ArticleNature communications2024
The tyrosine kinase KDR is essential for the survival of HTLV-1-infected T cells by stabilizing the Tax oncoprotein.
Article in Nature communications, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
What it found
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
6 citing papers in PubMed.
- Viral persistence and host-state remodeling in virus-associated cancers.Archives of microbiology · 2026Review
- Viral-driven oncogenesis in T/NK-cell lymphomas: parallels and divergences between HTLV-1 and EBV.International journal of hematology · 2026Review
- Multi-cohort cross-omics analysis reveals disease mechanisms and therapeutic targets in HTLV-1-associated myelopathy, a neglected retroviral neuroinflammatory disorder.Research square · 2025Article
- Comparative analysis of the genomic and expression profiles of ANLN and KDR as prognostic markers in breast Cancer.In silico pharmacology · 2025Article
- Oncogenic viruses rewire the epigenome in human cancer.Frontiers in cellular and infection microbiology · 2025Review
- Human T-cell leukemia virus type 1: oncogenic potential and vaccine development strategies.Frontiers in cellular and infection microbiology · 2025Review
Corrections and comments
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Authors and funding
8 authors.
Funding
Abstract
Human T-cell leukemia virus type 1 (HTLV-1) infection is linked to the development of adult T-cell leukemia/lymphoma (ATLL) and the neuroinflammatory disease, HTLV-1-associated myelopathy/tropical spastic paraparesis (HAM/TSP). The HTLV-1 Tax oncoprotein regulates viral gene expression and persistently activates NF-κB to maintain the viability of HTLV-1-infected T cells. Here, we utilize a kinome-wide shRNA screen to identify the tyrosine kinase KDR as an essential survival factor of HTLV-1-transformed cells. Inhibition of KDR specifically induces apoptosis of Tax expressing HTLV-1-transformed cell lines and CD4 + T cells from HAM/TSP patients. Furthermore, inhibition of KDR triggers the autophagic degradation of Tax resulting in impaired NF-κB activation and diminished viral transmission in co-culture assays. Tax induces the expression of KDR, forms a complex with KDR, and is phosphorylated by KDR. These findings suggest that Tax stability is dependent on KDR activity which could be exploited as a strategy to target Tax in HTLV-1-associated diseases.
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