Masaki Noda focuses on Osteopontin, Internal medicine, Endocrinology, Osteoblast and Bone remodeling. His research integrates issues of Cell, Pathology and Cell biology in his study of Osteopontin. His study on Internal medicine is mostly dedicated to connecting different topics, such as In vivo.
Endocrinology is closely attributed to Wild type in his study. His Osteoblast research is multidisciplinary, incorporating perspectives in Osteocalcin, Molecular biology, Gene expression and Cellular differentiation. His Bone remodeling research is multidisciplinary, relying on both Hindlimb, Osteoclast, Reduction and Deoxypyridinoline.
His scientific interests lie mostly in Internal medicine, Endocrinology, Cell biology, Osteopontin and Bone remodeling. His Internal medicine research incorporates elements of Bone morphogenetic protein and Cancellous bone. He has included themes like Osteoclast, Bone marrow and Osteoblast in his Endocrinology study.
Masaki Noda works mostly in the field of Cell biology, limiting it down to topics relating to Immunology and, in certain cases, Cartilage, as a part of the same area of interest. His Osteopontin study combines topics from a wide range of disciplines, such as Cancer research, Arthritis, Pathology, Integrin and Extracellular matrix. His Bone remodeling study integrates concerns from other disciplines, such as Cortical bone and Deoxypyridinoline.
His primary areas of study are Cell biology, Internal medicine, Endocrinology, Osteoblast and Osteoclast. His studies in Cell biology integrate themes in fields like Receptor and Bone remodeling. Masaki Noda has researched Internal medicine in several fields, including Cell migration and Bone morphogenetic protein.
The various areas that Masaki Noda examines in his Endocrinology study include Gene expression, Gene knockdown, Cellular differentiation, Adrenergic receptor and Cartilage. His work investigates the relationship between Osteoblast and topics such as In vivo that intersect with problems in Prenylation, Osteocalcin, Bone tissue, Protein prenylation and In vitro. His research investigates the connection with Osteoclast and areas like Membrane potential which intersect with concerns in Depolarization, Intracellular, Cell membrane and Ion channel.
Masaki Noda mostly deals with Endocrinology, Internal medicine, Cell biology, Osteoblast and Bone resorption. His work focuses on many connections between Endocrinology and other disciplines, such as Bone morphogenetic protein, that overlap with his field of interest in Ossification, Cartilage, Endochondral ossification, Chondrocyte and Mesenchyme. The Internal medicine study combines topics in areas such as In vitro and Protein prenylation.
His work deals with themes such as Wild type, Parathyroid hormone and TRPV4, which intersect with Cell biology. The concepts of his Osteoblast study are interwoven with issues in Matrix, Ullrich congenital muscular dystrophy, Osteocalcin, Extracellular matrix and In vivo. His studies deal with areas such as Bone remodeling, Bone density, Osteoporosis, Regulation of gene expression and Bone marrow as well as Bone resorption.
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Osteopontin as a means to cope with environmental insults: regulation of inflammation, tissue remodeling, and cell survival
David T. Denhardt;Masaki Noda;Anthony W. O’Regan;Dubravko Pavlin.
Journal of Clinical Investigation (2001)
Leptin regulation of bone resorption by the sympathetic nervous system and CART
Florent Elefteriou;Jong Deok Ahn;Shu Takeda;Michael Starbuck.
Osteopontin expression and function: Role in bone remodeling.
David T. Denhardt;Masaki Noda.
Journal of Cellular Biochemistry (1998)
SOX9 enhances aggrecan gene promoter/enhancer activity and is up-regulated by retinoic acid in a cartilage-derived cell line, TC6.
Ichiro Sekiya;Kunikazu Tsuji;Peter Koopman;Hideto Watanabe.
Journal of Biological Chemistry (2000)
Osteopontin-deficient mice are resistant to ovariectomy-induced bone resorption
Hiroyuki Yoshitake;Susan R. Rittling;David T. Denhardt;Masaki Noda.
Proceedings of the National Academy of Sciences of the United States of America (1999)
Mice Lacking Osteopontin Show Normal Development and Bone Structure but Display Altered Osteoclast Formation In Vitro
Susan R. Rittling;Hiroko N. Matsumoto;Marc D. Mckee;Antonio Nanci.
Journal of Bone and Mineral Research (1998)
Negative regulation of BMP/Smad signaling by Tob in osteoblasts.
Yutaka Yoshida;Sakae Tanaka;Hisashi Umemori;Osamu Minowa.
NF-κB p50 and p52 Regulate Receptor Activator of NF-κB Ligand (RANKL) and Tumor Necrosis Factor-induced Osteoclast Precursor Differentiation by Activating c-Fos and NFATc1
Teruhito Yamashita;Zhenqiang Yao;Fang Li;Qian Zhang.
Journal of Biological Chemistry (2007)
Establishment of tendon-derived cell lines exhibiting pluripotent mesenchymal stem cell-like property
R Salingcarnboriboon;H Yoshitake;K Tsuji;M Obinata.
Experimental Cell Research (2003)
Gene expression in osteoblastic cells
G A Rodan;M Noda.
Critical Reviews in Eukaryotic Gene Expression (1991)
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