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Heinz Bauer

Researcher at Robert Koch Institute

Publications -  11
Citations -  403

Heinz Bauer is an academic researcher from Robert Koch Institute. The author has contributed to research in topics: Oncornavirus & Virus. The author has an hindex of 10, co-authored 11 publications receiving 403 citations.

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Book ChapterDOI

Virion and Tumor Cell Antigens of C-Type RNA Tumor Viruses

TL;DR: This chapter reviews the structure, function, and immunological properties of C-type virus-directed macromolecules that are immunologically active, and therefore approachable by immunological techniques.
Journal ArticleDOI

Detection of oncornavirus-like particles in HeLa cells. I. Fine structure and comparative morphological classification.

TL;DR: The HeLa particles closely resemble two primate viruses, namely the Mason‐Pfizer monkey virus and a recently discovered virus derived from human brain cells, and a new morphological group of viruses emerges that might be specific for primates.
Journal ArticleDOI

Common tumor-Specific surface antigens on cells of different species transformed by avian RNA tumor viruses

TL;DR: No correlation could be found between group-specific antigen content and virogenicity of the cells and the quantitative expression of the TSSA, although within a given species (mouse) the antigen is expressed in varying amounts on the surface of cells from different cell lines, possibly reflecting antigenic modulation or antigenic conversion.
Journal ArticleDOI

Avian oncornavirus-induced tumor antigens of embryonic and unknown origin.

TL;DR: It could be demonstrated that mouse-specific and interspecies-specific embryonic antigens exist on the surface of normal and malignant cells and viral transformation leads to the retrogenetic expression of embryonic antigen(s) on both chicken and mouse cells which cannot be detected on the respective normal cells.
Journal ArticleDOI

Influence of dibutyryl cyclicAMP and theophylline on cell surface antigens on oncornavirus transformed cells.

TL;DR: Transformed cells are restored to controlled growth as they grow to lower saturation density and apparently become contact inhibited during treatment with dbcyclicAMP plus Th6–8,13.