysfunction may not be the direct cause of deafness. It is conceivable that pendrin dysfunction favors changes in the expression levels of proteins that are critical for the maintenance of the hearing function. Detailed studies aimed at identifying the direct cause of deafness in Pendred syndrome have recently become possible due to the generation of a pendrin-specific polyclonal antibody [9] and the development of Slc26a4-/- mice, which bear a targeted disruption of the mouse Slc26a4 gene [14]. The aim in the present study was to determine the location of pendrin and the cause of deafness in Slc26a4-/- mice."}

{"project":"craft-ca-core-dev","denotations":[{"id":"T638","span":{"begin":51,"end":60},"obj":"GO:0030849"},{"id":"T639","span":{"begin":169,"end":173},"obj":"SO:0000704"},{"id":"T640","span":{"begin":174,"end":181},"obj":"PR:000015039"},{"id":"T641","span":{"begin":211,"end":218},"obj":"PR:000015039"},{"id":"T642","span":{"begin":325,"end":329},"obj":"UBERON:0000033"},{"id":"T643","span":{"begin":487,"end":493},"obj":"CHEBI:16382"},{"id":"T644","span":{"begin":510,"end":526},"obj":"UBERON:0012246"},{"id":"T645","span":{"begin":552,"end":558},"obj":"CHEBI:16382"},{"id":"T646","span":{"begin":552,"end":575},"obj":"_FRAGMENT"},{"id":"T647","span":{"begin":587,"end":595},"obj":"GO:1904200"},{"id":"T648","span":{"begin":580,"end":598},"obj":"_FRAGMENT"},{"id":"T649","span":{"begin":624,"end":629},"obj":"GO:0016324"},{"id":"T650","span":{"begin":599,"end":612},"obj":"UBERON:0002046"},{"id":"T651","span":{"begin":599,"end":629},"obj":"CL:0002257"},{"id":"T652","span":{"begin":613,"end":623},"obj":"UBERON:0000483"},{"id":"T653","span":{"begin":646,"end":657},"obj":"CHEBI:49706"},{"id":"T654","span":{"begin":689,"end":708},"obj":"UBERON:0002279"},{"id":"T655","span":{"begin":780,"end":787},"obj":"PR:000015039"},{"id":"T656","span":{"begin":794,"end":799},"obj":"CHEBI:22563"},{"id":"T657","span":{"begin":829,"end":832},"obj":"CHEBI:17996"},{"id":"T658","span":{"begin":834,"end":836},"obj":"CHEBI:16382"},{"id":"T659","span":{"begin":838,"end":844},"obj":"CHEBI:17544"},{"id":"T660","span":{"begin":849,"end":856},"obj":"CHEBI:15740"},{"id":"T661","span":{"begin":864,"end":874},"obj":"GO:0010467"},{"id":"T662","span":{"begin":897,"end":906},"obj":"UBERON:0001846"},{"id":"T663","span":{"begin":911,"end":924},"obj":"UBERON:0002046"},{"id":"T664","span":{"begin":1005,"end":1012},"obj":"PR:000015039"},{"id":"T665","span":{"begin":1013,"end":1023},"obj":"GO:0010467"},{"id":"T666","span":{"begin":1046,"end":1052},"obj":"UBERON:0002113"},{"id":"T667","span":{"begin":1058,"end":1071},"obj":"UBERON:0001911"},{"id":"T668","span":{"begin":1078,"end":1084},"obj":"UBERON:0000995"},{"id":"T669","span":{"begin":1091,"end":1097},"obj":"UBERON:0000473"},{"id":"T671","span":{"begin":1125,"end":1135},"obj":"GO:0010467"},{"id":"T672","span":{"begin":1158,"end":1163},"obj":"UBERON:0007023"},{"id":"T673","span":{"begin":1164,"end":1169},"obj":"UBERON:0000955"},{"id":"T674","span":{"begin":1226,"end":1236},"obj":"GO:0010467"},{"id":"T675","span":{"begin":1240,"end":1247},"obj":"PR:000015039"},{"id":"T676","span":{"begin":1260,"end":1269},"obj":"UBERON:0001846"},{"id":"T677","span":{"begin":1317,"end":1324},"obj":"UBERON:0001844"},{"id":"T678","span":{"begin":1330,"end":1350},"obj":"UBERON:0001862"},{"id":"T679","span":{"begin":1359,"end":1376},"obj":"UBERON:0002223"},{"id":"T680","span":{"begin":1406,"end":1413},"obj":"PR:000015039"},{"id":"T681","span":{"begin":1422,"end":1432},"obj":"GO:0010467"},{"id":"T682","span":{"begin":1594,"end":1601},"obj":"PR:000015039"},{"id":"T683","span":{"begin":1678,"end":1685},"obj":"PR:000015039"},{"id":"T684","span":{"begin":1720,"end":1730},"obj":"GO:0010467"},{"id":"T685","span":{"begin":1795,"end":1802},"obj":"GO:0007605"},{"id":"T686","span":{"begin":1957,"end":1964},"obj":"PR:000015039"},{"id":"T687","span":{"begin":1985,"end":1993},"obj":"GO:0042571"},{"id":"T688","span":{"begin":2021,"end":2028},"obj":"PR:000015039"},{"id":"T689","span":{"begin":2032,"end":2036},"obj":"NCBITaxon:10088"},{"id":"T690","span":{"begin":2078,"end":2083},"obj":"NCBITaxon:10088"},{"id":"T691","span":{"begin":2084,"end":2091},"obj":"PR:000015039"},{"id":"T692","span":{"begin":2092,"end":2096},"obj":"SO:0000704"},{"id":"T693","span":{"begin":2165,"end":2172},"obj":"PR:000015039"},{"id":"T694","span":{"begin":2202,"end":2209},"obj":"PR:000015039"},{"id":"T695","span":{"begin":2213,"end":2217},"obj":"NCBITaxon:10088"},{"id":"T670","span":{"begin":1107,"end":1115},"obj":"UBERON:0001987"}],"relations":[{"id":"R327","pred":"_lexicallyChainedTo","subj":"T647","obj":"T646"},{"id":"R328","pred":"_lexicallyChainedTo","subj":"T649","obj":"T648"}],"text":"Background\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 anion exchanger that can transport Cl-, I-, HCO3 - and formate [6,7]. Expression has been found in the inner ear and thyroid gland consistent with the clinical signs of deafness and goiter [2,3,8]. In addition, pendrin expression has been found in the kidney [9], mammary gland [10], uterus [11], testes [12] and placenta [13]. No expression was found in fetal or adult brain, consistent with a peripheral cause of deafness [2,11].