PubMed:16322221 / 182-470
Annnotations
c_corpus
{"project":"c_corpus","denotations":[{"id":"T31","span":{"begin":21,"end":28},"obj":"SO:0000104"},{"id":"T30","span":{"begin":21,"end":28},"obj":"PR:000000001"},{"id":"T27","span":{"begin":21,"end":28},"obj":"GO:0003675"},{"id":"T28","span":{"begin":21,"end":28},"obj":"CHEBI:36080"},{"id":"T29","span":{"begin":21,"end":28},"obj":"CHEBI:11122"},{"id":"T32","span":{"begin":73,"end":87},"obj":"SO:0000289"},{"id":"T33","span":{"begin":73,"end":99},"obj":"D053842"},{"id":"T34","span":{"begin":73,"end":99},"obj":"D053842"},{"id":"T35","span":{"begin":122,"end":127},"obj":"PR:P40692"},{"id":"T36","span":{"begin":128,"end":132},"obj":"SO:0000704"},{"id":"T37","span":{"begin":166,"end":202},"obj":"D003123"},{"id":"T38","span":{"begin":166,"end":202},"obj":"D003123"},{"id":"T39","span":{"begin":190,"end":195},"obj":"UBERON:0001155"},{"id":"T43","span":{"begin":221,"end":226},"obj":"PR:P54278"}],"text":"Cells lacking either protein have a strong mutator phenotype and display microsatellite instability, yet mutations in the hMLH1 gene account for approximately 50% of hereditary nonpolyposis colon cancer families, whereas hPMS2 mutations are substantially less frequent and less penetrant."}
PubmedHPO
{"project":"PubmedHPO","denotations":[{"id":"T1","span":{"begin":190,"end":202},"obj":"HP_0003003"},{"id":"T2","span":{"begin":190,"end":202},"obj":"HP_0100273"},{"id":"T3","span":{"begin":196,"end":202},"obj":"HP_0002664"}],"text":"Cells lacking either protein have a strong mutator phenotype and display microsatellite instability, yet mutations in the hMLH1 gene account for approximately 50% of hereditary nonpolyposis colon cancer families, whereas hPMS2 mutations are substantially less frequent and less penetrant."}
UseCases_ArguminSci_Discourse
{"project":"UseCases_ArguminSci_Discourse","denotations":[{"id":"T3","span":{"begin":0,"end":288},"obj":"DRI_Outcome"}],"text":"Cells lacking either protein have a strong mutator phenotype and display microsatellite instability, yet mutations in the hMLH1 gene account for approximately 50% of hereditary nonpolyposis colon cancer families, whereas hPMS2 mutations are substantially less frequent and less penetrant."}