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Differential Expression Of Gap Junctions In Neurons And Astrocytes Dervied From P19 Embryonal Carcinoma Cells, Daniel Belliveau, J. Bechberger, K. Rodgers, C. Naus
Differential Expression Of Gap Junctions In Neurons And Astrocytes Dervied From P19 Embryonal Carcinoma Cells, Daniel Belliveau, J. Bechberger, K. Rodgers, C. Naus
Daniel J. Belliveau
The P19 embryonal carcinoma cell line represents a pluripotential stem cell that can differentiate along the neural or muscle cell lineage when exposed to different environments. Exposure to retinoic acid induces P19 cells to differentiate into neurons and astrocytes that express similar developmental markers as their embryonic counterparts. We examined the expression of gap junction genes during differentiation of these stem cells into neurons and astrocytes. Untreated P19 cells express at least two gap junction proteins, connexins 26 and 43. Connexin32 could not be detected in these cells. Treatment for 96 hr with 0.3 mM retinoic acid induced the P19 …
Blocking Nerve Growth Factor Binding To The P75 Neurotrophin Receptor On Sympathetic Neurons Transiently Reduces Trka Activation But Does Not Affect Neuronal Survival, C. Lachance, Daniel Belliveau, P. Barker
Blocking Nerve Growth Factor Binding To The P75 Neurotrophin Receptor On Sympathetic Neurons Transiently Reduces Trka Activation But Does Not Affect Neuronal Survival, C. Lachance, Daniel Belliveau, P. Barker
Daniel J. Belliveau
Nerve growth factor interacts with the trkA tyrosine kinase receptor and with the p75 neurotrophin receptor. It is clear that trkA mediates most, if not all, of the stereotypical responses of sympathetic neurons to nerve growth factor but the role of the p75 neurotrophin receptor is unclear. In this study, we have asked whether a functional interaction between p75 neurotrophin receptor and trkA exists in primary sympathetic neurons by disrupting nerve growth factor binding to p75 neurotrophin receptor. Acute assays reveal that blocking antibodies directed against p75 neurotrophin receptor reduce nerve growth factor-mediated trkA tyrosine phosphorylation and reduce the amount …
Transgenic Mice Expressing The Intracellular Domain Of The P75 Neurotrophin Receptor Undergo Neuronal Apoptosis, M. Majdan, C. Lachance, A. Gloster, R. Aloyz, C. Zeindler, S. Bamji, A. Bhakar, Daniel Belliveau, J. Fawcett, F. Miller, P. Barker
Transgenic Mice Expressing The Intracellular Domain Of The P75 Neurotrophin Receptor Undergo Neuronal Apoptosis, M. Majdan, C. Lachance, A. Gloster, R. Aloyz, C. Zeindler, S. Bamji, A. Bhakar, Daniel Belliveau, J. Fawcett, F. Miller, P. Barker
Daniel J. Belliveau
We have asked whether p75NTR may play a role in neuronal apoptosis by producing transgenic mice that express the p75NTR intracellular domain within peripheral and central neurons. These animals showed profound reductions in numbers of sympathetic and peripheral sensory neurons as well as cell loss in the neocortex, where there is normally little or no p75NTR expression. Developmental loss of facial motor neurons was not observed, but induced expression of the p75NTR intracellular domain within adult animals led to increased motor neuron death after axotomy. Biochemical analyses suggest that these effects were not attributable to a p75NTR-dependent reduction in trk …
Ngf And Neurotrophin-3 Both Activate Trka On Sympathetic Neurons But Differentially Regulate Survival And Neuritogenesis, Daniel Belliveau, I. Krivko, C. Lachance, J. Kohn, D. Rusakov, D. Kaplan, F. Miller
Ngf And Neurotrophin-3 Both Activate Trka On Sympathetic Neurons But Differentially Regulate Survival And Neuritogenesis, Daniel Belliveau, I. Krivko, C. Lachance, J. Kohn, D. Rusakov, D. Kaplan, F. Miller
Daniel J. Belliveau
In this report we examine the biological and molecular basis of the control of sympathetic neuron differentiation and survival by NGF and neurotrophin-3 (NT-3). NT-3 is as efficient as NGF in mediating neuritogenesis and expression of growth-associated genes in NGF-dependent sympathetic neurons, but it is 20-40-fold less efficient in supporting their survival. Both NT-3 and NGF induce similar sustained, long-term activation of TrkA, while NGF is 10-fold more efficient than NT-3 in mediating acute, short-term TrkA activity. At similar acute levels of TrkA activation, NT-3 still mediates neuronal survival two- to threefold less well than NGF. However, a mutant NT-3 …