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cellular role of annexin A7 is not well understood. It is thought to regulate and stabilize membrane domains and to have a role in Ca2+ homeostasis and Ca2+-dependent signaling pathways. These proposals are supported by data obtained from analysis of annexin A7 deficient mouse mutants. Two annexin A7 129Sv null mice strains were generated independently using a different strategy. The one of Srivastava et al. [16] is lethal. Heterozygous mice exhibit an insulin secretion defect and tumor phenotypes. The null strain reported by Herr et al. [17] is viable, healthy, and shows no insulin secretion defect or other obvious defects. However, in isolated cardiomyocytes the frequency-induced shortening is disturbed. Here we have focused on the analysis of red blood cells and platelets of the anxA7-/- mutant. Generally, red blood cells and platelets were thought not to contain annexin A7 and only recently the 47 kDa isoform has been reported as component of red blood cells [7]."}

    craft-ca-core-dev

    {"project":"craft-ca-core-dev","denotations":[{"id":"T830","span":{"begin":21,"end":31},"obj":"PR:000004080"},{"id":"T831","span":{"begin":73,"end":81},"obj":"GO:0065007"},{"id":"T832","span":{"begin":96,"end":112},"obj":"GO:0044425"},{"id":"T833","span":{"begin":135,"end":139},"obj":"CHEBI:29108"},{"id":"T834","span":{"begin":140,"end":151},"obj":"GO:0042592"},{"id":"T835","span":{"begin":156,"end":160},"obj":"CHEBI:29108"},{"id":"T836","span":{"begin":156,"end":189},"obj":"GO:0019722"},{"id":"T837","span":{"begin":255,"end":265},"obj":"PR:000004080"},{"id":"T838","span":{"begin":276,"end":281},"obj":"NCBITaxon:10088"},{"id":"T839","span":{"begin":295,"end":305},"obj":"PR:000004080"},{"id":"T840","span":{"begin":317,"end":321},"obj":"NCBITaxon:10088"},{"id":"T841","span":{"begin":445,"end":449},"obj":"NCBITaxon:10088"},{"id":"T842","span":{"begin":461,"end":468},"obj":"PR:000045358"},{"id":"T843","span":{"begin":586,"end":593},"obj":"PR:000045358"},{"id":"T844","span":{"begin":658,"end":672},"obj":"CL:0000746"},{"id":"T845","span":{"begin":760,"end":775},"obj":"CL:0000232"},{"id":"T846","span":{"begin":764,"end":769},"obj":"UBERON:0000178"},{"id":"T847","span":{"begin":780,"end":789},"obj":"CL:0000233"},{"id":"T848","span":{"begin":797,"end":802},"obj":"PR:000004080"},{"id":"T849","span":{"begin":825,"end":840},"obj":"CL:0000232"},{"id":"T850","span":{"begin":829,"end":834},"obj":"UBERON:0000178"},{"id":"T851","span":{"begin":845,"end":854},"obj":"CL:0000233"},{"id":"T852","span":{"begin":883,"end":893},"obj":"PR:000004080"},{"id":"T853","span":{"begin":923,"end":930},"obj":"SO:0001060"},{"id":"T854","span":{"begin":965,"end":980},"obj":"CL:0000232"},{"id":"T855","span":{"begin":969,"end":974},"obj":"UBERON:0000178"}],"text":"The cellular role of annexin A7 is not well understood. It is thought to regulate and stabilize membrane domains and to have a role in Ca2+ homeostasis and Ca2+-dependent signaling pathways. These proposals are supported by data obtained from analysis of annexin A7 deficient mouse mutants. Two annexin A7 129Sv null mice strains were generated independently using a different strategy. The one of Srivastava et al. [16] is lethal. Heterozygous mice exhibit an insulin secretion defect and tumor phenotypes. The null strain reported by Herr et al. [17] is viable, healthy, and shows no insulin secretion defect or other obvious defects. However, in isolated cardiomyocytes the frequency-induced shortening is disturbed. Here we have focused on the analysis of red blood cells and platelets of the anxA7-/- mutant. Generally, red blood cells and platelets were thought not to contain annexin A7 and only recently the 47 kDa isoform has been reported as component of red blood cells [7]."}

    2_test

    {"project":"2_test","denotations":[{"id":"12925238-10570150-8102388","span":{"begin":417,"end":419},"obj":"10570150"},{"id":"12925238-11390641-8102389","span":{"begin":549,"end":551},"obj":"11390641"},{"id":"12925238-11895795-8102390","span":{"begin":982,"end":983},"obj":"11895795"}],"text":"The cellular role of annexin A7 is not well understood. It is thought to regulate and stabilize membrane domains and to have a role in Ca2+ homeostasis and Ca2+-dependent signaling pathways. These proposals are supported by data obtained from analysis of annexin A7 deficient mouse mutants. Two annexin A7 129Sv null mice strains were generated independently using a different strategy. The one of Srivastava et al. [16] is lethal. Heterozygous mice exhibit an insulin secretion defect and tumor phenotypes. The null strain reported by Herr et al. [17] is viable, healthy, and shows no insulin secretion defect or other obvious defects. However, in isolated cardiomyocytes the frequency-induced shortening is disturbed. Here we have focused on the analysis of red blood cells and platelets of the anxA7-/- mutant. Generally, red blood cells and platelets were thought not to contain annexin A7 and only recently the 47 kDa isoform has been reported as component of red blood cells [7]."}

