Vpu was shown to inhibit I kBa wreckage in HIV 1 infected cultured T cells or HeLa CD4U cells, which resulted in a solid lowering of both TNFa and HIV induced activation of NF kB activity. Yet another study indicates that, by inhibiting the NF kB dependent expression of anti apoptotic factors of TNFR complex proteins and the Bcl 2 family, Vpu induced apoptosis through activation of the caspase pathway. Also, really recently, Vpu was demonstrated to compete for the interaction of tumor suppressor p53 with b TrCP, leading to inhibition of p53 ubiquitylation and proteasomal degradation. Resultant stabilization of p53 was demonstrated to improve p53 mediated apoptosis during HIV 1 disease. Since it was shown to render HIV infected cells more susceptible pro-peptide to FASinduced cell death. Vpu are often in a position to induce apoptosis via other pathways. Viralized transgenic Drosophila models have shown to be helpful to examine the function of different viral proteins at the amount of a whole organism. Three HIV viral proteins, Tat, Nef, and Vpu have already been analyzed using the Drosophila model. Appearance of the Tat protein throughout fly oogenesis affected oocyte polarization caused by interaction of Tat with tubulin and in inhibition of ribosomal rRNA precursor processing in nurse cell nucleoli. Nef phrase induced caspase dependent apoptosis in Drosophila developing side cells via the activation of the c Jun N terminal Kinase pathway and inhibited the Drosophila innate immune responses mediated by the Relish/NFkB pathway. Using transgenic Linifanib VEGFR inhibitor flies expressing Vpu, we previously demonstrated that Vpu can also inhibit the Drosophila NF kB dependent immune response in vivo. In today’s study we demonstrate that Vpu expression in the fly affects normal growth in particular reducing the size of the structure where it is stated, including wing and eye. We also show that the interaction between Vpu and human b TrCP is conserved between Vpu and SLIMB, the Drosophila b TrCP homolog, but this interaction is partially accountable for the phenotypes induced by Vpu. Hence, the Drosophila type can be utilized for evaluation of Vpu activity at the level of an entire wood, and for identification of novel useful interactions in vivo. We therefore performed a genetic screen to recognize modifiers of the Vpu induced phenotypes and discovered that overexpression of thread encoding Drosophila Inhibitor of Apoptosis Protein 1 very effectively suppressed the wing phenotypes. Next, we demonstrated that Vpu expression within the developing Drosophila wing caused apoptosis cell autonomously, which can be also counteracted by thread/ diap1 overexpression. We further showed that Vpu activated expression of the pro apoptotic reaper gene and downregulated DIAP1 accumulation in this tissue. Finally, the activity of the JNK pathway was found to be necessary for Vpu triggered apoptosis within the side. Altogether the info reported here provide the first evidence of an operating link between Vpu induced apoptosis and the activation of the conserved JNK signaling pathway.