Researcher Database

（Last updated : 2024-09-21 16:35:17）　

HORI Toshiyuki

Department / Course College of Life Sciences Department of Biomedical Sciences

Title / Position Professor

Other Affiliations
1.	Graduate School of Life Sciences
2.	Research Organization of Science and Technology The Institute of Science and Engineering

Academic background
1.	1988 Degree Acquisition	│ Kyoto University Ph.D. in Medical Science
2.	～1980	Department of Medicine │ Faculty of Medicine │ Kyoto University │ Graduated
3.	～1988	Doctoral course │ Graduate School, Division of Medicine │ Kyoto University │ Completed

Research activities
1.		Molecular Biology Society of Japan
2.		Japanese Cancer Association
3.		The Japanese Society of Hematology
4.		The Japanese Society of Internal Medicine
5.		Japanese Society for Immunology

Subject of research
1.	(1) Studies on the signaling system through Warts/Lats as a core molecule

Research summary
Biological studies on cancer and immunity We aim to get insights into the pathogenesis of intractable diseases, especially, life threatening cancer. Although it is certain that cancer is caused by mutations of the genes that regulate cellular growth and viability, precise mechanisms underlying most cancers remain unclear. Recently, evidence has indicated that abnormalities of a novel signal transduction pathway, Hippo pathway, are involved in many types of cancers. We identified and cloned kpm (LATS2) that is one of the core components of the Hippo pathway and, since then, we have been working on the Hippo pathway. We pursue such studies that will help diagnosis and treatment of intractable cancers. For this purpose, we choose model animals that are most suitable for our experiments in order to elucidate unknown regulatory mechanism of the Hippo pathway. =Research theme(1)= Since its discovery in tissue culture of normal fibroblasts, the phenomenon of contact inhibition has been considered to be an important trait of normal cells distinct from transformed or cancer cells. It has recently been suggested that the signaling pathway through Warts/Lats that we have studied is involved in this phenomenon. However, the molecular structure and function between the putative membrane receptor and Warts/Lats remains unclear even in Drosophila melanogaster. So we have started studies to address this problem by interspecies extrapolation with C. elegans as a simple animal model. =Research theme(2)= We previously reported that guanylyl cyclase-A, a receptor for atrial natriuretic peptide (ANP), and soluble guanylyl cyclase, a receptor for NO, are expressed on activated dendritic cells. We showed that both ANP and NO polarize dendritic cells toward a Th2-inducing phenotype through a second messenger of cGMP. We plan to further analyze these immunoregulatory functions of guanylyl

Present specialized field
Molecular Biology, Pathological Medical Chemistry, Experimental Pathology, Hematology, Immunology, Collagen Disease/Allergy/Infectious Disease Medicine (Keyword：Internal Medicine, Hematology, Immunology, Pathological Medical Chemistry, Warts/Lats, Hippo pathway, Contact inhibition, guanylyl cyclase, dendritic cell, immune regulation)

Books
1.	1991	Mechanism of Lymphocyte Activation and Immune Regulation III

Papers
1.	2019/11	BCR-ABL and Src Family Kinases Induce YAP Tyrosine Phosphorylation Resulting in Survivin and Cyclin D1 Expression in Chronic Myeloid Leukemia Cells │ Blood │ 134 (Issue Supplement 1),pp.5366
2.	2019/11	BCR‑ABL induces tyrosine phosphorylation of YAP leading to expression of Survivin and Cyclin D1 in chronic myeloid leukemia cells │ Int. J. Hematol. │ 110 (5),pp.591-598
3.	2024/09/09	Minimal Requirements for Cancer Initiation: A Comparative Consideration of Three Prototypes of Human Leukemia │ Cancers │ 16 (17),pp.3109-3109
4.	2021/12	Small B-cell neoplasm responding to ibrutinib after 17 years of cold agglutinin disease symptom │ ,pp.1678-1683
5.	2019/11/13	BCR-ABL and Src Family Kinases Induce YAP Tyrosine Phosphorylation Resulting in Survivin and Cyclin D1 Expression in Chronic Myeloid Leukemia Cells │ Blood │ ,pp.5366-5366
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Academic conference presentation
1.	2019/10/12	Tyrosine phosphorylation and activation of YAP is involved in tumorigenic growth of CML cells
2.	2018/09/27	Molecular mechanism underlying Survivin expression in FLT3-ITD+ AML cells
3.	2018/09/27	Molecular mechanism of Survivin expression in anaplastic large cell lymphoma
4.	2017/10/21	BCR-ABL induces expression of an apoptosis inhibitor Survivin via activation of YAP
5.	2017/09/29	BCR-ABL induces tyrosine phosphorylation of YAP and Survivin expression
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Message
1.	Laboratory of Medical Cell Biology We started a new laboratory in April of 2008. We have been interested in cancer and immunity. Recently we are focusing on the role of kpm/Lats2 that we molecularly cloned in the pathogenesis of various malignancies.