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Protein kinase C in synaptic plasticity: changes in the in situ phosphorylation state of identified pre- and postsynaptic substrates

Additionally, we identify the FHA domain of SNIP1 as a reader of P-SF3B1, guiding the recruitment and assembly of the RES complex during spliceosome activation, and show that mutations in the FHA domain, including the neurodevelopmental disorder-linked E366G variant, impair this interaction, resulting in defects in splicing and cellular proliferation

While significantly lower GSH:GSSG ratios were not seen using traditionally defined severity phenotypes, lower ratios corresponded to a greater history of exacerbations, lower lung function, and higher FeNO

& Olafsdottir, K

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