José António Belo

Prof. Dr. José António Belo

NOVA Medical School | Faculdade de Ciências Médicas, Lisbon, Lisboa, Portugal
orcid

Research Focus & Metrics

Academic Career Length

34Years (1993-Present)

(Calculated once Scilit publication data is synced: current year − year of first publication + 1)

Representative Publications

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1 February 2000 in Nature
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Journal Article
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DBDaniel Bachiller
Daniel Bachiller
JKJohn Klingensmith
John Klingensmith
CKC. Kemp
C. Kemp
JBJosé António Belo
José António Belo
RAR. M. Anderson
R. M. Anderson
ERE. M. De Robertis
E. M. De Robertis

1 November 1997 in Mechanisms of Development
Verified
Journal Article
Closed access
JBJosé António Belo
José António Belo
TBTewis Bouwmeester
Tewis Bouwmeester
LLLuc Leyns
Luc Leyns
NKNathalie Kertesz
Nathalie Kertesz
MGMichael Gallo
Michael Gallo
EREddy M De Robertis
Eddy M De Robertis

12 October 2012 in Science
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Journal Article
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SYSatoko Yoshiba
Satoko Yoshiba
HSHidetaka Shiratori
Hidetaka Shiratori
IKIvana Y. Kuo
Ivana Y. Kuo
AKAiko Kawasumi
Aiko Kawasumi
KSKyosuke Shinohara
Kyosuke Shinohara
HHHiroshi Hamada
Hiroshi Hamada
Distinguishing Right from Left: In most vertebrates during embryonic development, rotational movement of the cilia within a structure in the embryo, known as the node, generates unidirectional flow required for future left-right asymmetry of the internal organs. The flow may transport a determinant molecule or provide mechanical force. However, it is not clear how the flow is sensed. Yoshiba et al. (p. 226 , published online 13 September; see the Perspective by Norris and Grimes ) show that nodal flow in mouse embryos is sensed by the cilia of perinodal cells located at the edge of the node, in a manner dependent on Pkd2, a Ca 2+ -permeable cation channel that has been implicated in polycystic kidney disease in humans.

1 October 2004 in Genes & Development
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SMSara Marques
Sara Marques
ABAna Cristina Borges
Ana Cristina Borges
ASAna Cristina Silva
Ana Cristina Silva
SFSandra Freitas
Sandra Freitas
MCMichelangelo Cordenonsi
Michelangelo Cordenonsi
JBJosé António Belo
José António Belo
Correct establishment of the left/right (L/R) body asymmetry in the mouse embryo requires asymmetric activation of the evolutionarily conserved Nodal signaling cascade in the left lateral plate mesoderm (L-LPM). Furthermore, the presence of Nodal in the node is essential for its own expression in the L-LPM. Here, we have characterized the function of cerl-2, a novel Nodal antagonist, which displays a unique asymmetric expression on the right side of the mouse node. cerl-2 knockout mice display multiple laterality defects including randomization of the L/R axis. These defects can be partially rescued by removing one nodal allele. Our results demonstrate that Cerl-2 plays a key role in restricting the Nodal signaling pathway toward the left side of the mouse embryo by preventing its activity in the right side.

1 November 2005 in Developmental Cell
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Journal Article
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CKChiharu Kimura-Yoshida
Chiharu Kimura-Yoshida
HNHiroshi Nakano
Hiroshi Nakano
DODaiji Okamura
Daiji Okamura
KNKazuki Nakao
Kazuki Nakao
SYShigenobu Yonemura
Shigenobu Yonemura
IMIsao Matsuo
Isao Matsuo

1 January 2012 in Nature Communications
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TNTetsuya Nakamura
Tetsuya Nakamura
DSDaisuke Saito
Daisuke Saito
AKAiko Kawasumi
Aiko Kawasumi
KSKyosuke Shinohara
Kyosuke Shinohara
YAYasuko Asai
Yasuko Asai
HHHiroshi Hamada
Hiroshi Hamada
Breaking of left–right symmetry in mouse embryos requires fluid flow at the node, but the precise action of the flow has remained unknown. Here we show that the left–right asymmetry of Cerl2 expression around the node, a target of the flow, is determined post-transcriptionally by decay of Cerl2 mRNA in a manner dependent on its 3′ untranslated region. Cerl2 mRNA is absent specifically from the apical region of crown cells on the left side of the node. Preferential decay of Cerl2 mRNA on the left is initiated by the leftward flow and further enhanced by the operation of Wnt-Cerl2 interlinked feedback loops, in which Wnt3 upregulates Wnt3 expression and promotes Cerl2 mRNA decay, whereas Cerl2 promotes Wnt degradation. Mathematical modelling and experimental data suggest that these feedback loops behave as a bistable switch that can amplify in a noise-resistant manner a small bias conferred by fluid flow.