His primary areas of investigation include Connexin, Cell biology, Carcinogenesis, Gap junction and Molecular biology. Hiroshi Yamasaki interconnects Western blot, Transfection and Pathology in the investigation of issues within Connexin. His Transfection research is multidisciplinary, incorporating perspectives in Cancer cell and HeLa.
His research integrates issues of Cell, Cell culture, Cell junction, Cell–cell interaction and Cell growth in his study of Cell biology. The study incorporates disciplines such as Endometrium and Cancer research in addition to Carcinogenesis. Within one scientific family, Hiroshi Yamasaki focuses on topics pertaining to Gene mutation under Molecular biology, and may sometimes address concerns connected to Anatomy and Degenerative disease.
Hiroshi Yamasaki focuses on Molecular biology, Cell biology, Connexin, Carcinogenesis and Cell culture. His work in Molecular biology tackles topics such as Endocrinology which are related to areas like Endometrial cancer. He has researched Cell biology in several fields, including Immunology, Cell and Cell growth.
His studies in Connexin integrate themes in fields like Tumor suppressor gene, Transfection and Pathology. His Carcinogenesis research is multidisciplinary, relying on both Mutation, Cancer research, Immunohistochemistry and Carcinogen. He is interested in Cell–cell interaction, which is a branch of Cell culture.
Hiroshi Yamasaki spends much of his time researching Connexin, Molecular biology, Connexin 32, Cell biology and Internal medicine. Hiroshi Yamasaki works mostly in the field of Connexin, limiting it down to concerns involving Cell culture and, occasionally, Cell cycle. His work deals with themes such as Bystander effect, Carcinogenesis, Cancer cell, HeLa and Cell type, which intersect with Molecular biology.
His work carried out in the field of Connexin 32 brings together such families of science as Cell, Progenitor cell, Renal cell carcinoma, Pathology and Tumor suppressor gene. His research in Cell biology intersects with topics in Transfection and Cell growth. The various areas that he examines in his Internal medicine study include Immunology, Endocrinology and Oncology.
Hiroshi Yamasaki mainly investigates Connexin, Cell biology, Gap junction, Connexin 32 and Transfection. His Connexin research is multidisciplinary, incorporating elements of Immunohistochemistry, Molecular biology and Carcinogenesis. His Cell biology study combines topics in areas such as Transgene, Immunology and Cell growth.
His Gap junction study combines topics from a wide range of disciplines, such as Prostaglandin E2, Prostaglandin, Cell junction and Osteoblast. His Connexin 32 research includes elements of Cell, Cell–cell interaction and Pathology. The concepts of his Cell study are interwoven with issues in Tumor suppressor gene, Cell culture and Cancer research.
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Role of connexin genes in growth control.
Hiroshi Yamasaki;Christian C.G. Naus.
Carcinogenesis (1996)
Bystander killing of cancer cells by herpes simplex virus thymidine kinase gene is mediated by connexins.
Marc Mesnil;Colette Piccoli;Gerard Tiraby;Klaus Willecke.
Proceedings of the National Academy of Sciences of the United States of America (1996)
Regulation of connexin 43-mediated gap junctional intercellular communication by Ca2+ in mouse epidermal cells is controlled by E-cadherin.
W. M. F. Jongen;D. J. Fitzgerald;M. Asamoto;C. Piccoli.
Journal of Cell Biology (1991)
Bystander effect in herpes simplex virus-thymidine kinase/ganciclovir cancer gene therapy : role of gap-junctional intercellular communication
Marc Mesnil;Hiroshi Yamasaki.
Cancer Research (2000)
UV and skin cancer: specific p53 gene mutation in normal skin as a biologically relevant exposure measurement.
Hisayoshi Nakazawa;Dallas English;Peter L. Randell;Keiko Nakazawa.
Proceedings of the National Academy of Sciences of the United States of America (1994)
Negative growth control of HeLa cells by connexin genes: connexin species specificity.
M Mesnil;V Krutovskikh;C Piccoli;C Elfgang.
Cancer Research (1995)
Gap junctional communication and carcinogenesis
Hiroshi Yamasaki.
Carcinogenesis (1990)
Gap Junctional Intercellular Communication and Carcinogenesis
Hiroshi Yamasaki.
Carcinogenesis (1990)
Tumor promoters inhibit spontaneous and induced differentiation of murine erythroleukemia cells in culture
H Yamasaki;E Fibach;U Nudel;I B Weinstein.
Proceedings of the National Academy of Sciences of the United States of America (1977)
Altered homologous and heterologous gap‐junctional intercellular communication in primary human liver tumors associated with aberrant protein localization but not gene mutation of connexin 32
V. Krutovskikh;G. Mazzoleni;N. Mironov;Y. Omori.
International Journal of Cancer (2007)
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