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- Publications
- Influence
Semaphorin 3E and Plexin-D1 Control Vascular Pattern Independently of Neuropilins
- Chenghua Gu, Y. Yoshida, +7 authors D. Ginty
- Biology, Medicine
- Science
- 14 January 2005
The development of a patterned vasculature is essential for normal organogenesis. We found that signaling by semaphorin 3E (Sema3E) and its receptor plexin-D1 controls endothelial cell positioning… Expand
Induced Pluripotent Stem Cells Generated from Patients with ALS Can Be Differentiated into Motor Neurons
- John T. Dimos, Kit T. Rodolfa, +10 authors K. Eggan
- Medicine
- Science
- 29 August 2008
The generation of pluripotent stem cells from an individual patient would enable the large-scale production of the cell types affected by that patient's disease. These cells could in turn be used for… Expand
GDNF: a potent survival factor for motoneurons present in peripheral nerve and muscle.
- C. E. Henderson, H. Phillips, +9 authors A. Rosenthal
- Biology, Medicine
- Science
- 11 November 1994
For survival, embryonic motoneurons in vertebrates depend on as yet undefined neurotrophic factors present in the limb bud. Members of the neurotrophin family are currently the best candidates for… Expand
Persephin, a Novel Neurotrophic Factor Related to GDNF and Neurturin
- J. Milbrandt, F. Sauvage, +24 authors E. Johnson
- Biology, Medicine
- Neuron
- 1 February 1998
A novel neurotrophic factor named Persephin that is approximately 40% identical to glial cell line-derived neurotrophic factor (GDNF) and neurturin (NTN) has been identified using degenerate PCR.… Expand
Programmed Cell Death of Embryonic Motoneurons Triggered through the FAS Death Receptor
- C. Raoul, C. E. Henderson, B. Pettmann
- Biology, Medicine
- The Journal of cell biology
- 29 November 1999
About 50% of spinal motoneurons undergo programmed cell death (PCD) after target contact, but little is known about how this process is initiated. Embryonic motoneurons coexpress the death receptor… Expand
A functionally characterized test set of human induced pluripotent stem cells
- G. Boulting, Evangelos Kiskinis, +15 authors K. Eggan
- Biology, Medicine
- Nature Biotechnology
- 1 March 2011
Human induced pluripotent stem cells (iPSCs) present exciting opportunities for studying development and for in vitro disease modeling. However, reported variability in the behavior of iPSCs has… Expand
Accelerated High-Yield Generation of Limb-Innervating Motor Neurons from Human Stem Cells
- Mackenzie W Amoroso, G. Croft, +8 authors H. Wichterle
- Biology, Medicine
- The Journal of Neuroscience
- 9 January 2013
Human pluripotent stem cells are a promising source of differentiated cells for developmental studies, cell transplantation, disease modeling, and drug testing. However, their widespread use even for… Expand
Lentiviral-mediated silencing of SOD1 through RNA interference retards disease onset and progression in a mouse model of ALS
- C. Raoul, T. Abbas-Terki, +5 authors P. Aebischer
- Biology, Medicine
- Nature Medicine
- 13 March 2005
Mutations in Cu/Zn superoxide dismutase (encoded by SOD1), one of the causes of familial amyotrophic lateral sclerosis (ALS), lead to progressive death of motoneurons through a gain-of-function… Expand
Reg-2 is a motoneuron neurotrophic factor and a signalling intermediate in the CNTF survival pathway
- H. Nishimune, S. Vasseur, +5 authors C. E. Henderson
- Biology, Medicine
- Nature Cell Biology
- 1 December 2000
Cytokines that are related to ciliary neurotrophic factor (CNTF) are physiologically important survival factors for motoneurons, but the mechanisms by which they prevent neuronal cell death remain… Expand
Chronic activation in presymptomatic amyotrophic lateral sclerosis (ALS) mice of a feedback loop involving Fas, Daxx, and FasL.
- C. Raoul, Emmanuelle Buhler, +5 authors G. Haase
- Biology, Medicine
- Proceedings of the National Academy of Sciences…
- 11 April 2006
The reasons for the cellular specificity and slow progression of motoneuron diseases such as ALS are still poorly understood. We previously described a motoneuron-specific cell death pathway… Expand