![]() ![]() Accordingly, neuronal knockout of Atf4, but not of Chop, recapitulates the neuroprotection afforded by Perk deficiency, and Perk or Atf4 knockout impairs optic axon regeneration enabled by disrupting the tumor suppressor Pten. Using conditional knockout mice, we instead find that a canonical Atf4 response, inclusive of a modest contribution by Chop, couples pro-apoptotic and pro-regenerative transcription as the principal mediator of the stress-responsive kinase Perk. ![]() ![]() Results from CRISPR-based screening and chromatin accessibility profiling have suggested that two distinct neurodegenerative programs, mediated by Activating transcription factor-4 (Atf4) and C/ebp homologous protein (Chop), respectively, may operate independently of pro-regenerative programs after optic nerve injury. SummaryThe extent to which injury-activated transcriptional programs for apoptosis are mechanistically linked to those for axon regeneration has implications for efforts to promote neuronal survival without limiting CNS repair potential. ![]()
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