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CRISPR/Cas9-based knockout screening revealed GSK3beta as a key regulator for structural plasticity of axon initial segment
Du, Y.; Egawa, R.; Adachi, R.; Motohara, K.; Furumichi, K.; Fukaya, R.; Kuba, H.
GSK3beta-dependent microtubule remodeling drives axon initial segment structural plasticity, with knockout impairing and constitutively active GSK3beta facilitating the change.
Mild contradiction
1 prior failureOne documented clinical failure (Phase 1 or 2) overlaps with the claimed mechanism.
Abstract excerpt
The axon initial segment (AIS) undergoes structural plasticity to tune neuronal excitability, yet the underlying molecular mechanisms remain unclear. An in vivo CRISPR/Cas9 knockout platform identified that knockout of GSK3beta or Tau impaired developmental AIS shortening, while constitutively active GSK3beta facilitated shortening, an effect suppressed by microtubule stabilization. The findings identify GSK3beta-dependent microtubule remodeling as a mechanism underlying developmental AIS shortening.
Matching Claidex post-mortems
1 of 1 indexedThis is an automated contradiction flag, not an editorial judgment on the preprint's quality. Flags identify where the preclinical literature and the clinical failure record diverge.

