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Role for Akt/protein kinase B and activator protein-1 in cellular proliferation induced by the human T-cell leukemia virus type 1 tax oncoprotein.

Abstract
Human T-cell leukemia virus type 1 is an oncogenic retrovirus etiologically causal of adult T-cell leukemia. The virus encodes a Tax oncoprotein, which functions in transcriptional regulation, cell cycle control, and transformation. Because adult T-cell leukemia is a highly virulent cancer that is resistant to numerous chemotherapeutic treatments, to understand better this disease it is important to comprehend how human T-cell leukemia virus type 1 promotes cellular growth and survival. Most of the existing data point to Tax activation of NF-kappaB as important for cellular proliferation and transformation. We show here that Tax, in the absence of NF-kappaB signaling, can activate activator protein-1 to promote cellular proliferation and survival. Tax is shown to activate activator protein-1 through the phosphatidylinositol 3-kinase/Akt pathway.
AuthorsJean-Marie Peloponese Jr, Kuan-Teh Jeang
JournalThe Journal of biological chemistry (J Biol Chem) Vol. 281 Issue 13 Pg. 8927-38 (Mar 31 2006) ISSN: 0021-9258 [Print] United States
PMID16436385 (Publication Type: Journal Article, Research Support, N.I.H., Intramural)
Chemical References
  • Gene Products, tax
  • Transcription Factor AP-1
  • Luciferases
  • Proto-Oncogene Proteins c-akt
  • beta-Galactosidase
Topics
  • Animals
  • Cell Line, Transformed
  • Cell Proliferation
  • Cell Transformation, Viral
  • Cells, Cultured
  • Chlorocebus aethiops
  • Fibroblasts (metabolism, virology)
  • Gene Expression Regulation, Viral
  • Gene Products, tax (genetics, metabolism, physiology)
  • Genes, Reporter
  • Human T-lymphotropic virus 1 (physiology)
  • Humans
  • Jurkat Cells
  • Luciferases (metabolism)
  • Mice
  • Phosphatidylinositol 3-Kinases (metabolism)
  • Proto-Oncogene Proteins c-akt (analysis, metabolism, physiology)
  • T-Lymphocytes (metabolism, virology)
  • Transcription Factor AP-1 (metabolism, physiology)
  • Vero Cells
  • beta-Galactosidase (analysis, metabolism)

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