    craft-ca-core-ex-dev

    {"project":"craft-ca-core-ex-dev","denotations":[{"id":"T1040","span":{"begin":4,"end":12},"obj":"CL_GO_EXT:cell"},{"id":"T1041","span":{"begin":21,"end":31},"obj":"PR_EXT:000004080"},{"id":"T1042","span":{"begin":73,"end":81},"obj":"GO:0065007"},{"id":"T1043","span":{"begin":96,"end":112},"obj":"GO:0044425"},{"id":"T1044","span":{"begin":135,"end":139},"obj":"CHEBI:29108"},{"id":"T1045","span":{"begin":140,"end":151},"obj":"GO:0042592"},{"id":"T1046","span":{"begin":156,"end":160},"obj":"CHEBI:29108"},{"id":"T1047","span":{"begin":156,"end":189},"obj":"GO:0019722"},{"id":"T1048","span":{"begin":255,"end":265},"obj":"PR_EXT:000004080"},{"id":"T1049","span":{"begin":276,"end":281},"obj":"NCBITaxon:10088"},{"id":"T1050","span":{"begin":282,"end":289},"obj":"SO_EXT:sequence_altered_entity"},{"id":"T1051","span":{"begin":295,"end":305},"obj":"PR_EXT:000004080"},{"id":"T1052","span":{"begin":312,"end":316},"obj":"SO_EXT:sequence_nullness"},{"id":"T1053","span":{"begin":317,"end":321},"obj":"NCBITaxon:10088"},{"id":"T1054","span":{"begin":424,"end":430},"obj":"GO_EXT:fatality_or_lethality"},{"id":"T1055","span":{"begin":445,"end":449},"obj":"NCBITaxon:10088"},{"id":"T1056","span":{"begin":461,"end":468},"obj":"PR_EXT:000045358"},{"id":"T1057","span":{"begin":469,"end":478},"obj":"GO_EXT:secretion_entity_or_process"},{"id":"T1058","span":{"begin":512,"end":516},"obj":"SO_EXT:sequence_nullness"},{"id":"T1059","span":{"begin":586,"end":593},"obj":"PR_EXT:000045358"},{"id":"T1060","span":{"begin":594,"end":603},"obj":"GO_EXT:secretion_entity_or_process"},{"id":"T1061","span":{"begin":658,"end":672},"obj":"CL:0000746"},{"id":"T1062","span":{"begin":760,"end":775},"obj":"CL:0000232"},{"id":"T1063","span":{"begin":764,"end":769},"obj":"UBERON:0000178"},{"id":"T1064","span":{"begin":770,"end":775},"obj":"CL_GO_EXT:cell"},{"id":"T1065","span":{"begin":780,"end":789},"obj":"CL:0000233"},{"id":"T1066","span":{"begin":797,"end":802},"obj":"PR_EXT:000004080"},{"id":"T1067","span":{"begin":802,"end":803},"obj":"SO_EXT:sequence_nullness_or_absence"},{"id":"T1068","span":{"begin":804,"end":805},"obj":"SO_EXT:sequence_nullness_or_absence"},{"id":"T1069","span":{"begin":806,"end":812},"obj":"SO_EXT:sequence_altered_entity"},{"id":"T1070","span":{"begin":825,"end":840},"obj":"CL:0000232"},{"id":"T1071","span":{"begin":829,"end":834},"obj":"UBERON:0000178"},{"id":"T1072","span":{"begin":835,"end":840},"obj":"CL_GO_EXT:cell"},{"id":"T1073","span":{"begin":845,"end":854},"obj":"CL:0000233"},{"id":"T1074","span":{"begin":883,"end":893},"obj":"PR_EXT:000004080"},{"id":"T1075","span":{"begin":923,"end":930},"obj":"SO_EXT:0001060"},{"id":"T1076","span":{"begin":965,"end":980},"obj":"CL:0000232"},{"id":"T1077","span":{"begin":969,"end":974},"obj":"UBERON:0000178"},{"id":"T1078","span":{"begin":975,"end":980},"obj":"CL_GO_EXT:cell"}],"text":"The cellular role of annexin A7 is not well understood. It is thought to regulate and stabilize membrane domains and to have a role in Ca2+ homeostasis and Ca2+-dependent signaling pathways. These proposals are supported by data obtained from analysis of annexin A7 deficient mouse mutants. Two annexin A7 129Sv null mice strains were generated independently using a different strategy. The one of Srivastava et al. [16] is lethal. Heterozygous mice exhibit an insulin secretion defect and tumor phenotypes. The null strain reported by Herr et al. [17] is viable, healthy, and shows no insulin secretion defect or other obvious defects. However, in isolated cardiomyocytes the frequency-induced shortening is disturbed. Here we have focused on the analysis of red blood cells and platelets of the anxA7-/- mutant. Generally, red blood cells and platelets were thought not to contain annexin A7 and only recently the 47 kDa isoform has been reported as component of red blood cells [7]."}