AICAR 後mislocalization 的TDP-43 蛋白質相互作用。透過足夠UV
TDP-43 蛋白質互相作用，並經由引晶效應（seeding effect）使TDP-43
ALS 在疾病上的模型（disease model），且可以期待它在其它神經退
化性疾病中的廣泛討論與應用。;Photolytic device has been used widely in the controlled release of
chemicals. Previously we have identified the core sequence of TDP-43’s
C terminus and characterized its rapid aggregation and amyloidogenesis.
In this study, we synthesized a photochemically inducible peptide.
Provided that the amyloidogenicity of the peptide would be only activated
upon UV-initiated photocleavage. From 1) the ultrastructural changes
observed under a transmission electron microscope (TEM), 2) the
secondary structure alteration revealed by circular dichroism (CD), and 3)
the turbidity assessed by UV–visible spectrophotometer, the significant
changes of the peptide after UV illumination were reported. In addition to
the in vitro characterizations, the fluorophore was conjugated to the
peptide to learn its dynamics in neuronal cells since it also confers cell
membrane permeability. Of note, only UV-mediated release of this
peptide is capable of triggering cytosolic TDP-43 to form amyloid fiber.
Taken these together, this photochemically inducible peptide could serve
as a simple but powerful disease model of ALS and its further application
on neurodegenerative diseases is highly expected as well.