Abstract
Jumping translocation breakpoint protein (JTB) is suppressed in many cancers, implying it plays a role in the neoplastic transformation of cells. In order to explore the role of JTB in the carcinogenesis of liver, we used mammalian two-hybrid, co-immunoprecipitation, GST pull-down and laser scanning confocal to verify the interaction between HBs and JTB. According to the results, HBs interacts with JTB. In addition, we further determined that S region within HBs is sufficient for binding JTB. Overexpression of JTB conferred resistance to apoptosis induced by ultraviolet radiation, whereas this effect was compromised by the co-overexpression of HBs.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Apoptosis / physiology
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Apoptosis / radiation effects
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Blotting, Western
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Cell Transformation, Neoplastic / genetics
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Cell Transformation, Neoplastic / metabolism*
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Cell Transformation, Neoplastic / radiation effects
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Flow Cytometry
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Fluorescent Antibody Technique
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Hepatitis B Surface Antigens / metabolism*
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Hepatitis B, Chronic / complications
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Humans
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Immunoprecipitation
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Liver Neoplasms / genetics
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Liver Neoplasms / metabolism*
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Liver Neoplasms / virology
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Membrane Proteins / metabolism*
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Microscopy, Confocal
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Neoplasm Proteins / metabolism*
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Polymerase Chain Reaction
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Radiation Tolerance / physiology*
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Transfection
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Two-Hybrid System Techniques
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Ultraviolet Rays
Substances
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Hepatitis B Surface Antigens
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JTB protein, human
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Membrane Proteins
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Neoplasm Proteins