Post-Translational Modifications Modulate Proteinopathies of TDP-43, FUS and hnRNP-A/B in Amyotrophic Lateral Sclerosis

Ítems similars

• Phosphorylation of hnRNP K controls cytosolic accumulation of TDP-43
  per: White, Anthony, et al.
  Publicat: (2013)
• Functional mapping of the interaction between TDP-43 and hnRNP A2 in vivo
  per: D’Ambrogio, Andrea, et al.
  Publicat: (2009)
• TDP-43 regulates the alternative splicing of hnRNP A1 to yield an aggregation-prone variant in amyotrophic lateral sclerosis
  per: Deshaies, Jade-Emmanuelle, et al.
  Publicat: (2018)
• Interactions between the Intrinsically Disordered Regions of hnRNP-A2 and TDP-43 Accelerate TDP-43′s Conformational Transition
  per: Chiang, Wan-Chin, et al.
  Publicat: (2020)
• Inclusions in frontotemporal lobar degeneration with TDP-43 proteinopathy (FTLD-TDP) and amyotrophic lateral sclerosis (ALS), but not FTLD with FUS proteinopathy (FTLD-FUS), have properties of amyloid
  per: Bigio, Eileen H, et al.
  Publicat: (2013)