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Sensitivity to interferon-alpha and interferon-stimulated gene factor 3 binding activity in human chronic myelogenous leukemia cell line KT-1.

Abstract
The mechanism of responsiveness of chronic myelogenous leukemia (CML) cells to interferon (IFN)-alpha was examined by using two subclones of CML cell line KT-1 which exhibited significantly different sensitivities to the antiproliferative and apoptosis-inducing effects of IFN-alpha. IFN-stimulated gene factor 3 (ISGF3) formation by IFN-alpha was reduced in the IFN-alpha-resistant subclone compared to the IFN-alpha-sensitive subclone. We conclude that the level of ISGF3 formation is responsible for the difference in IFN-alpha responses between these subclones.
AuthorsH Yamauchi, I Sakai, H Narumi, S Soga, S Fujita
JournalActa haematologica (Acta Haematol) Vol. 104 Issue 1 Pg. 1-9 ( 2000) ISSN: 0001-5792 [Print] Switzerland
PMID11111114 (Publication Type: Comparative Study, Journal Article)
CopyrightCopyright 2000 S. Karger AG, Basel
Chemical References
  • Antineoplastic Agents
  • DNA-Binding Proteins
  • IRF9 protein, human
  • Interferon-Stimulated Gene Factor 3
  • Interferon-Stimulated Gene Factor 3, gamma Subunit
  • Interferon-alpha
  • Protein Subunits
  • RNA, Messenger
  • STAT1 Transcription Factor
  • STAT1 protein, human
  • STAT2 Transcription Factor
  • Trans-Activators
  • Transcription Factors
  • Protein-Tyrosine Kinases
Topics
  • Antineoplastic Agents (pharmacology)
  • Apoptosis (drug effects)
  • Blotting, Western
  • Cell Division (drug effects)
  • Clone Cells (drug effects)
  • DNA Fragmentation
  • DNA-Binding Proteins (drug effects, genetics, metabolism, pharmacology, physiology)
  • Electrophoresis, Agar Gel
  • Flow Cytometry
  • Humans
  • Interferon-Stimulated Gene Factor 3
  • Interferon-Stimulated Gene Factor 3, gamma Subunit
  • Interferon-alpha (genetics, pharmacology, physiology)
  • Leukemia, Myelogenous, Chronic, BCR-ABL Positive (pathology)
  • Promoter Regions, Genetic (drug effects)
  • Protein Binding (physiology)
  • Protein Subunits
  • Protein-Tyrosine Kinases (physiology)
  • RNA, Messenger (biosynthesis, drug effects)
  • Response Elements (drug effects)
  • STAT1 Transcription Factor
  • STAT2 Transcription Factor
  • Signal Transduction (drug effects)
  • Time Factors
  • Trans-Activators (drug effects, metabolism, physiology)
  • Transcription Factors (drug effects, genetics, metabolism, pharmacology)
  • Tumor Cells, Cultured (drug effects)

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