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This hypercatabolism is evident by our data demonstrating depletion of amino acids and upregulation of the urea cycle as judged by elevated levels of urea cycle metabolites such as citrulline

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loss of lobular plates, architecture, and/or occurrence of cellular atypia

While nucleosomal sites transiently made vacant by the dissociation of the RS variant could in principle allow WT H1.4 or other H1 isoforms to rebind and thereby mitigate the effects of the mutation, a nucleosome-bound RS variant causing chromatin to mimic the H1-free state would competitively inhibit such binding, preventing the rescue of chromatin structure and function