PubMed:17056596 JSONTXT

{"project":"Glycosmos15-CL","denotations":[{"id":"T1","span":{"begin":332,"end":338},"obj":"Cell"},{"id":"T2","span":{"begin":427,"end":440},"obj":"Cell"},{"id":"T3","span":{"begin":639,"end":645},"obj":"Cell"},{"id":"T4","span":{"begin":1408,"end":1414},"obj":"Cell"}],"attributes":[{"id":"A1","pred":"cl_id","subj":"T1","obj":"http://purl.obolibrary.org/obo/CL:0000084"},{"id":"A2","pred":"cl_id","subj":"T2","obj":"http://purl.obolibrary.org/obo/CL:0000898"},{"id":"A3","pred":"cl_id","subj":"T3","obj":"http://purl.obolibrary.org/obo/CL:0000084"},{"id":"A4","pred":"cl_id","subj":"T4","obj":"http://purl.obolibrary.org/obo/CL:0000084"}],"text":"Sustained activity of calcium release-activated calcium channels requires translocation of mitochondria to the plasma membrane.\nA rise of the intracellular Ca(2+) concentration has multiple signaling functions. Sustained Ca(2+) influx across plasma membrane through calcium release-activated calcium (CRAC) channels is required for T-cell development in the thymus, gene transcription, and proliferation and differentiation of naïve T-cells into armed effectors cells. Intracellular Ca(2+) signals are shaped by mitochondria, which function as a highly dynamic Ca(2+) buffer. However, the precise role of mitochondria for Ca(2+)-dependent T-cell activation is unknown. Here we have shown that mitochondria are translocated to the plasma membrane as a consequence of Ca(2+) influx and that this directed movement is essential to sustain Ca(2+) influx through CRAC channels. The decreased distance between mitochondria and the plasma membrane enabled mitochondria to take up large amounts of inflowing Ca(2+) at the plasma membrane, thereby preventing Ca(2+)-dependent inactivation of CRAC channels and sustaining Ca(2+) signals. Inhibition of kinesin-dependent mitochondrial movement along microtubules abolished mitochondrial translocation and reduced sustained Ca(2+) signals. Our results show how a directed movement of mitochondria is used to control important cellular functions such as Ca(2+)-dependent T-cell activation."}

{"project":"LitCoin-PubTator-for-Tuning","denotations":[{"id":"12","span":{"begin":156,"end":162},"obj":"ChemicalEntity"},{"id":"13","span":{"begin":221,"end":227},"obj":"ChemicalEntity"},{"id":"14","span":{"begin":483,"end":489},"obj":"ChemicalEntity"},{"id":"15","span":{"begin":561,"end":567},"obj":"ChemicalEntity"},{"id":"16","span":{"begin":622,"end":628},"obj":"ChemicalEntity"},{"id":"17","span":{"begin":766,"end":772},"obj":"ChemicalEntity"},{"id":"18","span":{"begin":836,"end":842},"obj":"ChemicalEntity"},{"id":"19","span":{"begin":1000,"end":1006},"obj":"ChemicalEntity"},{"id":"20","span":{"begin":1050,"end":1056},"obj":"ChemicalEntity"},{"id":"21","span":{"begin":1112,"end":1118},"obj":"ChemicalEntity"},{"id":"22","span":{"begin":1262,"end":1268},"obj":"ChemicalEntity"},{"id":"23","span":{"begin":1391,"end":1397},"obj":"ChemicalEntity"}],"attributes":[{"id":"A12","pred":"tao:has_database_id","subj":"12","obj":"MESH:D000069285"},{"id":"A13","pred":"tao:has_database_id","subj":"13","obj":"MESH:D000069285"},{"id":"A14","pred":"tao:has_database_id","subj":"14","obj":"MESH:D000069285"},{"id":"A15","pred":"tao:has_database_id","subj":"15","obj":"MESH:D000069285"},{"id":"A16","pred":"tao:has_database_id","subj":"16","obj":"MESH:D000069285"},{"id":"A17","pred":"tao:has_database_id","subj":"17","obj":"MESH:D000069285"},{"id":"A18","pred":"tao:has_database_id","subj":"18","obj":"MESH:D000069285"},{"id":"A19","pred":"tao:has_database_id","subj":"19","obj":"MESH:D000069285"},{"id":"A20","pred":"tao:has_database_id","subj":"20","obj":"MESH:D000069285"},{"id":"A21","pred":"tao:has_database_id","subj":"21","obj":"MESH:D000069285"},{"id":"A22","pred":"tao:has_database_id","subj":"22","obj":"MESH:D000069285"},{"id":"A23","pred":"tao:has_database_id","subj":"23","obj":"MESH:D000069285"}],"text":"Sustained activity of calcium release-activated calcium channels requires translocation of mitochondria to the plasma membrane.\nA rise of the intracellular Ca(2+) concentration has multiple signaling functions. Sustained Ca(2+) influx across plasma membrane through calcium release-activated calcium (CRAC) channels is required for T-cell development in the thymus, gene transcription, and proliferation and differentiation of naïve T-cells into armed effectors cells. Intracellular Ca(2+) signals are shaped by mitochondria, which function as a highly dynamic Ca(2+) buffer. However, the precise role of mitochondria for Ca(2+)-dependent T-cell activation is unknown. Here we have shown that mitochondria are translocated to the plasma membrane as a consequence of Ca(2+) influx and that this directed movement is essential to sustain Ca(2+) influx through CRAC channels. The decreased distance between mitochondria and the plasma membrane enabled mitochondria to take up large amounts of inflowing Ca(2+) at the plasma membrane, thereby preventing Ca(2+)-dependent inactivation of CRAC channels and sustaining Ca(2+) signals. Inhibition of kinesin-dependent mitochondrial movement along microtubules abolished mitochondrial translocation and reduced sustained Ca(2+) signals. Our results show how a directed movement of mitochondria is used to control important cellular functions such as Ca(2+)-dependent T-cell activation."}

