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- Fukumoto, SatoshiRemove Fukumoto, Satoshi filter
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Please choose a date range between 2018 and 2020.
Author
- Chiba, Yuta3
- Saito, Kan3
- Yoshizaki, Keigo3
- Bleck, Christopher KE2
- de Vega, Susana2
- Nakamura, Takashi2
- Rhodes, Craig2
- Yamada, Aya2
- Yamada, Yoshihiko2
- Arai, Chieko1
- Boger, Erich T1
- Chu, Emily Y1
- Funada, Keita1
- Han, Xue1
- He, Bing1
- Hino, Ryoko1
- Ikeuchi, Tomoko1
- Inuzuka, Hiroyuki1
- Ishijima, Muneaki1
- Martin, Daniel1
- Miyazaki, Kanako1
- Morell, Robert J1
- Stempinski, Erin1
Keyword
- gene knockout2
- tooth development2
- ameloblast1
- AmeloD1
- basic helix-loop-helix transcription factor (bHLH)1
- cadherin-1 (CDH1)1
- cell differentiation1
- cell migration1
- cell proliferation1
- craniofacial development1
- dental growth1
- development1
- ectodermal organ1
- epiprofin1
- epithelial cadherin (E-cadherin)1
- epithelial cell1
- epithelial-mesenchymal transition (EMT)1
- G-protein coupled receptor1
- GPCR1
- inner enamel epithelium1
- ion transporter1
- Nkx2-31
- odontogenesis1
- pH regulation1
- tissue-specific transcription factor1
Gene Regulation
3 Results
- Developmental BiologyOpen Access
G protein–coupled receptor Gpr115 (Adgrf4) is required for enamel mineralization mediated by ameloblasts
Journal of Biological ChemistryVol. 295Issue 45p15328–15341Published online: August 31, 2020- Yuta Chiba
- Keigo Yoshizaki
- Kan Saito
- Tomoko Ikeuchi
- Tsutomu Iwamoto
- Craig Rhodes
- and others
Cited in Scopus: 8Dental enamel, the hardest tissue in the human body, is derived from dental epithelial cell ameloblast-secreted enamel matrices. Enamel mineralization occurs in a strictly synchronized manner along with ameloblast maturation in association with ion transport and pH balance, and any disruption of these processes results in enamel hypomineralization. G protein–coupled receptors (GPCRs) function as transducers of external signals by activating associated G proteins and regulate cellular physiology. - Developmental BiologyOpen Access
The transcription factor AmeloD stimulates epithelial cell motility essential for tooth morphology
Journal of Biological ChemistryVol. 294Issue 10p3406–3418Published online: November 30, 2018- Yuta Chiba
- Bing He
- Keigo Yoshizaki
- Craig Rhodes
- Muneaki Ishijima
- Christopher K.E. Bleck
- and others
Cited in Scopus: 17The development of ectodermal organs, such as teeth, requires epithelial–mesenchymal interactions. Basic helix–loop–helix (bHLH) transcription factors regulate various aspects of tissue development, and we have previously identified a bHLH transcription factor, AmeloD, from a tooth germ cDNA library. Here, we provide both in vitro and in vivo evidence that AmeloD is important in tooth development. We created AmeloD-knockout (KO) mice to identify the in vivo functions of AmeloD that are critical for tooth morphogenesis. - Developmental BiologyOpen Access
The transcription factor NKX2-3 mediates p21 expression and ectodysplasin-A signaling in the enamel knot for cusp formation in tooth development
Journal of Biological ChemistryVol. 293Issue 38p14572–14584Published online: August 8, 2018- Xue Han
- Keigo Yoshizaki
- Kanako Miyazaki
- Chieko Arai
- Keita Funada
- Tomomi Yuta
- and others
Cited in Scopus: 17Tooth morphogenesis is initiated by reciprocal interactions between the ectoderm and neural crest–derived mesenchyme. During tooth development, tooth cusps are regulated by precise control of proliferation of cell clusters, termed enamel knots, that are present among dental epithelial cells. The interaction of ectodysplasin-A (EDA) with its receptor, EDAR, plays a critical role in cusp formation by these enamel knots, and mutations of these genes is a cause of ectodermal dysplasia. It has also been reported that deficiency in Nkx2-3, encoding a member of the NK2 homeobox family of transcription factors, leads to cusp absence in affected teeth.