Figure 6: Working model for the intrinsic propensities of TDP-43 GQN-rich C terminus in normal cellular functions and disease progression. | Nature Communications

Figure 6: Working model for the intrinsic propensities of TDP-43 GQN-rich C terminus in normal cellular functions and disease progression.

From: The self-interaction of native TDP-43 C terminus inhibits its degradation and contributes to early proteinopathies

Figure 6

As part of the normal physiological processes of the cell, the intrinsic propensity of the TDP-43 C terminus is to confer assembly of nuclear bodies, protein stability, and promote exon 9 skipping of CFTR by adopting flexible prion-like folding; however, if loss of TDP-43 N terminus by pathological cleavage, ALS-linked mutations or other unknown cellular factors could cause disruption of cellular prion-like folding of the TDP-43 C terminus, TDP-43 inclusions will form. EGCG induced oligomerisation of TDP-43 and reduced its degradation.

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