Human T-cell leukemia virus type 1 Tax protein transforms rat fibroblasts via two distinct pathways
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Summary
Results show that Tax transforms rat fibroblasts via two distinct pathways, and the activation of the CArG box pathway is essential for the transformation of REF by Tax.
- Type
- article
- Published
- 1997-06-01
- Cited by
- 154
- References
- 57
- Access
- Open access
- OpenAlex
- https://openalex.org/W1659625814
- Semantic Scholar
- https://api.semanticscholar.org/CorpusID:19699423
Keywords
Biology, Transcription (linguistics), Cell biology, Transformation (genetics), Molecular biology
References
- Tax protein of HTLV-1 destabilizes the complexes of NF-kappa B and I kappa B-alpha and induces nuclear translocation of NF-kappa B for transcriptional activation.
- Transactivation of the human interleukin-6 gene by human T-lymphotropic virus type 1 Tax protein.
- Tax protein of HTLV-1 interacts with the Rel homology domain of NF-kappa B p65 and c-Rel proteins bound to the NF-kappa B binding site and activates transcription.
- A transcriptional enhancer sequence of HTLV‐I is responsible for trans‐activation mediated by p40 chi HTLV‐I.
- Transactivation of the c-myc promoter by human T cell leukemia virus type 1 tax is mediated by NF kappa B.
- Identification of p40x-responsive regulatory sequences within the human T-cell leukemia virus type I long terminal repeat
- Proliferative response of Tax1-transduced primary human T cells to anti-CD3 antibody stimulation by an interleukin-2-independent pathway
- Constitutive activation of NF‐kappa B is essential for transformation of rat fibroblasts by the human T‐cell leukemia virus type I Tax protein.
- Role of human T-cell leukemia virus type 1 X region proteins in immortalization of primary human lymphocytes in culture
- Human T-cell leukemia virus type 1 Tax activates transcription of the human fra-1 gene through multiple cis elements responsive to transmembrane signals
- Human T-cell leukemia virus type I Tax associates with and is negatively regulated by the NF-kappa B2 p100 gene product: implications for viral latency
- The human T-lymphotropic virus type I tax gene can cooperate with the ras oncogene to induce neoplastic transformation of cells
- Coupling of a signal response domain in I kappa B alpha to multiple pathways for NF-kappa B activation
- Single amino acid substitution (58Pro-->Ser) in HTLV-I tax results in loss of ras cooperative focus formation in rat embryo fibroblasts.
- Regulation of the human interleukin-2 receptor alpha chain promoter: activation of a nonfunctional promoter by the transactivator gene of HTLV-I.
- Human T-cell lymphotropic virus type I (HTLV-I) transcriptional activator, Tax, enhances CREB binding to HTLV-I 21-base-pair repeats by protein-protein interaction.
- HTLV-1 transactivator induces interleukin-2 receptor expression through an NF-κB-like factor
- Transactivation of the transforming growth factor beta 1 (TGF-beta 1) gene by human T lymphotropic virus type 1 tax: a potential mechanism for the increased production of TGF-beta 1 in adult T cell leukemia
- Isolation and characterization of retrovirus from cell lines of human adult T-cell leukemia and its implication in the disease.
- Three distinct IL-2 signaling pathways mediated by bcl-2, c-myc, and lck cooperate in hematopoietic cell proliferation.
Cited by
- The multifaceted oncoprotein Tax: subcellular localization, posttranslational modifications, and NF-κB activation.
- Human T-cell leukemia virus type I oncoprotein Tax represses Smad-dependent transforming growth factor beta signaling through interaction with CREB-binding protein/p300.
- Expression of human inducible nitric oxide synthase gene in T-cell lines infected with human T-cell leukemia virus type-I and primary adult T-cell leukemia cells.
- Review Article Aberration in Signal Transduction Pathway in Human T-Cell Leukemia Virus Type I-Infected T Cells
- Rôle des protéines AID et Bfl-1 dans les processus d'instabilité génomique et de survie cellulaire induits par l'oncoprotéine Tax au cours de la lymphomagénèse associée à l'infection par HTLV-1
- HTLV-1 Tax Stimulates Ubiquitin E3 Ligase, Ring Finger Protein 8, to Assemble Lysine 63-Linked Polyubiquitin Chains for TAK1 and IKK Activation
- The involvement of retroviruses in human T cell leukaemias and lymphomas
- Human T-cell leukemia virus type-I Tax induces the expression of CD83 on T cells
- Ubiquitin Dependent Regulation of Innate Antiviral Signaling
- CREB − a real culprit in oncogenesis
- Human T‐cell leukemia virus type 1 Tax protein stimulates the interferon‐responsive enhancer element via NF‐κB activity 1
- Human T cell leukemia virus type I tax-induced IκB-ζ modulates tax-dependent and tax-independent gene expression in T cells.
- Constitutive expression of IRF-5 in HTLV-1-infected T cells.
- Seizing of T cells by human T-cell leukemia/lymphoma virus type 1.
- NF-κB Hyper-Activation by HTLV-1 Tax Induces Cellular Senescence, but Can Be Alleviated by the Viral Anti-Sense Protein HBZ
- Human T-cell leukemia virus type 1 tax protein activates transcription through AP-1 site by inducing DNA binding activity in T cells.
- Elevated expression of CCL5/RANTES in adult T‐cell leukemia cells: Possible transactivation of the CCL5 gene by human T‐cell leukemia virus type I tax
- The HTLV-I Tax oncoprotein targets the retinoblastoma protein for proteasomal degradation
- MicroRNA miR‐146a is induced by HTLV‐1 tax and increases the growth of HTLV‐1‐infected T‐cells
- CD69 overexpression by human T-cell leukemia virus type 1 Tax transactivation.
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