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subj":"T6800","obj":"T6799"},{"id":"R4164","pred":"prep","subj":"T6801","obj":"T6799"},{"id":"R4165","pred":"det","subj":"T6802","obj":"T6803"},{"id":"R4166","pred":"pobj","subj":"T6803","obj":"T6801"},{"id":"R4167","pred":"prep","subj":"T6804","obj":"T6803"},{"id":"R4168","pred":"nmod","subj":"T6805","obj":"T6806"},{"id":"R4169","pred":"pobj","subj":"T6806","obj":"T6804"},{"id":"R4170","pred":"amod","subj":"T6807","obj":"T6806"},{"id":"R4171","pred":"punct","subj":"T6808","obj":"T6782"}],"text":"Female mice carrying an Atrx null allele (Atrx WT/null;GATA1-cre +/−) were detected at 9.5 dpc (Table 1) and recovered at birth (unpublished data), although at both time points the number of carrier females was lower than that of wild-type (Atrx WT/WT;GATA1-cre +/−) females, suggesting that a proportion of carrier female embryos died in utero. Surviving adult carrier female mice were not phenotypically normal and exhibited mild behavioural abnormalities, although some could reproduce. For all Atrx WT/null carrier female embryos presented in Table 1, the Atrx WT allele was paternally derived, while the Atrx null allele was maternally derived. In the mouse, X chromosome inactivation is subject to parental imprinting in the trophectoderm and primitive endoderm lineages that give rise to the extraembryonic tissues, resulting in inactivation of the paternal X chromosome (Xp) [18]. In contrast, in tissues of the embryo proper (derived from the inner cell mass of the blastocyst) X-inactivation is random [19]. Thus, in the extraembryonic compartment of Atrx WT/null carrier females, normal imprinted X-inactivation would be expected to result in silencing of the paternally derived Atrx WT allele, leaving only the Atrx null allele on the active maternal X (Xm) and thereby render the extraembryonic tissues null for full-length Atrx protein. However, the absence of Atrx in the extraembryonic compartment is lethal in Atrx null/Y males. This suggested the possibility of an escape from imprinted inactivation of the paternally derived Atrx WT allele in the extraembryonic compartment of a proportion of carrier female embryos."}
craft-ca-core-ex-dev
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bearer_of_femaleness"},{"id":"T6353","span":{"begin":1098,"end":1122},"obj":"GO:0060819"},{"id":"T6354","span":{"begin":1108,"end":1109},"obj":"GO:0000805"},{"id":"T6355","span":{"begin":1154,"end":1163},"obj":"GO:0016458"},{"id":"T6356","span":{"begin":1190,"end":1194},"obj":"PR_EXT:000004503"},{"id":"T6357","span":{"begin":1195,"end":1197},"obj":"SO_EXT:wild_type_entity_or_quality"},{"id":"T6358","span":{"begin":1198,"end":1204},"obj":"SO_EXT:0001023"},{"id":"T6359","span":{"begin":1223,"end":1227},"obj":"PR_EXT:000004503"},{"id":"T6360","span":{"begin":1228,"end":1232},"obj":"SO_EXT:sequence_nullness"},{"id":"T6361","span":{"begin":1233,"end":1239},"obj":"SO_EXT:0001023"},{"id":"T6362","span":{"begin":1263,"end":1264},"obj":"GO:0000805"},{"id":"T6363","span":{"begin":1293,"end":1315},"obj":"UBERON:0005292"},{"id":"T6364","span":{"begin":1316,"end":1320},"obj":"SO_EXT:sequence_nullness"},{"id":"T6365","span":{"begin":1337,"end":1341},"obj":"PR_EXT:000004503"},{"id":"T6366","span":{"begin":1342,"end":1349},"obj":"CHEBI_PR_EXT:protein"},{"id":"T6367","span":{"begin":1375,"end":1379},"obj":"PR_EXT:000004503"},{"id":"T6368","span":{"begin":1392,"end":1401},"obj":"UBERON:0000922"},{"id":"T6369","