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The plethora of structural information, together with the increasing power of computational facilities and refinement of binding prediction tools (110, 112, 119), open the possibility to design peptides/peptidomimetics able to target the translation complexes, with the aim to decrease protein synthesis of specific neuronal mRNAs and rescuing a healthy phenotype in individuals affected by FXS
This review aims to elucidate the role of ferroptosis in RBI and its therapeutic implications
Kremer et al., 2024) with an indispensable role of STAT3 activation due to methylation at a CpG site in the GFAP promoter (Takizawa et al., 2001), and in TET1/2/3-mediated DNA demethylation for establishing neural stem cell identity and enabling glial (e.g., astrocyte and oligodendrocyte) differentiation (MacArthur et al., 2024)
The Jarisch-Herxheimer reaction: revisited
