Xenopus, an ideal model system to study vertebrate left‐right asymmetry

No abstract is available for this paper.

• Publication year

  2009

• Venue

  Developmental Dynamics

• Publication date

  2009-06-01

• Fields of study

  Biology, Medicine

• Identifiers
  DOI 10.1002/dvdy.21855PMID 19208433
• External record

  Open on Semantic Scholar

• Source metadata

  Semantic Scholar, PubMed

• No claims are published for this paper.

• No concepts are published for this paper.

• Evolution of leftward flow.

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• H,K-ATPase protein localization and Kir4.1 function reveal concordance of three axes during early determination of left-right asymmetry.

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• Asymmetries in H / K-ATPase and Cell Membrane Potentials Comprise a Very Early Step in Left

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• The ion channel polycystin-2 is required for left-right axis determination in mice.

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• Left–right development: Conserved function for embryonic nodal cilia

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• Overexpression of the Xenopus tight-junction protein claudin causes randomization of the left-right body axis.

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• A role for BMP signalling in heart looping morphogenesis in Xenopus.

  2001cited by this paper
• Regulation of left-right patterning in mice by growth/differentiation factor-1

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• Antivin, a novel and divergent member of the TGFbeta superfamily, negatively regulates mesoderm induction.

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• Gap junction-mediated transfer of left-right patterning signals in the early chick blastoderm is upstream of Shh asymmetry in the node.

  1999cited by this paper
• The novel Cer-like protein Caronte mediates the establishment of embryonic left–right asymmetry

  1999cited by this paper
• Gap junction-mediated transfer of left-right patterning signals in the early chick blastoderm is upstream of Shh asymmetry in the node

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• The homeobox gene Pitx2: mediator of asymmetric left-right signaling in vertebrate heart and gut looping.

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• Regulation of midline development by antagonism of lefty and nodal signaling.

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• Gap junctions are involved in the early generation of left-right asymmetry.

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  1998cited by this paper
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  1998cited by this paper
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• Mutations of the Connexin43 gap-junction gene in patients with heart malformations and defects of laterality.

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