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Notch signaling contributes to proliferation and tumor formation of human T-cell leukemia virus type 1–associated adult T-cell leukemia
- J. Pancewicz, Johnm . Taylor, +4 authors C. Nicot
- Biology, Medicine
- Proceedings of the National Academy of Sciences
- 7 September 2010
It is demonstrated that inhibition of Notch signaling by γ-secretase inhibitors reduced tumor cell proliferation and tumor formation in ATL-engrafted mice, suggesting that activated Notch may be important to ATL pathogenesis and reveal Notch1 as a target for therapeutic intervention in ATL patients. Expand
HTLV-1 Yin and Yang: Rex and p30 master regulators of viral mRNA trafficking.
How human T-cell lymphotropic virus type 1 p30 is involved in the nuclear retention of the tax/rex mRNA leading to inhibition of virus expression and establishment of viral latency is discussed. Expand
Critical role of hnRNP A1 in HTLV-1 replication in human transformed T lymphocytes
Observations provide an insight into a new cellular control of HTLV-1 replication and suggest that hnRNP A1 is likely part of the regulatory mechanisms of the life cycle of this human retrovirus in T cells. Expand
Platelet-derived growth factor protects neurons against gp120-mediated toxicity
PDGF-BB could be considered as a therapeutic agent that can mitigate gp120-mediated neurotoxicity in HAD, and PDGF-mediated protection against gp120 involved the phosphoinositide 3-kinase/Akt pathway. Expand
HTLV-I p30: a versatile protein modulating virus replication and pathogenesis.
2010 Elsevier Ltd. All rights reserved.
Human T-lymphotropic type 1 virus p30 inhibits homologous recombination and favors unfaithful DNA repair.
This study describes how the HTLV-1 p30 viral protein inhibits conservative homologous recombination (HR) DNA repair by targeting the MRE11/RAD50/NBS1 complex and favors the error-prone nonhomologous-end-joining (NHEJ) DNA-repair pathway instead. Expand
HTLV-I Tax-dependent and -independent events associated with immortalization of human primary T lymphocytes.
The results confirmed previous observations that Tax activates the anaphase-promoting complex, however, Tax did not affect the mitotic spindle checkpoint, which was also functional in HTLV-I-transformed cells. Expand
HTLV-I Tax Increases Genetic Instability by Inducing DNA Double Strand Breaks during DNA Replication and Switching Repair to NHEJ
A novel function of HTLV-I oncoprotein Tax is shown as an inducer of genomic DNA double strand breaks (DDSB) during DNA replication and it is demonstrated that during S phase, Tax-associated DDSB are preferentially repaired using the error-prone non-homologous end joining (NHEJ) pathway. Expand
HTLV-I p30 inhibits multiple S phase entry checkpoints, decreases cyclin E-CDK2 interactions and delays cell cycle progression
It is reported that the HTLV-I p30 delays cell cycle progression while its homologue,HTLV-II p28, does not, providing evidence for important differences between these two related retrovirus proteins. Expand
Regulation of the human T-cell leukemia virus gene expression depends on the localization of regulatory proteins Tax, Rex and p30II in specific nuclear subdomains.
The results suggest that transcripts originating from Tax-induced activation of gene expression at the boundaries of the Tax bodies are transported out of the nucleus by nucleoplasmic Rex/CRM-1 complexes that are first assembled in nucleolar foci. Expand