\nExpression of pendrin mRNA in the inner ear has been found in several places including the cochlea, the vestibular labyrinth and the endolymphatic sac [8]. The precise location of pendrin protein expression, however, has not yet been determined. The variability of deafness in Pendred syndrome and the observation that deafness is sometimes late in onset suggest that pendrin dysfunction may not be the direct cause of deafness. It is conceivable that pendrin dysfunction favors changes in the expression levels of proteins that are critical for the maintenance of the hearing function. Detailed studies aimed at identifying the direct cause of deafness in Pendred syndrome have recently become possible due to the generation of a pendrin-specific polyclonal antibody [9] and the development of Slc26a4-/- mice, which bear a targeted disruption of the mouse Slc26a4 gene [14]. The aim in the present study was to determine the location of pendrin and the cause of deafness in Slc26a4-/- mice."}

{"project":"2_test","denotations":[{"id":"15320950-9398842-12070934","span":{"begin":220,"end":221},"obj":"9398842"},{"id":"15320950-10650967-12070935","span":{"begin":432,"end":433},"obj":"10650967"},{"id":"15320950-10843192-12070936","span":{"begin":631,"end":632},"obj":"10843192"},{"id":"15320950-10700480-12070937","span":{"begin":776,"end":777},"obj":"10700480"},{"id":"15320950-10192399-12070938","span":{"begin":858,"end":859},"obj":"10192399"},{"id":"15320950-10644529-12070939","span":{"begin":860,"end":861},"obj":"10644529"},{"id":"15320950-9398842-12070940","span":{"begin":984,"end":985},"obj":"9398842"},{"id":"15320950-10650967-12070941","span":{"begin":986,"end":987},"obj":"10650967"},{"id":"15320950-10449762-12070942","span":{"begin":988,"end":989},"obj":"10449762"},{"id":"15320950-11274445-12070943","span":{"begin":1054,"end":1055},"obj":"11274445"},{"id":"15320950-12388138-12070944","span":{"begin":1073,"end":1075},"obj":"12388138"},{"id":"15320950-11836344-12070945","span":{"begin":1086,"end":1088},"obj":"11836344"},{"id":"15320950-11248751-12070946","span":{"begin":1099,"end":1101},"obj":"11248751"},{"id":"15320950-11095481-12070947","span":{"begin":1117,"end":1119},"obj":"11095481"},{"id":"15320950-9398842-12070948","span":{"begin":1219,"end":1220},"obj":"9398842"},{"id":"15320950-11836344-12070949","span":{"begin":1221,"end":1223},"obj":"11836344"},{"id":"15320950-10449762-12070950","span":{"begin":1378,"end":1379},"obj":"10449762"},{"id":"15320950-11274445-12070951","span":{"begin":1995,"end":1996},"obj":"11274445"},{"id":"15320950-11152663-12070952","span":{"begin":2098,"end":2100},"obj":"11152663"}],"text":"Background\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 anion exchanger that can transport Cl-, I-, HCO3 - and formate [6,7]. Expression has been found in the inner ear and thyroid gland consistent with the clinical signs of deafness and goiter [2,3,8]. In addition, pendrin expression has been found in the kidney [9], mammary gland [10], uterus [11], testes [12] and placenta [13]. No expression was found in fetal or adult brain, consistent with a peripheral cause of deafness [2,11].\nExpression of pendrin mRNA in the inner ear has been found in several places including the cochlea, the vestibular labyrinth and the endolymphatic sac [8]. The precise location of pendrin protein expression, however, has not yet been determined. The variability of deafness in Pendred syndrome and the observation that deafness is sometimes late in onset suggest that pendrin dysfunction may not be the direct cause of deafness. It is conceivable that pendrin dysfunction favors changes in the expression levels of proteins that are critical for the maintenance of the hearing function. Detailed studies aimed at identifying the direct cause of deafness in Pendred syndrome have recently become possible due to the generation of a pendrin-specific polyclonal antibody [9] and the development of Slc26a4-/- mice, which bear a targeted disruption of the mouse Slc26a4 gene [14]. The aim in the present study was to determine the location of pendrin and the cause of deafness in Slc26a4-/- mice."}