A
Akira Kudo
Researcher at Tokyo Institute of Technology
Publications - 197
Citations - 14593
Akira Kudo is an academic researcher from Tokyo Institute of Technology. The author has contributed to research in topics: Periostin & Gene. The author has an hindex of 61, co-authored 197 publications receiving 13558 citations. Previous affiliations of Akira Kudo include Basel Institute for Immunology & Kyushu University.
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Identification and characterization of a novel protein, periostin, with restricted expression to periosteum and periodontal ligament and increased expression by transforming growth factor β
Keisuke Horiuchi,Norio Amizuka,Sunao Takeshita,Hiroyuki Takamatsu,Mieko Katsuura,Hidehiro Ozawa,Yoshiaki Toyama,Lynda F. Bonewald,Akira Kudo +8 more
TL;DR: Immunohistochemistry and reverse transcription‐ polymerase chain reaction analysis suggest that periostin may play a role in the recruitment and attachment of osteoblast precursors in theperiosteum.
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Tumor necrosis factor-alpha induces differentiation of and bone resorption by osteoclasts.
TL;DR: It is revealed that TNF-α directly induced the formation of tartrate-resistant acid phosphatase (TRAP)-positive multinucleated cells (MNCs), which produced resorption pits on bone in vitro in the presence of M-CSF, suggesting that TNP and M- CSF play an important role in local osteolysis in chronic inflammatory diseases.
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Identification and characterization of the new osteoclast progenitor with macrophage phenotypes being able to differentiate into mature osteoclasts
TL;DR: The differentiation potential of mouse bone marrow macrophages into mature osteoclasts is characterized and the transition of morphology, surface markers, and gene expression from the early to mature stage in osteoclast differentiation is shown.
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A critical role of λ5 protein in B cell development
TL;DR: The lambda 5 gene is a homolog of immunoglobulin J lambda-C lambda genes, expressed specifically in immature B-lineage cells as discussed by the authors, and it is inactivated by targeted gene disruption in embryonic stem cells.
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The gamete fusion process is defective in eggs of Cd9-deficient mice.
Keisuke Kaji,Shoji Oda,Tomohide Shikano,Tatsuya Ohnuki,Yoshikatsu Uematsu,Junko Sakagami,Norihiro Tada,Shunichi Miyazaki,Akira Kudo +8 more
TL;DR: The results show that Cd9 is important in the gamete fusion process at fertilization, and that homozygous mutant females were infertile.