The Journal of Neuroscience, September 6, 2006, ():
Protecting Motor Neurons from Toxic Insult by Antagonism of Adenosine A2a and Trk Receptors
J. Neurosci. Mojsilovic-Petrovic et al.
26: 9250
Supplemental data
Files in this Data Supplement:
- supplemental material
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Supplemental Figure. Model for transactivation of TrkB receptors by adenosine A2a receptors. A complex of adenosine A2a receptors, src non-receptor kinases and Trk receptor kinases is depicted in the lipid raft portion of the plasma membrane. This complex is also known to reside in non-lipid raft membrane. Adenosine A2a receptors have 7 transmembrane domains, src associates with membranes through lipid modification and Trk receptors have a single transmembrane domain. Binding of adenosine (yellow star) to adenosine A2a receptors leads to activation of src, which then phosphorylates Trk receptors. Phosphorylated Trk receptors, through a series of associated proteins (not shown) leads to the activation of downstream signaling molecules such as MAP kinase and PI3’K. Activity of these signaling molecules influences the vulnerability of neurons to toxic insults. Several aspects of this model are not well-defined. First, it is not known whether these proteins exist in a tri-molecular complex and/or multiple binary complexes. Second, it is not known if these proteins exist as a complex constitutively or whether their association is dynamic. Third, it is not known if there are differences in the qualitative and/or quantitative nature of the signals derived from lipid raft versus non-lipid raft complexes. Fourth, it is not known if this complex exists in intracellular membranes (i.e., endosomes or the Golgi) and how this influences the signaling landscape. Fifth, the stoichometric composition of complex(es) is not known.
