Institution
Collège de France
Education•Paris, France•
About: Collège de France is a education organization based out in Paris, France. It is known for research contribution in the topics: Population & Dopamine. The organization has 6541 authors who have published 11983 publications receiving 648742 citations. The organization is also known as: College de France.
Topics: Population, Dopamine, Dopaminergic, Receptor, Neural crest
Papers published on a yearly basis
Papers
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TL;DR: Two novel glial‐specific markers, expressed earlier than any previously described myelin components, have been identified and partly characterised and are related to the divergence of glial and neuronal cell lineages.
Abstract: We have been studying how and when the different peripheral glial cell lineages individualize during avian embryonic development. Three different and complementary experimental approaches were used for this purpose: (1) the quail/chick chimera system allowed the tracing in vivo of the origin of the various types of peripheral glial cells (Schwann cells of nerves, satellite glial cells of sensory and autonomic ganglia, and enteric glial cells), and the analysis of the non-neuronal cell population of ganglia; (2) characterisation of early cell-type specific markers that discriminate between the different glial cell subpopulations; and (3) analysis of the progeny of neural crest cells in clonal cultures. As a result of these approaches, two novel glial-specific markers, expressed earlier than any previously described myelin components, have been identified and partly characterised. The divergence of glial and neuronal cell lineages is a process that is not completely terminated during the phase of neural crest migration. Whereas some cells are apparently already totally committed to a glial fate at this stage, others retain dual neuronal/glial potentialities.
134 citations
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TL;DR: Observations suggest that, within RXR‐R AR heterodimers, RAR can adopt a structure distinct from that of the active holo‐RAR, thus allowing RXR to become transcriptionally responsive to agonists.
Abstract: Mutations of a single residue in the retinoid X receptor alpha (RXRalpha) ligand-binding pocket (LBP) generate constitutive, ligand-binding-competent mutants with structural and functional characteristics similar to those of agonist-bound wild-type RXR. Modelling of the mouse RXRalphaF318A LBP suggests that, like agonist binding, the mutation disrupts a cluster of van der Waals interactions that maintains helix H11 in the apo-receptor location, thereby shifting the thermodynamic equilibrium to the holo form. Heterodimerization with some apo-receptors (retinoic acid, thyroid hormone and vitamin D3 receptors) results in 'silencing' of RXRalphaF318A constitutive activity, which, on the other hand, efficiently contributes to synergistic transactivation within NGFI-B-RXR heterodimers. RAR mutants disabled for corepressor binding and/or lacking a functional AF-2 activation domain, do not relieve RXR 'silencing'. Not only RAR agonists, but also the RAR antagonist BMS614 induce conformational changes allowing RXR to exert constitutive (RXRalphaF318A) or agonist-induced (wild-type RXR) activity in heterodimers. Interestingly, the RXRalphaF318A constitutive activity generated within heterodimers in the presence of BMS614 requires the integrity of both RXR and RAR AF-2 domains. These observations suggest that, within RXR-RAR heterodimers, RAR can adopt a structure distinct from that of the active holo-RAR, thus allowing RXR to become transcriptionally responsive to agonists.
134 citations
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TL;DR: A French pedigree with seven affected individuals in which two affected individuals also have adrenal tumors and two others have micronodular adrenal hyperplasia is studied, giving a rare opportunity to study the regulation and action of the hybrid gene causing the disease.
Abstract: Glucocorticoid-suppressible hyperaldosteronism is a dominantly inherited form of hypertension believed to be caused by the presence of a hybrid CYP11B1/CYP11B2 gene which has arisen from an unequal crossing over between the two CYP11B genes in a previous meiosis. We have studied a French pedigree with seven affected individuals in which two affected individuals also have adrenal tumors and two others have micronodular adrenal hyperplasia. One of the adrenal tumors and the surrounding adrenal tissue has been removed, giving a rare opportunity to study the regulation and action of the hybrid gene causing the disease. The hybrid CYP11B gene was demonstrated to be expressed at higher levels than either CYP11B1 or CYP11B2 in the cortex of the adrenal by RT-PCR and Northern blot analysis. In situ hybridization showed that both CYP11B1 and the hybrid gene were expressed in all three zones of the cortex. In cell culture experiments hybrid gene expression was stimulated by ACTH leading to increased production of aldosterone and the hybrid steroids characteristic of glucocorticoid-suppressible hyperaldosteronism. The genetic basis of the adrenal pathologies in this family is not known but may be related to the duplication causing the hyperaldosteronism.
134 citations
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TL;DR: In vivo the local effects of opiates on the release of DA in the cat caudate nucleus are examined and it is found that both morphine and more markedly, D-Ala2-Met-enkephalinamide stimulate DA release.
Abstract: Morphine and δ-opiate agonists locally stimulate in vivo dopamine release in cat caudate nucleus
133 citations
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TL;DR: The pathophysiological mechanisms of NR are described and the tools available for diagnosing it are described, which may provide relevant therapeutic targets for reducing NR and improving the prognosis for patients.
133 citations
Authors
Showing all 6597 results
Name | H-index | Papers | Citations |
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Pierre Chambon | 211 | 884 | 161565 |
Irving L. Weissman | 201 | 1141 | 172504 |
David R. Williams | 178 | 2034 | 138789 |
Kari Alitalo | 174 | 817 | 114231 |
Pierre Bourdieu | 153 | 592 | 194586 |
Stanislas Dehaene | 149 | 456 | 86539 |
Howard L. Weiner | 144 | 1047 | 91424 |
Alain Fischer | 143 | 770 | 81680 |
Yves Agid | 141 | 669 | 74441 |
Michel Foucault | 140 | 499 | 191296 |
Jean-Pierre Changeux | 138 | 672 | 76462 |
Jean-Marie Tarascon | 136 | 853 | 137673 |
K. Ganga | 132 | 272 | 99004 |
Jacques Delabrouille | 131 | 354 | 94923 |
G. Patanchon | 128 | 241 | 87233 |