span":{"begin":1417,"end":1423},"obj":"GO_EXT:fatality_or_lethality"},{"id":"T6370","span":{"begin":1427,"end":1431},"obj":"PR_EXT:000004503"},{"id":"T6371","span":{"begin":1432,"end":1436},"obj":"SO_EXT:sequence_nullness"},{"id":"T6372","span":{"begin":1437,"end":1438},"obj":"GO:0000806"},{"id":"T6373","span":{"begin":1439,"end":1444},"obj":"PATO_UBERON_EXT:male_or_bearer_of_maleness"},{"id":"T6374","span":{"begin":1495,"end":1504},"obj":"GO:0071514"},{"id":"T6375","span":{"begin":1544,"end":1548},"obj":"PR_EXT:000004503"},{"id":"T6376","span":{"begin":1549,"end":1551},"obj":"SO_EXT:wild_type_entity_or_quality"},{"id":"T6377","span":{"begin":1552,"end":1558},"obj":"SO_EXT:0001023"},{"id":"T6378","span":{"begin":1571,"end":1580},"obj":"UBERON:0000922"},{"id":"T6379","span":{"begin":1620,"end":1626},"obj":"PATO_UBERON_EXT:female_or_bearer_of_femaleness"},{"id":"T6380","span":{"begin":1627,"end":1634},"obj":"UBERON:0000922"}],"relations":[{"id":"R3856","pred":"_lexicallyChainedTo","subj":"T6337","obj":"T6336"},{"id":"R3857","pred":"_lexicallyChainedTo","subj":"T6338","obj":"T6336"}],"text":"Female mice carrying an Atrx null allele (Atrx WT/null;GATA1-cre +/−) were detected at 9.5 dpc (Table 1) and recovered at birth (unpublished data), although at both time points the number of carrier females was lower than that of wild-type (Atrx WT/WT;GATA1-cre +/−) females, suggesting that a proportion of carrier female embryos died in utero. Surviving adult carrier female mice were not phenotypically normal and exhibited mild behavioural abnormalities, although some could reproduce. For all Atrx WT/null carrier female embryos presented in Table 1, the Atrx WT allele was paternally derived, while the Atrx null allele was maternally derived. In the mouse, X chromosome inactivation is subject to parental imprinting in the trophectoderm and primitive endoderm lineages that give rise to the extraembryonic tissues, resulting in inactivation of the paternal X chromosome (Xp) [18]. In contrast, in tissues of the embryo proper (derived from the inner cell mass of the blastocyst) X-inactivation is random [19]. Thus, in the extraembryonic compartment of Atrx WT/null carrier females, normal imprinted X-inactivation would be expected to result in silencing of the paternally derived Atrx WT allele, leaving only the Atrx null allele on the active maternal X (Xm) and thereby render the extraembryonic tissues null for full-length Atrx protein. However, the absence of Atrx in the extraembryonic compartment is lethal in Atrx null/Y males. This suggested the possibility of an escape from imprinted inactivation of the paternally derived Atrx WT allele in the extraembryonic compartment of a proportion of carrier female embryos."}
2_test
{"project":"2_test","denotations":[{"id":"16628246-1152998-85799757","span":{"begin":884,"end":886},"obj":"1152998"},{"id":"16628246-6185603-85799758","span":{"begin":1013,"end":1015},"obj":"6185603"},{"id":"T777","span":{"begin":884,"end":886},"obj":"1152998"},{"id":"T63330","span":{"begin":1013,"end":1015},"obj":"6185603"}],"text":"Female mice carrying an Atrx null allele (Atrx WT/null;GATA1-cre +/−) were detected at 9.5 dpc (Table 1) and recovered at birth (unpublished data), although at both time points the number of carrier females was lower than that of wild-type (Atrx WT/WT;GATA1-cre +/−) females, suggesting that a proportion of carrier female embryos died in utero. Surviving adult carrier female mice were not