The formation of skeletal muscle: from somite to limb
- M. Buckingham, L. Bajard, F. Relaix
- BiologyJournal of Anatomy
- 1 January 2003
The oligoclonal origin of postnatal muscles points to a small number of founder cells, whether or not these have additional origins to the progenitor cells of the somite which form the first skeletal muscles, as discussed here for the embryonic limb.
KLHL3 mutations cause familial hyperkalemic hypertension by impairing ion transport in the distal nephron
- Hélène Louis-dit-Picard, J. Barc, X. Jeunemaître
- BiologyNature Genetics
- 1 April 2012
A role is established for KLHL3 as a new member of the complex signaling pathway regulating ion homeostasis in the distal nephron and indirectly blood pressure.
Rotation of the Myocardial Wall of the Outflow Tract Is Implicated in the Normal Positioning of the Great Arteries
- F. Bajolle, S. Zaffran, M. Buckingham
- BiologyCirculation Research
- 17 February 2006
Results suggest that embryonic laterality affects rotation of the myocardial wall during OFT maturation, and propose that failure of normal rotation of OFT myocardium may underlie major forms of congenital heart disease.
Regulation of Renal Electrolyte Transport by WNK and SPAK-OSR1 Kinases.
- J. Hadchouel, D. Ellison, G. Gamba
- BiologyAnnual Review of Physiology
- 10 February 2016
A review of the remarkable advances in serine-threonine kinases regulates electrolyte transport in the distal nephron in the past 10 years is presented.
WNK1-related Familial Hyperkalemic Hypertension results from an increased expression of L-WNK1 specifically in the distal nephron
- E. Vidal-Petiot, Emilie Elvira-Matelot, J. Hadchouel
- Biology, MedicineProceedings of the National Academy of Sciences
- 12 August 2013
New insights are provided into the in vivo mechanisms underlying the pathogenesis of WNK1-mediated FHHt and the importance of W NK1 in ion homeostasis and blood pressure is corroborated.
Modular long-range regulation of Myf5 reveals unexpected heterogeneity between skeletal muscles in the mouse embryo.
- J. Hadchouel, S. Tajbakhsh, M. Buckingham
- BiologyDevelopment
- 15 October 2000
A YAC transgenic approach to identify regulatory sequences that direct the complex spatiotemporal expression of this gene during myogenesis in the mouse embryo reveals unexpected heterogeneity between muscle masses, which may underlie the observed restriction of myopathies to particular muscle subgroups.
KLHL3 mutations cause familial hyperkalemic hypertension by impairing ion transport in the distal nephron
- Hélène Louis-dit-Picard, J. Barc, X. Jeunemaître
- BiologyNature Genetics
- 1 May 2012
Hélène Louis-Dit-Picard, Julien Barc, Daniel Trujillano, Stéphanie Miserey-Lenkei, Nabila Bouatia-Naji, Olena Pylypenko, Geneviève Beaurain, Amélie Bonnefond, Olivier Sand, Christophe Simian,…
The early epaxial enhancer is essential for the initial expression of the skeletal muscle determination gene Myf5 but not for subsequent, multiple phases of somitic myogenesis.
- L. Teboul, J. Hadchouel, P. Daubas, D. Summerbell, M. Buckingham, P. Rigby
- BiologyDevelopment
- 1 October 2002
It is proposed that the first phase of Myf5 epaxial expression is necessary for early myotome formation, while the subsequent phases are associated with cytodifferentiation within the myotomes.
Decreased ENaC expression compensates the increased NCC activity following inactivation of the kidney-specific isoform of WNK1 and prevents hypertension
- J. Hadchouel, Christelle Soukaseum, X. Jeunemaître
- BiologyProceedings of the National Academy of Sciences
- 4 October 2010
This study suggests that the activation of Na–Cl cotransporter is not sufficient by itself to induce a hyperkalemic hypertension and that the deregulation of other channels, such as the Epithelial Na+ channel (ENaC), is probably required.
Myf5 is a novel early axonal marker in the mouse brain and is subjected to post-transcriptional regulation in neurons.
- P. Daubas, S. Tajbakhsh, J. Hadchouel, M. Primig, M. Buckingham
- BiologyDevelopment
- 15 January 2000
It is shown that cells expressing Wnt1 can activate neuronal Myf5-nlacZ gene expression in dissected head explants isolated from E9.5 embryos, and the gene encoding the basic Helix-Loop-Helix transcription factor mSim 1 is expressed in adjacent cells in both the somite and the brain, suggesting that signalling molecules necessary for the activation of mSim1 as well as Myf4 are present at these different sites in the embryo.
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