PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 29524538-3 2018 We recently found that ceftriaxone, a beta-lactam antibiotic able to overcome the blood-brain barrier, successfully eliminated the cellular toxic effects of misfolded proteins as Glial Fibrillary Acidic Protein (GFAP) and alpha-synuclein. Ceftriaxone 23-34 synuclein alpha Homo sapiens 222-237 34189904-6 2021 Western blot and immunofluorescence revealed that incorporation of CL in a lipid bilayer ameliorated the docking of CEF-FK506-nilotinib-GSH-CL-liposomes at alpha-synuclein (alpha-syn), indicating a better targeting capability of the liposomes to degenerated neurons. Ceftriaxone 116-119 synuclein alpha Homo sapiens 156-171 34189904-6 2021 Western blot and immunofluorescence revealed that incorporation of CL in a lipid bilayer ameliorated the docking of CEF-FK506-nilotinib-GSH-CL-liposomes at alpha-synuclein (alpha-syn), indicating a better targeting capability of the liposomes to degenerated neurons. Ceftriaxone 116-119 synuclein alpha Homo sapiens 173-182 29524538-9 2018 General significance These results, in addition to our previous studies on alpha-synuclein and GFAP, confirm the property of ceftriaxone to inhibit the pathological protein aggregation of lysozyme also by a chaperone-like mechanism, extending the potential therapeutic application of this molecule to some forms of human hereditary systemic amyloidosis. Ceftriaxone 125-136 synuclein alpha Homo sapiens 75-90 27133445-7 2016 GENERAL SIGNIFICANCE: This result, in addition to our previous works in which we documented that ceftriaxone interacts with alpha-synuclein inhibiting its pathological aggregation and that a cyclical treatment with this molecule in a patient with adult-onset Alexander"s disease halted, and partly reversed, the progression of neurodegeneration, suggests the possibility of a chaperone-like effect of ceftriaxone on protein involved in specific neurodegenerative diseases. Ceftriaxone 97-108 synuclein alpha Homo sapiens 124-139 27133445-7 2016 GENERAL SIGNIFICANCE: This result, in addition to our previous works in which we documented that ceftriaxone interacts with alpha-synuclein inhibiting its pathological aggregation and that a cyclical treatment with this molecule in a patient with adult-onset Alexander"s disease halted, and partly reversed, the progression of neurodegeneration, suggests the possibility of a chaperone-like effect of ceftriaxone on protein involved in specific neurodegenerative diseases. Ceftriaxone 401-412 synuclein alpha Homo sapiens 124-139