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genes for Plg, PAI-1, and α2-antiplasmin reside on the three chromosomes identified for QTL for rebleeding time and may or may not be coincidental to the observed phenotypes found in the A/J mice and CSS. It is not likely that merely the concentration of these components explains the increased rebleeding time and reduced arterial occlusion time in the A/J mice. When compared to the B6 mice, the A/J mice and the three strains with elevated rebleeding time had variable Plg, PAI-1, and α2-antiplasmin. Two allelic forms of the mouse Plg gene have been reported for B6 and A/J mice [40]. Plg concentration was increased in A/J mice compared to B6 mice. Although we did not detect differences in Plg structure, this would not exclude possible functional differences. A congenic strain (specific for a homosomic region from A/J and the remaining Chr and background is from B6 mice) of A/J chromosome 17 that includes the Plg gene was tested in the bleeding assay. Values for bleeding and rebleeding in this congenic strain were similar to values from B6 mice, indicating that the QTL is not Plg. There are genes for other proteases and matrix proteins that reside on chromosome 17 in addition to unknown genes. DNA base pair sequence data for the PAI-1 gene or the α2-antiplasmin gene in B6 and A/J mice have reported no differences [51], but regulatory genes upstream of the coding region may be important. Our results suggest that novel or unknown genes may interact with the Plg system components to modify their function."}

craft-ca-core-ex-dev

{"project":"craft-ca-core-ex-dev","denotations":[{"id":"T18466","span":{"begin":14,"end":17},"obj":"PR_EXT:000012867"},{"id":"T18465","span":{"begin":4,"end":9},"obj":"SO_EXT:0000704"},{"id":"T18516","span":{"begin":1481,"end":1484},"obj":"PR_EXT:000012867"},{"id":"T18515","span":{"begin":1453,"end":1458},"obj":"SO_EXT:0000704"},{"id":"T18514","span":{"begin":1379,"end":1392},"obj":"SO_EXT:coding_sequence"},{"id":"T18513","span":{"begin":1363,"end":1371},"obj":"SO_EXT:sequence_upstreamness"},{"id":"T18512","span":{"begin":1357,"end":1362},"obj":"SO_EXT:0000704"},{"id":"T18511","span":{"begin":1346,"end":1356},"obj":"GO:0065007"},{"id":"T18510","span":{"begin":1302,"end":1306},"obj":"NCBITaxon:10088"},{"id":"T18509","span":{"begin":1283,"end":1287},"obj":"SO_EXT:0000704"},{"id":"T18508","span":{"begin":1268,"end":1282},"obj":"PR_EXT:000014706"},{"id":"T18507","span":{"begin":1256,"end":1260},"obj":"SO_EXT:0000704"},{"id":"T18506","span":{"begin":1250,"end":1255},"obj":"PR_EXT:000014702"},{"id":"T18505","span":{"begin":1228,"end":1236},"obj":"SO_EXT:biological_sequence"},{"id":"T18504","span":{"begin":1218,"end":1227},"obj":"SO_EXT:0000028"},{"id":"T18503","span":{"begin":1218,"end":1222},"obj":"CHEBI_SO_EXT:base"},{"id":"T18502","span":{"begin":1214,"end":1217},"obj":"CHEBI_SO_EXT:DNA"},{"id":"T18501","span":{"begin":1207,"end":1212},"obj":"SO_EXT:0000704"},{"id":"T18500","span":{"begin":1170,"end":1180},"obj":"GO_SO_EXT:chromosome"},{"id":"T18499","span":{"begin":1146,"end":1154},"obj":"CHEBI_PR_EXT:protein"},{"id":"T18498","span":{"begin":1139,"end":1145},"obj":"GO:0031012"},{"id":"T18497","span":{"begin":1125,"end":1134},"obj":"GO_EXT:0008233"},{"id":"T18496","span":{"begin":1109,"end":1114},"obj":"SO_EXT:0000704"},{"id":"T18495","span":{"begin":1094,"end":1097},"obj":"PR_EXT:000012867"},{"id":"T18494","span":{"begin":1083,"end":1086},"obj":"SO_EXT:0000771"},{"id":"T18493","span":{"begin":1057,"end":1061},"obj":"NCBITaxon:10088"},{"id":"T18492","span":{"begin":928,"end":932},"obj":"SO_EXT:0000704"},{"id":"T18491","span":{"begin":924,"end":927},"obj":"PR_EXT:000012867"},{"id":"T18490","span":{"begin":892,"end":902},"obj":"GO_SO_EXT:chromosome"},{"id":"T18489","span":{"begin":879,"end":883},"obj":"NCBITaxon:10088"},{"id":"T18488","span":{"begin":849,"end":852},"obj":"GO_SO_EXT:chromosome"},{"id":"T18487","span":{"begin":700,"end":703},"obj":"PR_EXT:000012867"},{"id":"T18486","span":{"begin":652,"end":656},"obj":"NCBITaxon:10088"},{"id":"T18485","span":{"begin":632,"end":636},"obj":"NCBITaxon:10088"},{"id":"T18484","span":{"begin":593,"end":596},"obj":"PR_EXT:000012867"},{"id":"T18483","span":{"begin":582,"end":586},"obj":"NCBITaxon:10088"},{"id":"T18482","span":{"begin":543,"end":547},"obj":"SO_EXT:0000704"},{"id":"T18481","span":{"begin":539,"end":542},"obj":"PR_EXT:000012867"},{"id":"T18480","span":{"begin":533,"end":538},"obj":"NCBITaxon:10088"},{"id":"T18479","span":{"begin":512,"end":519},"obj":"SO_EXT:0001023"},{"id":"T18478","span":{"begin":492,"end":506},"obj":"PR_EXT:000014706"},{"id":"T18477","span":{"begin":481,"end":486},"obj":"PR_EXT:000014702"},{"id":"T18476","span":{"begin":476,"end":479},"obj":"PR_EXT:000012867"},{"id":"T18475","span":{"begin":406,"end":410},"obj":"NCBITaxon:10088"},{"id":"T18474","span":{"begin":392,"end":396},"obj":"NCBITaxon:10088"},{"id":"T18473","span":{"begin":362,"end":366},"obj":"NCBITaxon:10088"},{"id":"T18472","span":{"begin":327,"end":335},"obj":"UBERON:0001637"},{"id":"T18471","span":{"begin":195,"end":199},"obj":"NCBITaxon:10088"},{"id":"T18470","span":{"begin":92,"end":95},"obj":"SO_EXT:0000771"},{"id":"T18469","span":{"begin":65,"end":76},"obj":"GO_SO_EXT:chromosome"},{"id":"T18468","span":{"begin":30,"end":44},"obj":"PR_EXT:000014706"},{"id":"T18467","span":{"begin":19,"end":24},"obj":"PR_EXT:000014702"}],"text":"The genes for Plg, PAI-1, and α2-antiplasmin reside on the three chromosomes identified for QTL for rebleeding time and may or may not be coincidental to the observed phenotypes found in the A/J mice and CSS. It is not likely that merely the concentration of these components explains the increased rebleeding time and reduced arterial occlusion time in the A/J mice. When compared to the B6 mice, the A/J mice and the three strains with elevated rebleeding time had variable Plg, PAI-1, and α2-antiplasmin. Two allelic forms of the mouse Plg gene have been reported for B6 and A/J mice [40]. Plg concentration was increased in A/J mice compared to B6 mice. Although we did not detect differences in Plg structure, this would not exclude possible functional differences. A congenic strain (specific for a homosomic region from A/J and the remaining Chr and background is from B6 mice) of A/J chromosome 17 that includes the Plg gene was tested in the bleeding assay. Values for bleeding and rebleeding in this congenic strain were similar to values from B6 mice, indicating that the QTL is not Plg. There are genes for other proteases and matrix proteins that reside on chromosome 17 in addition to unknown genes. DNA base pair sequence data for the PAI-1 gene or the α2-antiplasmin gene in B6 and A/J mice have reported no differences [51], but regulatory genes upstream of the coding region may be important. Our results suggest that novel or unknown genes may interact with the Plg system components to modify their function."}

