Abstract:The Nucleoporin 98KD (Nup98) is one of the most promiscuous translocation partners in hematological malignancies, contributing to at least 31 different truncation—fusion proteins. To date, nearly all disease models of Nup98 translocations involve ectopic expression of transgenes recapitulating the fusion protein under study, leaving the endogenous Nup98 loci unperturbed. Overlooked in these approaches is that translocation leads to the loss of one copy of normal Nup98 in addition to the loss of Nup96, a second… Show more
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