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Isabel Fariñas
Researcher at University of Valencia
Publications - 105
Citations - 15950
Isabel Fariñas is an academic researcher from University of Valencia. The author has contributed to research in topics: Neural stem cell & Neurogenesis. The author has an hindex of 50, co-authored 98 publications receiving 14927 citations. Previous affiliations of Isabel Fariñas include University of California, San Francisco & Spanish National Research Council.
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Mice Lacking α-Synuclein Display Functional Deficits in the Nigrostriatal Dopamine System
Asa Abeliovich,Yvonne Schmitz,Isabel Fariñas,DL Choi-Lundberg,Wei Hsien Ho,Pablo E. Castillo,Natasha Shinsky,José Manuel García Verdugo,Mark Armanini,Anne M. Ryan,Mary Hynes,Heidi S. Phillips,David Sulzer,Arnon Rosenthal +13 more
TL;DR: The hypothesis that alpha-Syn is an essential presynaptic, activity-dependent negative regulator of DA neurotransmission is supported.
Journal ArticleDOI
Renal and neuronal abnormalities in mice lacking GDNF.
Mark W. Moore,Robert D. Klein,Isabel Fariñas,Hansjorg Sauer,Mark Armanini,Heidi S. Phillips,Louis F. Reichardt,Anne M. Ryan,Karen Carver-Moore,Arnon Rosenthal +9 more
TL;DR: It is shown that at postnatal day 0 (P0), GDNF-deficient mice have deficits in dorsal root ganglion, sympathetic and nodose neurons, but not in hindbrain noradrenergic or midbrain dopaminergic neurons, and GDNF is important for the development and/or survival of enteric, sympathetic, and sensory neurons and the renal system, but is not essential for catecholaminergic neuron in the central nervous system (CNS).
Journal ArticleDOI
Targeted disruption of the BDNF gene perturbs brain and sensory neuron development but not motor neuron development
TL;DR: The BDNF mutant homozygotes have substantially reduced numbers of cranial and spinal sensory neurons and expression of neuropeptide Y and calcium-binding proteins is altered in many neurons, suggesting they do not function normally.
Journal ArticleDOI
Development of several organs that require inductive epithelial-mesenchymal interactions is impaired in LEF-1-deficient mice.
C van Genderen,Ross M Okamura,Isabel Fariñas,R G Quo,Tristram G. Parslow,L Bruhn,Rudolf Grosschedl +6 more
TL;DR: The pattern of defects suggest an essential role for LEF-1 in the formation of several organs and structures that require inductive tissue interactions in mice carrying a homozygous germ-line mutation in the LEf-1 gene.