The Schwann cell promoter is present in the downstream region of the human dystrophin gene that gives shortened transcript that are again synthesized in a tissue-specific manner.

[4] The vertebrate nervous system relies on the myelin sheath for insulation and as a method of decreasing membrane capacitance in the axon.

Following this process, the Schwann cells can guide regeneration by forming a type of tunnel that leads toward the target neurons.

Successful axons can, therefore, reconnect with the muscles or organs they previously controlled with the help of Schwann cells, but specificity is not maintained and errors are frequent, especially when long distances are involved.

[8][9] When SOX10 is inactivated in mice, satellite glia and Schwann cell precursors fail to develop, though neurons are generated normally without issue.

[8] In the absence of SOX10, neural crest cells survive and are free to generate neurons, but glial specification is blocked.

It is required for neural crest cells to migrate past the site of dorsal root ganglia to find the ventral regions of sympathetic gangliogenesis.

In mice that lack the transmembrane III isoform, Schwann cell precursors are eventually eliminated from spinal nerves.

[18] Several important transcription factors are also expressed and involved at various stages in development changing the features on the Schwann cells from an immature to mature state.

It has been shown to control a set of genes responsible for interfering with this feature in the axon changing it from a pro-myelinating to myelinating state.

[19] In this way, in Krox-20 double knock out mice, it has been recorded that hindbrain segmentation is affected as well as myelination of Schwann cell associated axons.

In addition, recent studies have also proven the importance of this transcription factor in maintaining the myelination phenotype (and requires the co-expression of Sox 10) as its inactivation leads to dedifferentiation of the Schwann cells.

[20] A number of experimental studies since 2001 have implanted Schwann cells in an attempt to induce remyelination in multiple sclerosis-afflicted patients.

[21] In the past two decades, many studies have demonstrated positive results and potential for Schwann cell transplantation as a therapy for spinal cord injury, both in aiding regrowth and myelination of damaged CNS axons.

[22] Schwann cell transplants in combination with other therapies such as Chondroitinase ABC have also been shown to be effective in functional recovery from spinal cord injury.