NME1-NME2 readthrough fusion protein (NME1-NME2)

NME1-NME2 readthrough is a naturally occurring fusion transcript and protein generated by read-through transcription between the neighboring NME1 and NME2 genes. These proteins are members of the NME (non-metastatic cells) family, which are multifunctional enzymes chiefly known for their nucleoside diphosphate kinase activity—essential for cellular nucleotide homeostasis. NME1 acts primarily as a metastasis suppressor in various cancers, exhibiting 3′–5′ exonuclease activity essential for DNA repair and gene regulation, while NME2 functions as a transcriptional regulator that binds and remodels DNA at promoter regions (notably *MYC* and telomerase promoters), leading to DNA cleavage or activation/repression of transcription. The fusion protein is expected to retain both kinase and DNA-modifying activities, with implications for cell proliferation, differentiation, DNA repair, and cancer suppression or progression depending on cellular context[1][2][3][4]. Note: The explicit biological and therapeutic relevance of the NME1-NME2 fusion protein (as opposed to NME1 and NME2 individually) is not well established; most functional data refer to the two proteins separately, and the fusion transcript is less commonly discussed as an independent drug target[2]. If structured therapeutic targeting is desirable, the canonical entities would likely be "Nucleoside diphosphate kinase A (NME1)" and "Nucleoside diphosphate kinase B (NME2)" individually.

Other names

NME1-NME2 fusionNME/NM23 nucleoside diphosphate kinase A/B readthroughNM23-H1/NM23-H2 readthrough

For associated drugs (none specific), general mechanisms include inhibition or modulation of kinase activity, DNA repair inhibition, or gene expression modulation