Publications
Neuronal subtypes show diverse injury responses, but the molecular underpinnings remain elusive. Using transgenic mice that allow reliable visualization of axonal fate, we demonstrate that intrinsically photosensitive retinal ganglion cells (ipRGCs) are both resilient to cell death and highly regenerative. Read more “Thrombospondin-1 Mediates Axon Regeneration in Retinal Ganglion Cells”
![Figure 4 Dusp14 regulates axon regeneration through dephosphorylation of the MAPK family in vivo. (A) No change in Dusp14 expression was detectable at 5 and 14 days after optic nerve crush. (B) Dusp14 expression decreased after intravitreal injection of AAV2-Dusp14-shRNA in vivo (arrows). (C–F) Dusp14 knockdown significantly increased the number of pERK1/2-positive cells (D) and pERK1/2 fluorescent intensity (E) in retinas treated with BDNF. (*P < 0.05, Student's t-test; n = 4 [D, E]) Scale bars: 25 μm in (A) to (C), 500 μm in (D). Error bars, SEM.](https://i0.wp.com/idsc.miami.edu/wp-content/uploads/2020/12/axon-regeneration-940x530-1.jpg?resize=730%2C350&ssl=1)
Publications
Adult central nervous system (CNS) neurons are unable to regenerate their axons after injury. Krüppel-like transcription factor (KLF) family members regulate intrinsic axon growth ability in vitro and in vivo, but mechanisms downstream of these transcription factors are not known. Read more “The Krüppel-Like Factor Gene Target Dusp14 Regulates Axon Growth and Regeneration”
Publications
Axon regeneration is a necessary step toward functional recovery after spinal cord injury. The AP-1 transcription factor c-Jun has long been known to play an important role in directing the transcriptional response of Dorsal Root Ganglion (DRG) neurons to peripheral axotomy that results in successful axon regeneration. Read more “The Effect of Jun Dimerization on Neurite Outgrowth and Motif Binding”
Publications
Several studies have demonstrated that the intrinsic ability of neurons to regenerate their axons can be stimulated by maneuvers that favor the open state of chromatin, such as inhibiting histone deacetylase activity or increasing histone acetyltransferase activity. Taken together, these experiments suggest . . . Read more “Can Chromatin Accessibility be Exploited for Axon Regeneration?”