PMC:539297 / 25325-25810 JSONTXT

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    craft-ca-core-dev

    {"project":"craft-ca-core-dev","denotations":[{"id":"T5013","span":{"begin":4,"end":12},"obj":"GO:0016020"},{"id":"T5014","span":{"begin":4,"end":24},"obj":"GO:0055085"},{"id":"T5015","span":{"begin":29,"end":42},"obj":"GO:0005739"},{"id":"T5016","span":{"begin":76,"end":78},"obj":"UBERON:0002037"},{"id":"T5017","span":{"begin":78,"end":82},"obj":"PR:000005591"},{"id":"T5018","span":{"begin":129,"end":137},"obj":"CL:0000540"},{"id":"T5019","span":{"begin":184,"end":200},"obj":"GO:0031988"},{"id":"T5020","span":{"begin":193,"end":210},"obj":"GO:0016192"},{"id":"T5021","span":{"begin":230,"end":240},"obj":"GO:0008152"},{"id":"T5022","span":{"begin":263,"end":270},"obj":"CL:0000540"},{"id":"T5023","span":{"begin":286,"end":294},"obj":"PR:000005591"},{"id":"T5024","span":{"begin":364,"end":366},"obj":"UBERON:0002037"},{"id":"T5025","span":{"begin":366,"end":370},"obj":"PR:000005591"},{"id":"T5026","span":{"begin":377,"end":387},"obj":"UBERON:0002037"},{"id":"T5027","span":{"begin":445,"end":453},"obj":"PR:000005591"}],"text":"The membrane trafficking and mitochondrial deficits uncovered in homozygous CbCln3Δex7/8 cells are likely to particularly impact neuronal function. Neurotransmission heavily relies on membrane vesicle transport, and a high-energy metabolism may further sensitize neurons to the loss of battenin activity. Thus, our panel of wild-type, heterozygous, and homozygous CbCln3Δex7/8 cerebellar cells provide an ideal model system to further elucidate battenin function and JNCL pathogenesis."}

    craft-sa-dev

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membrane trafficking and mitochondrial deficits uncovered in homozygous CbCln3Δex7/8 cells are likely to particularly impact neuronal function. Neurotransmission heavily relies on membrane vesicle transport, and a high-energy metabolism may further sensitize neurons to the loss of battenin activity. Thus, our panel of wild-type, heterozygous, and homozygous CbCln3Δex7/8 cerebellar cells provide an ideal model system to further elucidate battenin function and JNCL pathogenesis."}

    craft-ca-core-ex-dev

    {"project":"craft-ca-core-ex-dev","denotations":[{"id":"T5035","span":{"begin":148,"end":165},"obj":"GO_EXT:neurotransmission"},{"id":"T5036","span":{"begin":184,"end":200},"obj":"GO:0031988"},{"id":"T5037","span":{"begin":193,"end":210},"obj":"GO:0016192"},{"id":"T5038","span":{"begin":230,"end":240},"obj":"GO:0008152"},{"id":"T5039","span":{"begin":263,"end":270},"obj":"CL:0000540"},{"id":"T5040","span":{"begin":286,"end":294},"obj":"PR_EXT:000005591"},{"id":"T5041","span":{"begin":324,"end":333},"obj":"SO_EXT:wild_type_entity_or_quality"},{"id":"T5042","span":{"begin":364,"end":366},"obj":"UBERON:0002037"},{"id":"T5043","span":{"begin":366,"end":370},"obj":"PR_EXT:000005591"},{"id":"T5044","span":{"begin":377,"end":387},"obj":"UBERON:0002037"},{"id":"T5045","span":{"begin":388,"end":393},"obj":"CL_GO_EXT:cell"},{"id":"T5046","span":{"begin":445,"end":453},"obj":"PR_EXT:000005591"},{"id":"T5028","span":{"begin":4,"end":12},"obj":"GO:0016020"},{"id":"T5029","span":{"begin":4,"end":24},"obj":"GO:0055085"},{"id":"T5030","span":{"begin":29,"end":42},"obj":"GO:0005739"},{"id":"T5031","span":{"begin":76,"end":78},"obj":"UBERON:0002037"},{"id":"T5032","span":{"begin":78,"end":82},"obj":"PR_EXT:000005591"},{"id":"T5033","span":{"begin":89,"end":94},"obj":"CL_GO_EXT:cell"},{"id":"T5034","span":{"begin":129,"end":137},"obj":"CL:0000540"}],"text":"The membrane trafficking and mitochondrial deficits uncovered in homozygous CbCln3Δex7/8 cells are likely to particularly impact neuronal function. Neurotransmission heavily relies on membrane vesicle transport, and a high-energy metabolism may further sensitize neurons to the loss of battenin activity. Thus, our panel of wild-type, heterozygous, and homozygous CbCln3Δex7/8 cerebellar cells provide an ideal model system to further elucidate battenin function and JNCL pathogenesis."}