Kyushu University Academic Staff Educational and Research Activities Database
Search by Keyword How ro search
Keyword
Search Criteria
 
Detailed Search

Researcher information (To researchers) Need Help? How to update
Keiko Kitajima Last modified date：2023.11.22

Assistant Professor / Department of Basic Medicine
Department of Basic Medicine
Faculty of Medical Sciences




Homepage
https://kyushu-u.elsevierpure.com/en/persons/keiko-kitajima
　Reseacher Profiling Tool　Kyushu University Pure
http://www.med.kyushu-u.ac.jp/dev/
Academic Degree
Doctor of Philosophy
Country of degree conferring institution (Overseas)
No
Field of Specialization
Developmental Biology
Total Priod of education and research career in the foreign country
00years00months
Outline Activities
Research for axes formation between development, using techniques of Developmental and Molecular Biology
Research
Research Interests
  • Molecular mechanisms of body axis formation
    keyword : mouse, development, body axes
    2006.04Research for body axes formation during embryogenesis, using techniques of Developmental and Molecular Biology..
Academic Activities
Papers
 Show All Papers >>
1. 北島 桂子, 角 智行, 沖 真弥, 大川 恭行, 目野 主税, Wnt signaling regulates left-right axis formation in the node of mouse embryos., Developmental Biology, 10.1016/j.ydbio.2013.05.011, 380, 2, 222-232, 2013.08, The node triggers formation of the left-right axis in mouse embryos by establishing local asymmetry of Nodal and Cerl2 expression. We found that Wnt3 is expressed in perinodal crown cells preferentially on the left side. The enhancer responsible for Wnt3 expression was identified and found to be regulated by Foxa2 and Rbpj under the control of Notch signaling. Rbpj binding sites suppress enhancer activity in pit cells of the node, thereby ensuring crown cell-specific expression. In addition, we found that the expression of Gdf1 and Cerl2 is also regulated by Notch signaling, suggesting that such signaling may induce the expression of genes related to left-right asymmetry as a set. Furthermore, Cerl2 expression became symmetric in response to inhibition of Wnt-β-catenin signaling. Our results suggest that Wnt signaling regulates the asymmetry of Cerl2 expression, which likely generates a left-right difference in Nodal activity at the node for further amplification in lateral plate mesoderm..
2. Oki S, Kitajima K, Meno C., Dissecting the role of Fgf signaling during gastrulation and left-right axis formation in mouse embryos using chemical inhibitors., Developmental Dynamics, 10.1002/dvdy.22282, 239, 6, 1768-1778, 2010.06.
3. Oki S., Kitajima K., Marques S., Belo JA., Yokoyama T., Hamada H., Meno C., Reversal of left-right asymmetry induced by aberrant Nodal signaling in the node of mouse embryos., Development, 136, 23, 3917-3925, 2009.12.
Presentations
 Show All Presentations >>
1. 北島 桂子, 角 智行, 沖 真弥, 目野 主税, Wnt signaling regulates the left-right axis formation in the node of mouse embryos, 46th Annual Meeting of JSDB, 2013.05.
2. 北島 桂子, 角 智行, 沖 真弥, 目野 主税, Wnt signaling regulates the left-right axis formation in the node, MOUSE MOLECULAR GENETICS, 2013.09, The node triggers formation of the left-right axis in mouse embryos by establishing local asymmetry of Nodal and Cerl2 expression. We found that Wnt3 is expressed in perinodal crown cells preferentially on the left side. The enhancer responsible for Wnt3 expression was identified and found to be regulated by Foxa2 and Rbpj under the control of Notch signaling. Rbpj binding sites suppress enhancer activity in pit cells of the node, thereby ensuring crown cell–specific expression. In addition, we found that the expression of Gdf1 and Cerl2 is also regulated by Notch signaling, suggesting that such signaling may induce the expression of genes related to left-right asymmetry as a set. Furthermore, Cerl2 expression became symmetric in response to inhibition of Wnt–β-catenin signaling. Our results suggest that Wnt signaling regulates the asymmetry of Cerl2 expression, which likely generates a left-right difference in Nodal activity at the node for further amplification in lateral plate mesoderm..


Unauthorized reprint of the contents of this database is prohibited.

Copyright © 2006, Kyushu University. All rights reserved.