In this issue of Blood, O’Brien and colleagues1 demonstrate impaired growth of circulating red-cell progenitor cells ex vivo from patients with Diamond-Blackfan anemia (DBA) with ribosomal protein (RP) or GATA1… Click to show full abstract
In this issue of Blood, O’Brien and colleagues1 demonstrate impaired growth of circulating red-cell progenitor cells ex vivo from patients with Diamond-Blackfan anemia (DBA) with ribosomal protein (RP) or GATA1 mutations. Distinct transcriptional profiles in erythroid cells from patients with RP and GATA1 mutations indicate potential mechanisms underlying dysregulation of translation.1
               
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