A transgenic Drosophila melanogaster model to study human T-lymphotropic virus oncoprotein Tax-1-driven transformation in vivo
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24 janvier 2025
- 10938/29096
- 25995252.0
- 2-s2.0-84937705501
Ce document est lié à :
Journal of Virology
Mots-clés
Animals Cell transformation, viral Disease models, animal Drosophila melanogaster Eye Gene products, tax Htlv-i infections Human t-lymphotropic virus 1 Human t-lymphotropic virus 2 Humans I kappa b kinase gamma Oncoprotein Protein tax 1 Protein tax 2 Transactivator protein Unclassified drug Tax protein Tax protein, human t-lymphotrophic virus 1 Tax protein, human t-lymphotrophic virus 2 Animal cell Animal experiment Animal model Animal tissue Article Cell proliferation Cell transformation Controlled study Disease model Disease severity Eye development Eye disease Gal4 gene Gene Gene dosage Gene expression regulation Gene function Gene identification Gene interaction Gene overexpression Gmr gene In vivo study Lymphocyte transformation Molecular cloning Nonhuman Oncogene Phenotype Plasma cell Priority journal Promoter region Protein function Protein protein interaction Rna interference Rough eye disease Scanning electron microscopy Tax 1 gene Transcription regulation Transgenic drosophila Animal Genetics Human Human t cell leukemia virus infection Metabolism Pathology Physiology Virology Virus cell transformationSujets proches
Eyes Eyeball Visual system illnessCiter ce document
Shirinian et al., « A transgenic Drosophila melanogaster model to study human T-lymphotropic virus oncoprotein Tax-1-driven transformation in vivo », American University of Beirut ScholarWorks
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Résumé
Human T-cell lymphotropic virus type 1 (HTLV-1)-induced adult T-cell leukemia/lymphoma is an aggressive malignancy. HTLV-2 is genetically related to HTLV-1 but does not cause any malignant disease. HTLV-1 Tax transactivator (Tax-1) contributes to leukemogenesis via NF-κB. We describe transgenic Drosophila models expressing Tax in the compound eye and plasmatocytes. We demonstrate that Tax-1 but not Tax-2 induces ommatidial perturbation and increased plasmatocyte proliferation and that the eye phenotype is dependent on Kenny (IKKγ/NEMO), thus validating this new in vivo model. © 2015, American Society for Microbiology.
