PMC:3654953 / 25612-26593 JSONTXT

{"project":"AxD_symptoms","denotations":[{"id":"T66","span":{"begin":221,"end":238},"obj":"Phenotype"},{"id":"T67","span":{"begin":364,"end":381},"obj":"Phenotype"},{"id":"T68","span":{"begin":632,"end":649},"obj":"Phenotype"},{"id":"T69","span":{"begin":789,"end":806},"obj":"Phenotype"}],"attributes":[{"id":"A66","pred":"hp_id","subj":"T66","obj":"http://purl.obolibrary.org/obo/HP_0002180"},{"id":"A67","pred":"hp_id","subj":"T67","obj":"http://purl.obolibrary.org/obo/HP_0002180"},{"id":"A68","pred":"hp_id","subj":"T68","obj":"http://purl.obolibrary.org/obo/HP_0002180"},{"id":"A69","pred":"hp_id","subj":"T69","obj":"http://purl.obolibrary.org/obo/HP_0002180"}],"text":"Taken together, these observations indicate HDAC6 as a master regulator of different neuroprotective mechanisms, partly mediated by controlling MTOC biogenesis and function, [23] and predict a role for defective HDAC6 in neurodegeneration, particularly in MND [26]. As for mammalian models, although a first strain of HDAC6 knockout (KO) mice presented no sign of neurodegeneration, [29] altered emotional behaviors suggested a contribution of HDAC6 to maintain proper neuronal activity [30]. Moreover, a second KO HDAC6 strain displayed ubiquitin-positive aggregates and increased apoptosis of brain nerve cells, both hallmarks of neurodegeneration, starting from 6 months of age [31]. These and other results suggest for HDAC6 a complex role in contributing to either neuroprotection or neurodegeneration, depending on the specific pathological condition [7,26,32]. These opposite effects can indeed hamper the development of therapeutic strategies based on HDAC6 modulation [7]."}

{"project":"2_test","denotations":[{"id":"23634874-20940043-81641099","span":{"begin":175,"end":177},"obj":"20940043"},{"id":"23634874-22372633-81641100","span":{"begin":261,"end":263},"obj":"22372633"},{"id":"23634874-18180281-81641101","span":{"begin":384,"end":386},"obj":"18180281"},{"id":"23634874-22328923-81641102","span":{"begin":488,"end":490},"obj":"22328923"},{"id":"23634874-20075865-81641103","span":{"begin":682,"end":684},"obj":"20075865"},{"id":"23634874-21377170-81641104","span":{"begin":858,"end":859},"obj":"21377170"},{"id":"23634874-22372633-81641105","span":{"begin":860,"end":862},"obj":"22372633"},{"id":"23634874-23184605-81641106","span":{"begin":863,"end":865},"obj":"23184605"},{"id":"23634874-21377170-81641107","span":{"begin":978,"end":979},"obj":"21377170"},{"id":"T33489","span":{"begin":175,"end":177},"obj":"20940043"},{"id":"T15726","span":{"begin":261,"end":263},"obj":"22372633"},{"id":"T48149","span":{"begin":384,"end":386},"obj":"18180281"},{"id":"T65385","span":{"begin":488,"end":490},"obj":"22328923"},{"id":"T39909","span":{"begin":682,"end":684},"obj":"20075865"},{"id":"T10435","span":{"begin":858,"end":859},"obj":"21377170"},{"id":"T16572","span":{"begin":860,"end":862},"obj":"22372633"},{"id":"T60470","span":{"begin":863,"end":865},"obj":"23184605"},{"id":"T66386","span":{"begin":978,"end":979},"obj":"21377170"}],"text":"Taken together, these observations indicate HDAC6 as a master regulator of different neuroprotective mechanisms, partly mediated by controlling MTOC biogenesis and function, [23] and predict a role for defective HDAC6 in neurodegeneration, particularly in MND [26]. As for mammalian models, although a first strain of HDAC6 knockout (KO) mice presented no sign of neurodegeneration, [29] altered emotional behaviors suggested a contribution of HDAC6 to maintain proper neuronal activity [30]. Moreover, a second KO HDAC6 strain displayed ubiquitin-positive aggregates and increased apoptosis of brain nerve cells, both hallmarks of neurodegeneration, starting from 6 months of age [31]. These and other results suggest for HDAC6 a complex role in contributing to either neuroprotection or neurodegeneration, depending on the specific pathological condition [7,26,32]. These opposite effects can indeed hamper the development of therapeutic strategies based on HDAC6 modulation [7]."}