{"project":"sentences","denotations":[{"id":"T1","span":{"begin":0,"end":127},"obj":"Sentence"},{"id":"T2","span":{"begin":128,"end":210},"obj":"Sentence"},{"id":"T3","span":{"begin":211,"end":468},"obj":"Sentence"},{"id":"T4","span":{"begin":469,"end":575},"obj":"Sentence"},{"id":"T5","span":{"begin":576,"end":668},"obj":"Sentence"},{"id":"T6","span":{"begin":669,"end":872},"obj":"Sentence"},{"id":"T7","span":{"begin":873,"end":1127},"obj":"Sentence"},{"id":"T8","span":{"begin":1128,"end":1277},"obj":"Sentence"},{"id":"T9","span":{"begin":1278,"end":1426},"obj":"Sentence"}],"namespaces":[{"prefix":"_base","uri":"http://pubannotation.org/ontology/tao.owl#"}],"text":"Sustained activity of calcium release-activated calcium channels requires translocation of mitochondria to the plasma membrane.\nA rise of the intracellular Ca(2+) concentration has multiple signaling functions. Sustained Ca(2+) influx across plasma membrane through calcium release-activated calcium (CRAC) channels is required for T-cell development in the thymus, gene transcription, and proliferation and differentiation of naïve T-cells into armed effectors cells. Intracellular Ca(2+) signals are shaped by mitochondria, which function as a highly dynamic Ca(2+) buffer. However, the precise role of mitochondria for Ca(2+)-dependent T-cell activation is unknown. Here we have shown that mitochondria are translocated to the plasma membrane as a consequence of Ca(2+) influx and that this directed movement is essential to sustain Ca(2+) influx through CRAC channels. The decreased distance between mitochondria and the plasma membrane enabled mitochondria to take up large amounts of inflowing Ca(2+) at the plasma membrane, thereby preventing Ca(2+)-dependent inactivation of CRAC channels and sustaining Ca(2+) signals. Inhibition of kinesin-dependent mitochondrial movement along microtubules abolished mitochondrial translocation and reduced sustained Ca(2+) signals. Our results show how a directed movement of mitochondria is used to control important cellular functions such as Ca(2+)-dependent T-cell activation."}

{"project":"Glycosmos6-MAT","denotations":[{"id":"T1","span":{"begin":358,"end":364},"obj":"http://purl.obolibrary.org/obo/MAT_0000080"}],"text":"Sustained activity of calcium release-activated calcium channels requires translocation of mitochondria to the plasma membrane.\nA rise of the intracellular Ca(2+) concentration has multiple signaling functions. Sustained Ca(2+) influx across plasma membrane through calcium release-activated calcium (CRAC) channels is required for T-cell development in the thymus, gene transcription, and proliferation and differentiation of naïve T-cells into armed effectors cells. Intracellular Ca(2+) signals are shaped by mitochondria, which function as a highly dynamic Ca(2+) buffer. However, the precise role of mitochondria for Ca(2+)-dependent T-cell activation is unknown. Here we have shown that mitochondria are translocated to the plasma membrane as a consequence of Ca(2+) influx and that this directed movement is essential to sustain Ca(2+) influx through CRAC channels. The decreased distance between mitochondria and the plasma membrane enabled mitochondria to take up large amounts of inflowing Ca(2+) at the plasma membrane, thereby preventing Ca(2+)-dependent inactivation of CRAC channels and sustaining Ca(2+) signals. Inhibition of kinesin-dependent mitochondrial movement along microtubules abolished mitochondrial translocation and reduced sustained Ca(2+) signals. Our results show how a directed movement of mitochondria is used to control important cellular functions such as Ca(2+)-dependent T-cell activation."}

