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Pascal Dollé

Researcher at French Institute of Health and Medical Research

Publications -  169
Citations -  26799

Pascal Dollé is an academic researcher from French Institute of Health and Medical Research. The author has contributed to research in topics: Retinoic acid & Retinoic acid receptor. The author has an hindex of 82, co-authored 167 publications receiving 25579 citations. Previous affiliations of Pascal Dollé include University of Strasbourg & Paris Descartes University.

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The expression pattern of the mouse receptor tyrosine kinase gene MDK1 is conserved through evolution and requires Hoxa-2 for rhombomere-specific expression in mouse embryos.

TL;DR: The isolation of the zebrafish orthologue of the mouse RTK gene MDK1 which belongs to the Eph receptor subfamily is reported and it is shown that the major expression domains of the Mouse and the Zebrafish genes have been conserved through evolution.
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The Mouse Hox-1.4 Gene: Primary Structure, Evidence for Promoter Activity and Expression During Development

TL;DR: The Hox-1.4 expression pattern is in good agreement with recent proposals concerning the involvement of such genes in the establishment of the vertebrate body plan as well as the relationship between the positions of these genes within their clusters and the anteroposterior restriction of their expression domains.
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Retinaldehyde dehydrogenase 2 and Hoxc8 are required in the murine brachial spinal cord for the specification of Lim1+ motoneurons and the correct distribution of Islet1+ motoneurons.

TL;DR: It is shown that Hoxc8 mutant mice, which exhibit a similar congenital forepaw defect, display at embryonic stages molecular defects that phenocopy the Raldh2L–/– motoneuron abnormalities, and interdependent RA signaling and Hox gene functions are required for the specification of brachial motoneurons in the mouse.
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Retinoic acid signalling is required for specification of pronephric cell fate

TL;DR: Timed antagonist treatments show that RA signalling is required during gastrulation for expression of Xlim-1 and XPax-8 in pronephric precursors, and experiments conducted with a protein synthesis inhibitor indicate that RA may directly regulate X Lim-1.
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Developing with lethal RA levels: genetic ablation of Rarg can restore the viability of mice lacking Cyp26a1.

TL;DR: Ablation of the gene for RARγ (Rarg) rescues Cyp26a1-null mutant animals from caudal regression and embryonic lethality, thus demonstrating that CYP26A1 suppresses the RA-mediated downregulation of WNT3A and FGF8 signaling pathways by eliminating ectopic RA in gastrulating tail bud mesoderm.