M
Mohamed Jaber
Researcher at University of Bordeaux
Publications - 31
Citations - 9089
Mohamed Jaber is an academic researcher from University of Bordeaux. The author has contributed to research in topics: Dopamine & Dopaminergic. The author has an hindex of 18, co-authored 23 publications receiving 8659 citations. Previous affiliations of Mohamed Jaber include Howard Hughes Medical Institute & Duke University.
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Journal ArticleDOI
The dopamine transporter: A crucial component regulating dopamine transmission
TL;DR: The results establish not only the central importance of the transporter as the key element controlling dopamine levels in the brain, but also its role as an obligatory target for the behavioral and biochemical action of amphetamine and cocaine.
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Absence of MPTP-induced neuronal death in mice lacking the dopamine transporter.
Erwan Bezard,Christian E. Gross,Marie-Christine Fournier,Sandra Dovero,Bertrand Bloch,Mohamed Jaber +5 more
TL;DR: The results shed light on the degenerative process of dopamine neurons and suggest that individual differences in developing Parkinson's disease in human may be related to differences of uptake through the DAT of a yet unidentified neurotoxin.
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Anterior Pituitary Hypoplasia and Dwarfism in Mice Lacking the Dopamine Transporter
Roger Bossé,Fabio Fumagalli,Mohamed Jaber,Bruno Giros,Raul R. Gainetdinov,William C. Wetsel,Cristina Missale,Marc G. Caron +7 more
TL;DR: The results reveal an unexpected and important role or DA in the control of developmental events in the pituitary gland and assign a critical role for hypothalamic DA reuptake in regulating these events.
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Control of Myocardial Contractile Function by the Level of β-Adrenergic Receptor Kinase 1 in Gene-targeted Mice
Howard A. Rockman,Dong-Ju Choi,Shahab A. Akhter,Mohamed Jaber,Bruno Giros,Robert J. Lefkowitz,Robert J. Lefkowitz,Marc G. Caron,Marc G. Caron,Walter J. Koch +9 more
TL;DR: Data demonstrate that contractile function can be modulated by the level of βark1 activity and suggests that βARK1 should be considered as a therapeutic target in this situation, and even partial inhibition of βarks1 activity enhances β-adrenergic receptor signaling leading to improved functional catecholamine responsiveness.
Journal ArticleDOI
Differential regulation of tyrosine hydroxylase in the basal ganglia of mice lacking the dopamine transporter.
Mohamed Jaber,Brigitte Dumartin,Corinne Sagné,John W. Haycock,Christine Roubert,Bruno Giros,Bertrand Bloch,Marc G. Caron +7 more
TL;DR: The paradoxical hyperdopaminergia in the DAT KO mice despite a marked decrease in TH and dopamine levels suggests a parallel to Parkinson's disease implying that blockade of DAT may be beneficial in this condition.