{"project":"PubmedHPO","denotations":[{"id":"T1","span":{"begin":1160,"end":1173},"obj":"HP_0001427"},{"id":"T2","span":{"begin":1212,"end":1225},"obj":"HP_0001427"}],"text":"Sustained activity of calcium release-activated calcium channels requires translocation of mitochondria to the plasma membrane.\nA rise of the intracellular Ca(2+) concentration has multiple signaling functions. Sustained Ca(2+) influx across plasma membrane through calcium release-activated calcium (CRAC) channels is required for T-cell development in the thymus, gene transcription, and proliferation and differentiation of naïve T-cells into armed effectors cells. Intracellular Ca(2+) signals are shaped by mitochondria, which function as a highly dynamic Ca(2+) buffer. However, the precise role of mitochondria for Ca(2+)-dependent T-cell activation is unknown. Here we have shown that mitochondria are translocated to the plasma membrane as a consequence of Ca(2+) influx and that this directed movement is essential to sustain Ca(2+) influx through CRAC channels. The decreased distance between mitochondria and the plasma membrane enabled mitochondria to take up large amounts of inflowing Ca(2+) at the plasma membrane, thereby preventing Ca(2+)-dependent inactivation of CRAC channels and sustaining Ca(2+) signals. Inhibition of kinesin-dependent mitochondrial movement along microtubules abolished mitochondrial translocation and reduced sustained Ca(2+) signals. Our results show how a directed movement of mitochondria is used to control important cellular functions such as Ca(2+)-dependent T-cell activation."}

{"project":"NCBITAXON","denotations":[{"id":"T1","span":{"begin":358,"end":364},"obj":"OrganismTaxon"}],"attributes":[{"id":"A1","pred":"db_id","subj":"T1","obj":"49990"}],"text":"Sustained activity of calcium release-activated calcium channels requires translocation of mitochondria to the plasma membrane.\nA rise of the intracellular Ca(2+) concentration has multiple signaling functions. Sustained Ca(2+) influx across plasma membrane through calcium release-activated calcium (CRAC) channels is required for T-cell development in the thymus, gene transcription, and proliferation and differentiation of naïve T-cells into armed effectors cells. Intracellular Ca(2+) signals are shaped by mitochondria, which function as a highly dynamic Ca(2+) buffer. However, the precise role of mitochondria for Ca(2+)-dependent T-cell activation is unknown. Here we have shown that mitochondria are translocated to the plasma membrane as a consequence of Ca(2+) influx and that this directed movement is essential to sustain Ca(2+) influx through CRAC channels. The decreased distance between mitochondria and the plasma membrane enabled mitochondria to take up large amounts of inflowing Ca(2+) at the plasma membrane, thereby preventing Ca(2+)-dependent inactivation of CRAC channels and sustaining Ca(2+) signals. Inhibition of kinesin-dependent mitochondrial movement along microtubules abolished mitochondrial translocation and reduced sustained Ca(2+) signals. Our results show how a directed movement of mitochondria is used to control important cellular functions such as Ca(2+)-dependent T-cell activation."}

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{"project":"Anatomy-MAT","denotations":[{"id":"T1","span":{"begin":358,"end":364},"obj":"Body_part"}],"attributes":[{"id":"A1","pred":"mat_id","subj":"T1","obj":"http://purl.obolibrary.org/obo/MAT_0000080"}],"text":"Sustained activity of calcium release-activated calcium channels requires translocation of mitochondria to the plasma membrane.\nA rise of the intracellular Ca(2+) concentration has multiple signaling functions. Sustained Ca(2+) influx across plasma membrane through calcium release-activated calcium (CRAC) channels is required for T-cell development in the thymus, gene transcription, and proliferation and differentiation of naïve T-cells into armed effectors cells. Intracellular Ca(2+) signals are shaped by mitochondria, which function as a highly dynamic Ca(2+) buffer. However, the precise role of mitochondria for Ca(2+)-dependent T-cell activation is unknown. Here we have shown that mitochondria are translocated to the plasma membrane as a consequence of Ca(2+) influx and that this directed movement is essential to sustain Ca(2+) influx through CRAC channels. The decreased distance between mitochondria and the plasma membrane enabled mitochondria to take up large amounts of inflowing Ca(2+) at the plasma membrane, thereby preventing Ca(2+)-dependent inactivation of CRAC channels and sustaining Ca(2+) signals. Inhibition of kinesin-dependent mitochondrial movement along microtubules abolished mitochondrial translocation and reduced sustained Ca(2+) signals. Our results show how a directed movement of mitochondria is used to control important cellular functions such as Ca(2+)-dependent T-cell activation."}