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. 2023 Sep 26;18:67. doi: 10.1186/s13024-023-00659-8

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© The Author(s) 2023

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated in a credit line to the data.

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Fig. 1 — Static imaging of GFP-BAX expressing cells in BALB/cByJ mice showing the time course for GFP-BAX translocation as a function of time after optic nerve crush (ONC). Previously, we had documented that the translocated GFP-BAX forms puncta localized to mitochondria in these cells [25]. A-F Static imaging of GFP-BAX expressing cells in retinal whole mounts at times post-ONC (pONC) showing localization changes from diffuse to punctate distribution of the fusion protein. In some cells, punctate GFP-BAX is also evident in the axon originating from the cell (arrows in B, F). Scale bar = 20 µm. G Graph showing the change in percentage of GFP-BAX transduced cells that exhibit punctate labeling pONC. A significant increase in punctate cells is evident at 3, 5, 7 and 14 days pONC relative to contralateral eyes (*P = 0.012, *** P < 0.0001, individual t-tests). This pattern is consistent with descriptions of BAX accumulation in cells of the ganglion cell layer after optic nerve damage in rats and mice reported by others [25, 32, 48, 50]