The acute avian leukaemia retroviruses AMV and E26 both induce myeloblastosis in vivo and transform myeloblasts in vitro. Both viruses contain the oncogene v-myb first described for AMV. Unlike AMV, E26 has the additional capacity to induce erythroblastosis in vivo and to transform erythroblasts. Previous analyses indicated that the genome of E26 also contained nucleotide sequences distinct from v-myb and unrelated to viral replicative genes. Using a molecularly cloned E26 provirus, we have now identified a novel nucleotide sequence designated v-ets (for E-twenty-six specific) of approximately 1.5 kilobase pairs (kbp) located next to v-myb. v-ets possesses all the structural characteristics of a putative new oncogene: it has a conserved cellular counterpart c-ets which is transcribed in some normal chicken cells as a major 7.5-kb polyadenylated RNA. Although our results now await elucidation of their biological significance, we propose that v-ets could be a new oncogene accounting for the additional transforming properties of E26, or potentiating the transforming properties of the v-myb oncogene.

Understanding how ultrasmall gold nanoparticles (metal core ∼1–1.5 nm), so-called gold nanoclusters (Au NCs), interact with biological barriers has become highly important for their future bioapplications. The properties of Au NCs with tunable hydrophobicity were extensively characterized in three different biological situations: (i) interaction with serum in solution, (ii) interaction with synthetic free-standing lipid bilayers integrated in a microfluidic device, and (iii) cell studies with two different cell types (U87MG human primary glioblastoma and A375 melanoma cell lines). Our results indicate a significant impact of the precise tailoring of the hydrophilicity/hydrophobicity balance on the Au NC surfaces, which could prevent the formation of biomolecular absorption while maintaining excellent colloidal stability in solutions with high serum contents. Increasing the surface hydrophobicity of the Au NCs enabled more efficient lipid bilayer membrane insertion and induced faster cellular uptake. We showed the existence of a hydrophobicity threshold, which resulted in colloidal instability, lipid bilayer damage, and acute cytotoxicity. We also demonstrated a significant influence of metal–ligand shell hydrophobicity on the fluorescence signal of the Au NCs, increasing it in the near-infrared region. A twofold signal enhancement was achieved by simple replacement of methyl groups with ethyl groups.