craft-ca-core-dev

{"project":"craft-ca-core-dev","denotations":[{"id":"T18250","span":{"begin":1481,"end":1484},"obj":"PR:000012867"},{"id":"T18249","span":{"begin":1453,"end":1458},"obj":"SO:0000704"},{"id":"T18248","span":{"begin":1357,"end":1362},"obj":"SO:0000704"},{"id":"T18247","span":{"begin":1346,"end":1356},"obj":"GO:0065007"},{"id":"T18246","span":{"begin":1302,"end":1306},"obj":"NCBITaxon:10088"},{"id":"T18245","span":{"begin":1283,"end":1287},"obj":"SO:0000704"},{"id":"T18244","span":{"begin":1268,"end":1282},"obj":"PR:000014706"},{"id":"T18243","span":{"begin":1256,"end":1260},"obj":"SO:0000704"},{"id":"T18242","span":{"begin":1250,"end":1255},"obj":"PR:000014702"},{"id":"T18241","span":{"begin":1218,"end":1227},"obj":"SO:0000028"},{"id":"T18240","span":{"begin":1207,"end":1212},"obj":"SO:0000704"},{"id":"T18239","span":{"begin":1139,"end":1145},"obj":"GO:0031012"},{"id":"T18238","span":{"begin":1109,"end":1114},"obj":"SO:0000704"},{"id":"T18237","span":{"begin":1094,"end":1097},"obj":"PR:000012867"},{"id":"T18236","span":{"begin":1083,"end":1086},"obj":"SO:0000771"},{"id":"T18235","span":{"begin":1057,"end":1061},"obj":"NCBITaxon:10088"},{"id":"T18234","span":{"begin":928,"end":932},"obj":"SO:0000704"},{"id":"T18233","span":{"begin":924,"end":927},"obj":"PR:000012867"},{"id":"T18232","span":{"begin":879,"end":883},"obj":"NCBITaxon:10088"},{"id":"T18231","span":{"begin":700,"end":703},"obj":"PR:000012867"},{"id":"T18230","span":{"begin":652,"end":656},"obj":"NCBITaxon:10088"},{"id":"T18229","span":{"begin":632,"end":636},"obj":"NCBITaxon:10088"},{"id":"T18228","span":{"begin":593,"end":596},"obj":"PR:000012867"},{"id":"T18227","span":{"begin":582,"end":586},"obj":"NCBITaxon:10088"},{"id":"T18226","span":{"begin":543,"end":547},"obj":"SO:0000704"},{"id":"T18225","span":{"begin":539,"end":542},"obj":"PR:000012867"},{"id":"T18224","span":{"begin":533,"end":538},"obj":"NCBITaxon:10088"},{"id":"T18223","span":{"begin":512,"end":519},"obj":"SO:0001023"},{"id":"T18222","span":{"begin":492,"end":506},"obj":"PR:000014706"},{"id":"T18221","span":{"begin":481,"end":486},"obj":"PR:000014702"},{"id":"T18220","span":{"begin":476,"end":479},"obj":"PR:000012867"},{"id":"T18219","span":{"begin":406,"end":410},"obj":"NCBITaxon:10088"},{"id":"T18218","span":{"begin":392,"end":396},"obj":"NCBITaxon:10088"},{"id":"T18217","span":{"begin":362,"end":366},"obj":"NCBITaxon:10088"},{"id":"T18216","span":{"begin":327,"end":335},"obj":"UBERON:0001637"},{"id":"T18215","span":{"begin":195,"end":199},"obj":"NCBITaxon:10088"},{"id":"T18214","span":{"begin":92,"end":95},"obj":"SO:0000771"},{"id":"T18213","span":{"begin":30,"end":44},"obj":"PR:000014706"},{"id":"T18212","span":{"begin":19,"end":24},"obj":"PR:000014702"},{"id":"T18211","span":{"begin":14,"end":17},"obj":"PR:000012867"},{"id":"T18210","span":{"begin":4,"end":9},"obj":"SO:0000704"}],"text":"The genes for Plg, PAI-1, and α2-antiplasmin reside on the three chromosomes identified for QTL for rebleeding time and may or may not be coincidental to the observed phenotypes found in the A/J mice and CSS. It is not likely that merely the concentration of these components explains the increased rebleeding time and reduced arterial occlusion time in the A/J mice. When compared to the B6 mice, the A/J mice and the three strains with elevated rebleeding time had variable Plg, PAI-1, and α2-antiplasmin. Two allelic forms of the mouse Plg gene have been reported for B6 and A/J mice [40]. Plg concentration was increased in A/J mice compared to B6 mice. Although we did not detect differences in Plg structure, this would not exclude possible functional differences. A congenic strain (specific for a homosomic region from A/J and the remaining Chr and background is from B6 mice) of A/J chromosome 17 that includes the Plg gene was tested in the bleeding assay. Values for bleeding and rebleeding in this congenic strain were similar to values from B6 mice, indicating that the QTL is not Plg. There are genes for other proteases and matrix proteins that reside on chromosome 17 in addition to unknown genes. DNA base pair sequence data for the PAI-1 gene or the α2-antiplasmin gene in B6 and A/J mice have reported no differences [51], but regulatory genes upstream of the coding region may be important. Our results suggest that novel or unknown genes may interact with the Plg system components to modify their function."}

2_test

{"project":"2_test","denotations":[{"id":"17022820-2081600-8600409","span":{"begin":588,"end":590},"obj":"2081600"}],"text":"The genes for Plg, PAI-1, and α2-antiplasmin reside on the three chromosomes identified for QTL for rebleeding time and may or may not be coincidental to the observed phenotypes found in the A/J mice and CSS. It is not likely that merely the concentration of these components explains the increased rebleeding time and reduced arterial occlusion time in the A/J mice. When compared to the B6 mice, the A/J mice and the three strains with elevated rebleeding time had variable Plg, PAI-1, and α2-antiplasmin. Two allelic forms of the mouse Plg gene have been reported for B6 and A/J mice [40]. Plg concentration was increased in A/J mice compared to B6 mice. Although we did not detect differences in Plg structure, this would not exclude possible functional differences. A congenic strain (specific for a homosomic region from A/J and the remaining Chr and background is from B6 mice) of A/J chromosome 17 that includes the Plg gene was tested in the bleeding assay. Values for bleeding and rebleeding in this congenic strain were similar to values from B6 mice, indicating that the QTL is not Plg. There are genes for other proteases and matrix proteins that reside on chromosome 17 in addition to unknown genes. DNA base pair sequence data for the PAI-1 gene or the α2-antiplasmin gene in B6 and A/J mice have reported no differences [51], but regulatory genes upstream of the coding region may be important. Our results suggest that novel or unknown genes may interact with the Plg system components to modify their function."}