phenotypically normal and exhibited mild behavioural abnormalities, although some could reproduce. For all Atrx WT/null carrier female embryos presented in Table 1, the Atrx WT allele was paternally derived, while the Atrx null allele was maternally derived. In the mouse, X chromosome inactivation is subject to parental imprinting in the trophectoderm and primitive endoderm lineages that give rise to the extraembryonic tissues, resulting in inactivation of the paternal X chromosome (Xp) [18]. In contrast, in tissues of the embryo proper (derived from the inner cell mass of the blastocyst) X-inactivation is random [19]. Thus, in the extraembryonic compartment of Atrx WT/null carrier females, normal imprinted X-inactivation would be expected to result in silencing of the paternally derived Atrx WT allele, leaving only the Atrx null allele on the active maternal X (Xm) and thereby render the extraembryonic tissues null for full-length Atrx protein. However, the absence of Atrx in the extraembryonic compartment is lethal in Atrx null/Y males. This suggested the possibility of an escape from imprinted inactivation of the paternally derived Atrx WT allele in the extraembryonic compartment of a proportion of carrier female embryos."}
craft-ca-core-dev
{"project":"craft-ca-core-dev","denotations":[{"id":"T6160","span":{"begin":7,"end":11},"obj":"NCBITaxon:10088"},{"id":"T6161","span":{"begin":24,"end":28},"obj":"PR:000004503"},{"id":"T6162","span":{"begin":34,"end":40},"obj":"SO:0001023"},{"id":"T6163","span":{"begin":42,"end":46},"obj":"PR:000004503"},{"id":"T6164","span":{"begin":55,"end":60},"obj":"PR:000007857"},{"id":"T6165","span":{"begin":122,"end":127},"obj":"GO:0007567"},{"id":"T6166","span":{"begin":241,"end":245},"obj":"PR:000004503"},{"id":"T6167","span":{"begin":252,"end":257},"obj":"PR:000007857"},{"id":"T6168","span":{"begin":323,"end":330},"obj":"UBERON:0000922"},{"id":"T6169","span":{"begin":331,"end":335},"obj":"GO:0016265"},{"id":"T6170","span":{"begin":356,"end":361},"obj":"UBERON:0007023"},{"id":"T6171","span":{"begin":377,"end":381},"obj":"NCBITaxon:10088"},{"id":"T6172","span":{"begin":479,"end":488},"obj":"GO:0000003"},{"id":"T6173","span":{"begin":498,"end":502},"obj":"PR:000004503"},{"id":"T6174","span":{"begin":526,"end":533},"obj":"UBERON:0000922"},{"id":"T6175","span":{"begin":560,"end":564},"obj":"PR:000004503"},{"id":"T6176","span":{"begin":568,"end":574},"obj":"SO:0001023"},{"id":"T6177","span":{"begin":609,"end":613},"obj":"PR:000004503"},{"id":"T6178","span":{"begin":619,"end":625},"obj":"SO:0001023"},{"id":"T6179","span":{"begin":657,"end":662},"obj":"NCBITaxon:10088"},{"id":"T6180","span":{"begin":664,"end":676},"obj":"GO:0000805"},{"id":"T6181","span":{"begin":664,"end":689},"obj":"GO:0009048"},{"id":"T6182","span":{"begin":713,"end":723},"obj":"GO:0071514"},{"id":"T6183","span":{"begin":731,"end":744},"obj":"UBERON:0004345"},{"id":"T6184","span":{"begin":749,"end":767},"obj":"UBERON:0008776"},{"id":"T6185","span":{"begin":799,"end":821},"obj":"UBERON:0005292"},{"id":"T6186","span":{"begin":836,"end":851},"obj":"_FRAGMENT"},{"id":"T6187","span":{"begin":856,"end":877},"obj":"GO:0060817"},{"id":"T6188","span":{"begin":879,"end":881},"obj":"GO:0060817"},{"id":"T6189","span":{"begin":865,"end":877},"obj":"GO:0000805"},{"id":"T6190","span":{"begin":905,"end":912},"obj":"UBERON:0000479"},{"id":"T6191","span":{"begin":920,"end":926},"obj":"UBERON:0000922"},{"id":"T6192","span":{"begin":952,"end