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DLK is required for the majority of gene expression changes in RGCs initiated by injury, including induction of both proapoptotic and regeneration-associated genes. Deletion of DLK in retina results in robust and sustained protection of RGCs from degeneration after optic nerve injury. Despite this improved survival, the number of axons that regrow beyond the injury site is substantially reduced, even when the tumor suppressor phosphatase and tensin homolog (PTEN) is deleted to enhance intrinsic growth potential. These findings demonstrate that these seemingly contradictory responses to injury are mechanistically coupled through a DLK-based damage detection mechanism.<\/jats:p>","DOI":"10.1073\/pnas.1211074110","type":"journal-article","created":{"date-parts":[[2013,2,20]],"date-time":"2013-02-20T01:56:59Z","timestamp":1361325419000},"page":"4039-4044","update-policy":"https:\/\/doi.org\/10.1073\/pnas.cm10313","source":"Crossref","is-referenced-by-count":327,"title":["DLK initiates a transcriptional program that couples apoptotic and regenerative responses to axonal injury"],"prefix":"10.1073","volume":"110","author":[{"given":"Trent A.","family":"Watkins","sequence":"first","affiliation":[{"name":"Neurodegeneration Laboratories, Department of Neuroscience,"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Bei","family":"Wang","sequence":"additional","affiliation":[{"name":"Neurodegeneration Laboratories, Department of Neuroscience,"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Sarah","family":"Huntwork-Rodriguez","sequence":"additional","affiliation":[{"name":"Neurodegeneration Laboratories, Department of Neuroscience,"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jing","family":"Yang","sequence":"additional","affiliation":[{"name":"Neurodegeneration Laboratories, Department of Neuroscience,"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Zhiyu","family":"Jiang","sequence":"additional","affiliation":[{"name":"Neurodegeneration Laboratories, Department of Neuroscience,"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jeffrey","family":"Eastham-Anderson","sequence":"additional","affiliation":[{"name":"Department of Pathology,"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Zora","family":"Modrusan","sequence":"additional","affiliation":[{"name":"Department of Molecular Biology, and"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Joshua S.","family":"Kaminker","sequence":"additional","affiliation":[{"name":"Department of Bioinformatics and Computational Biology, Genentech, Inc., South San Francisco, CA 94080"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Marc","family":"Tessier-Lavigne","sequence":"additional","affiliation":[{"name":"Neurodegeneration Laboratories, Department of Neuroscience,"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Joseph W.","family":"Lewcock","sequence":"additional","affiliation":[{"name":"Neurodegeneration Laboratories, Department of Neuroscience,"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"341","published-online":{"date-parts":[[2013,2,19]]},"reference":[{"key":"e_1_3_3_1_2","doi-asserted-by":"publisher","DOI":"10.1167\/iovs.07-0542"},{"key":"e_1_3_3_2_2","first-page":"774","article-title":"Retinal ganglion cell death in experimental glaucoma and after axotomy occurs by apoptosis","volume":"36","author":"Quigley HA","year":"1995","unstructured":"HA Quigley, et al., Retinal ganglion cell death in experimental glaucoma and after axotomy occurs by apoptosis. 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