Výsledky vyhledávání - "MIZUHO KITTAKA"

Akademický článek

Osteocytes directly regulate osteolysis via MYD88 signaling in bacterial bone infection

Autor: Tetsuya Yoshimoto, Mizuho Kittaka, Andrew Anh Phuong Doan, Rina Urata, Matthew Prideaux, Roxana E. Rojas, Clifford V. Harding, W. Henry Boom, Lynda F. Bonewald, Edward M. Greenfield, Yasuyoshi Ueki

Publikováno v: Nature Communications, Vol 13, Iss 1, Pp 1-19 (2022)

MYD88 mediates the signal of bacterial infection. Here, in the context of periodontal infection, the authors show that the MYD88 pathway in osteocytes plays a dominant role in regulating osteolysis.

Externí odkaz: https://doaj.org/article/e16f005c0ee94c278ec83641515e371c

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Akademický článek

Osteocyte-Derived CaMKK2 Regulates Osteoclasts and Bone Mass in a Sex-Dependent Manner through Secreted Calpastatin

Autor: Justin N. Williams, Mavis Irwin, Yong Li, Anuradha Valiya Kambrath, Brett T. Mattingly, Sheel Patel, Mizuho Kittaka, Rebecca N. Collins, Nicholas A. Clough, Emma H. Doud, Amber L. Mosley, Teresita Bellido, Angela Bruzzaniti, Lilian I. Plotkin, Jonathan C. Trinidad, William R. Thompson, Lynda F. Bonewald, Uma Sankar

Publikováno v: International Journal of Molecular Sciences, Vol 24, Iss 5, p 4718 (2023)

Calcium/calmodulin (CaM)-dependent protein kinase kinase 2 (CaMKK2) regulates bone remodeling through its effects on osteoblasts and osteoclasts. However, its role in osteocytes, the most abundant bone cell type and the master regulator of bone remod

Externí odkaz: https://doaj.org/article/d9164afb0eaa4ffda13dc2ff3c098267

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Akademický článek

OC_Finder: Osteoclast Segmentation, Counting, and Classification Using Watershed and Deep Learning

Autor: Xiao Wang, Mizuho Kittaka, Yilin He, Yiwei Zhang, Yasuyoshi Ueki, Daisuke Kihara

Publikováno v: Frontiers in Bioinformatics, Vol 2 (2022)

Osteoclasts are multinucleated cells that exclusively resorb bone matrix proteins and minerals on the bone surface. They differentiate from monocyte/macrophage lineage cells in the presence of osteoclastogenic cytokines such as the receptor activator

Externí odkaz: https://doaj.org/article/c76e88be9b594650b3f8d83463694eaf

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Akademický článek

Microbe‐Dependent Exacerbated Alveolar Bone Destruction in Heterozygous Cherubism Mice

Autor: Mizuho Kittaka, Tetsuya Yoshimoto, Collin Schlosser, Mikihito Kajiya, Hidemi Kurihara, Ernst J Reichenberger, Yasuyoshi Ueki

Publikováno v: JBMR Plus, Vol 4, Iss 6, Pp n/a-n/a (2020)

ABSTRACT Cherubism (OMIM#118400) is a craniofacial disorder characterized by destructive jaw expansion. Gain‐of‐function mutations in SH3‐domain binding protein 2 (SH3BP2) are responsible for this rare disorder. We have previously shown that ho

Externí odkaz: https://doaj.org/article/771a4998294a42b7801c0c626ba58eb0

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Akademický článek

RANKL-independent osteoclastogenesis in the SH3BP2 cherubism mice

Autor: Mizuho Kittaka, Tetsuya Yoshimoto, Henry Hoffman, Marcus Evan Levitan, Yasuyoshi Ueki

Publikováno v: Bone Reports, Vol 12, Iss , Pp 100258- (2020)

Even though the receptor activator of the nuclear factor-κB ligand (RANKL) and its receptor RANK have an exclusive role in osteoclastogenesis, the possibility of RANK/RANKL-independent osteoclastogenesis has been the subject of a long-standing debat

Externí odkaz: https://doaj.org/article/8a18c3724bfa47d594a4248bef8b32be

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Akademický článek

Enhanced TLR-MYD88 Signaling Stimulates Autoinflammation in SH3BP2 Cherubism Mice and Defines the Etiology of Cherubism

Autor: Teruhito Yoshitaka, Tomoyuki Mukai, Mizuho Kittaka, Lisa M. Alford, Salome Masrani, Shu Ishida, Ken Yamaguchi, Motohiko Yamada, Noriyoshi Mizuno, Bjorn R. Olsen, Ernst J. Reichenberger, Yasuyoshi Ueki

Publikováno v: Cell Reports, Vol 8, Iss 6, Pp 1752-1766 (2014)

Cherubism is caused by mutations in SH3BP2. Studies of cherubism mice showed that tumor necrosis factor α (TNF-α)-dependent autoinflammation is a major cause of the disorder but failed to explain why human cherubism lesions are restricted to jaws a

Externí odkaz: https://doaj.org/article/5453dcbdd4d64aed8b946a1fbb2113bc

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Akademický článek

SH3BP2 gain-of-function mutation exacerbates inflammation and bone loss in a murine collagen-induced arthritis model.

Autor: Tomoyuki Mukai, Richard Gallant, Shu Ishida, Teruhito Yoshitaka, Mizuho Kittaka, Keiichiro Nishida, David A Fox, Yoshitaka Morita, Yasuyoshi Ueki

Publikováno v: PLoS ONE, Vol 9, Iss 8, p e105518 (2014)

SH3BP2 is a signaling adapter protein which regulates immune and skeletal systems. Gain-of-function mutations in SH3BP2 cause cherubism, characterized by jawbone destruction. This study was aimed to examine the role of SH3BP2 in inflammatory bone los

Externí odkaz: https://doaj.org/article/55344c38147d466ba48414f194b2723d

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