":967},"obj":"UBERON:0000087"},{"id":"T6193","span":{"begin":975,"end":985},"obj":"UBERON:0000358"},{"id":"T6194","span":{"begin":987,"end":988},"obj":"GO:0000805"},{"id":"T6195","span":{"begin":987,"end":1001},"obj":"GO:0009048"},{"id":"T6196","span":{"begin":1036,"end":1045},"obj":"UBERON:0000922"},{"id":"T6197","span":{"begin":1061,"end":1065},"obj":"PR:000004503"},{"id":"T6198","span":{"begin":1098,"end":1122},"obj":"GO:0060819"},{"id":"T6199","span":{"begin":1108,"end":1109},"obj":"GO:0000805"},{"id":"T6200","span":{"begin":1154,"end":1163},"obj":"GO:0016458"},{"id":"T6201","span":{"begin":1190,"end":1194},"obj":"PR:000004503"},{"id":"T6202","span":{"begin":1198,"end":1204},"obj":"SO:0001023"},{"id":"T6203","span":{"begin":1223,"end":1227},"obj":"PR:000004503"},{"id":"T6204","span":{"begin":1233,"end":1239},"obj":"SO:0001023"},{"id":"T6205","span":{"begin":1263,"end":1264},"obj":"GO:0000805"},{"id":"T6206","span":{"begin":1293,"end":1315},"obj":"UBERON:0005292"},{"id":"T6207","span":{"begin":1337,"end":1341},"obj":"PR:000004503"},{"id":"T6208","span":{"begin":1375,"end":1379},"obj":"PR:000004503"},{"id":"T6209","span":{"begin":1392,"end":1401},"obj":"UBERON:0000922"},{"id":"T6210","span":{"begin":1427,"end":1431},"obj":"PR:000004503"},{"id":"T6211","span":{"begin":1437,"end":1438},"obj":"GO:0000806"},{"id":"T6212","span":{"begin":1495,"end":1504},"obj":"GO:0071514"},{"id":"T6213","span":{"begin":1544,"end":1548},"obj":"PR:000004503"},{"id":"T6214","span":{"begin":1552,"end":1558},"obj":"SO:0001023"},{"id":"T6215","span":{"begin":1571,"end":1580},"obj":"UBERON:0000922"},{"id":"T6216","span":{"begin":1627,"end":1634},"obj":"UBERON:0000922"}],"relations":[{"id":"R3853","pred":"_lexicallyChainedTo","subj":"T6187","obj":"T6186"},{"id":"R3854","pred":"_lexicallyChainedTo","subj":"T6188","obj":"T6186"}],"text":"Female mice carrying an Atrx null allele (Atrx WT/null;GATA1-cre +/−) were detected at 9.5 dpc (Table 1) and recovered at birth (unpublished data), although at both time points the number of carrier females was lower than that of wild-type (Atrx WT/WT;GATA1-cre +/−) females, suggesting that a proportion of carrier female embryos died in utero. Surviving adult carrier female mice were not phenotypically normal and exhibited mild behavioural abnormalities, although some could reproduce. For all Atrx WT/null carrier female embryos presented in Table 1, the Atrx WT allele was paternally derived, while the Atrx null allele was maternally derived. In the mouse, X chromosome inactivation is subject to parental imprinting in the trophectoderm and primitive endoderm lineages that give rise to the extraembryonic tissues, resulting in inactivation of the paternal X chromosome (Xp) [18]. In contrast, in tissues of the embryo proper (derived from the inner cell mass of the blastocyst) X-inactivation is random [19]. Thus, in the extraembryonic compartment of Atrx WT/null carrier females, normal imprinted X-inactivation would be expected to result in silencing of the paternally derived Atrx WT allele, leaving only the Atrx null allele on the active maternal X (Xm) and thereby render the extraembryonic tissues null for full-length Atrx protein. However, the absence of Atrx in the extraembryonic compartment is lethal in Atrx null/Y males. This suggested the possibility of an escape from imprinted inactivation of the paternally derived Atrx WT allele in the extraembryonic compartment of a proportion of carrier female embryos."}