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No doubt, Van Aelst clarifies that the loss of bad results OPHN1 signaling destabilization of the structure of dendritic spines and synaptic AMPA receptors, resulting in impaired synaptic plasticity and, possibly, spines and NMDA receptors. This string events was observed in rats permanently.
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The protein normally encoded by the gene OPHN1 belongs to what scientists call the Rho subfamily of G proteins The members of this family are known to be key regulators of the actin cytoskeleton and affect many aspects of neuronal development, says Van Aelst . The actin cytoskeleton is gauze, thread-like structure that provides the scaffolding for the content of the cell. All mutations that we have in mind OPHN1 gene OPHN1 proteins that do not work, said Van Aelst. This naturally raised the question of what the normal function of the protein is at the level of excitatory synapses, and what goes wrong when he developed a genetic mutation.
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Another way to promote axon regeneration, based on the results of the team, could directly stimulate the signaling pathway that SOCS3 inhibits, known as JAK / STAT, adds Fang Sun, Ph.D., who shares Fatherhood first post with Patrice Smith, PhD (both also FM Kirby Neurobiology Center at Children’s Hospital in Boston). Sun is currently testing some STAT activators.
In the new study, he and his colleagues used a second set of genetic techniques in mice to delete a suppressor of inflammatory signaling, known as SOCS3, in retinal ganglion cells – and saw the axonal growth after solid lesion. The greatest effect was observed after one week, when there were signs that the mTOR pathway has been reactivated.