His primary areas of study are Osteoclast, Cell biology, RANKL, Osteoimmunology and Signal transduction. Hiroshi Takayanagi combines subjects such as Cellular differentiation, Transcription factor, NFAT, NFATC Transcription Factors and Bone regeneration with his study of Osteoclast. He interconnects Internal medicine, Bone remodeling, Endocrinology and Immunology in the investigation of issues within Cell biology.
His study in Immunology is interdisciplinary in nature, drawing from both Receptor, Bone resorption and CD40. His RANKL research incorporates elements of Macrophage colony-stimulating factor, Osteoprotegerin and Cytokine. Hiroshi Takayanagi focuses mostly in the field of Signal transduction, narrowing it down to matters related to Cancer research and, in some cases, Arthritis, Autoimmune disease, Experimental autoimmune encephalomyelitis and Mitogen-activated protein kinase kinase.
His primary areas of investigation include Cell biology, RANKL, Osteoclast, Immunology and Osteoimmunology. His work in Cell biology covers topics such as RANK Ligand which are related to areas like Fc receptor. His biological study spans a wide range of topics, including Cancer research, Signal transduction and Cytokine.
He combines subjects such as Endocrinology, Bone resorption, Transcription factor and Cellular differentiation with his study of Osteoclast. As part of one scientific family, Hiroshi Takayanagi deals mainly with the area of Bone resorption, narrowing it down to issues related to the Bone remodeling, and often Bone remodeling period. His research integrates issues of Cell signaling, Neuroscience, Immunity and Monocyte in his study of Osteoimmunology.
His primary scientific interests are in Cell biology, RANKL, Immune system, Osteoclast and Inflammation. Hiroshi Takayanagi is interested in Signal transduction, which is a field of Cell biology. Hiroshi Takayanagi does research in RANKL, focusing on Osteoimmunology specifically.
As part of the same scientific family, Hiroshi Takayanagi usually focuses on Osteoimmunology, concentrating on Neuroscience and intersecting with Chemokine, Cell signaling and Haematopoiesis. His Immune system research is multidisciplinary, incorporating elements of Bone cell and Bone remodeling. His Osteoclast study combines topics from a wide range of disciplines, such as Osteoprotegerin and Endocrinology.
His scientific interests lie mostly in RANKL, Immune system, Bone cell, Osteoimmunology and Bone remodeling. His studies in RANKL integrate themes in fields like Osteoclast and Cancer research. His Osteoclast study incorporates themes from Carcinogenesis, Endocrinology, Melanoma and Stromal cell.
His work carried out in the field of Immune system brings together such families of science as Periodontitis and Neuroscience. As a part of the same scientific family, Hiroshi Takayanagi mostly works in the field of Osteoimmunology, focusing on Bone marrow and, on occasion, CD14. The various areas that Hiroshi Takayanagi examines in his Receptor study include Immunohistochemistry, Dental alveolus, Osteocyte, Bone resorption and Cell biology.
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Induction and activation of the transcription factor NFATc1 (NFAT2) integrate RANKL signaling in terminal differentiation of osteoclasts.
Hiroshi Takayanagi;Sunhwa Kim;Takako Koga;Takako Koga;Hiroshi Nishina.
Developmental Cell (2002)
Osteoimmunology: shared mechanisms and crosstalk between the immune and bone systems
Hiroshi Takayanagi.
Nature Reviews Immunology (2007)
Th17 functions as an osteoclastogenic helper T cell subset that links T cell activation and bone destruction
Kojiro Sato;Ayako Suematsu;Kazuo Okamoto;Akira Yamaguchi.
Journal of Experimental Medicine (2006)
Evidence for osteocyte regulation of bone homeostasis through RANKL expression
Tomoki Nakashima;Mikihito Hayashi;Takanobu Fukunaga;Kosaku Kurata.
Nature Medicine (2011)
T-cell-mediated regulation of osteoclastogenesis by signalling cross-talk between RANKL and IFN-gamma.
Hiroshi Takayanagi;Kouetsu Ogasawara;Shigeaki Hida;Tomoki Chiba.
Nature (2000)
The molecular understanding of osteoclast differentiation.
Masataka Asagiri;Hiroshi Takayanagi.
Bone (2007)
Estrogen Prevents Bone Loss via Estrogen Receptor α and Induction of Fas Ligand in Osteoclasts
Takashi Nakamura;Yuuki Imai;Yuuki Imai;Takahiro Matsumoto;Shingo Sato.
Cell (2007)
Pathogenic conversion of Foxp3+ T cells into TH17 cells in autoimmune arthritis.
Noriko Komatsu;Kazuo Okamoto;Shinichiro Sawa;Tomoki Nakashima.
Nature Medicine (2014)
Costimulatory signals mediated by the ITAM motif cooperate with RANKL for bone homeostasis
Takako Koga;Masanori Inui;Kazuya Inoue;Sunhwa Kim.
Nature (2004)
Autoamplification of NFATc1 expression determines its essential role in bone homeostasis.
Masataka Asagiri;Kojiro Sato;Takako Usami;Sae Ochi.
Journal of Experimental Medicine (2005)
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