These results implicate Pin1 as a possible modulator of stress-induced NF-H phosphorylation as seen in neurodegenerative disorders like AD and amyotrophic lateral sclerosis.
This study highlights a novel signaling role of PP2A by Pin1 and implicates Pin1 as a therapeutic target to reduce aberrant phosphorylation of NF proteins in neurodegenerative disorders such as AD, PD, and ALS.
We have confirmed the involvement of specific proteins previously associated with ALS (Galectin 2 (<i>LGALS3</i>), Transthyretin (<i>TTR</i>), Protein S100-A6 (<i>S100A6</i>), and Protein S100-A11 (<i>S100A11</i>)) and have shown the involvement of proteins not previously described in the ALS context (Methanethiol oxidase (<i>SELENBP1</i>), Peptidyl-prolyl cis-trans isomerase NIMA-interacting 1 (<i>PIN-1</i>), Calcyclin-binding protein (<i>CACYBP</i>) and Rho-associated protein kinase 2 (<i>ROCK2</i>)).