Figure - PMC

Skip to main content

An official website of the United States government

Here's how you know

Here's how you know

Official websites use .gov
A .gov website belongs to an official government organization in the United States.

Secure .gov websites use HTTPS
A lock ( ) or https:// means you've safely connected to the .gov website. Share sensitive information only on official, secure websites.

View full-text article in PMC

. 2020 Mar 6;10:4189. doi: 10.1038/s41598-020-60699-8

Search in PMC
Search in PubMed
View in NLM Catalog
Add to search

© The Author(s) 2020

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 license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license 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 license, visit http://creativecommons.org/licenses/by/4.0/.

PMC Copyright notice

Optic nerves of adult TTR null mice display higher concentrations of phosphorylated AKT compared to wild type mice. (A) Western blot analysis of total protein lysate (5 µg) from optic nerves of wild type and TTR null mice (n = 18–20 optic nerves from 9–10 mice per genotype), identifying bands of corresponding molecular weights for proteins: pAKT, AKT, pERK1, pERK2, ERK1, ERK2, β-actin and TTR. (B) Densitometric analysis of immunoblots (n = 3) comparing wild type and TTR null mice displayed as a phosphorylated to non-phosphorylated protein ratio for AKT and ERK1, ERK2, normalised against β-actin. (C) Densitometric analysis of immunoblots (n = 3) from comparing the fold change of TTR null to wild type mice of phosphorylated to non-phosphorylated AKT, ERK1 and ERK2. (D) Immunoprecipitation and Western blotting of AKT, ERK1 and ERK2 from total protein lysates (100 µg) (n = 18–20 optic nerves from 9–10 mice per genotype). (E) Densitometric analysis of immunoblots (n = 3) following immunoprecipitation of anti-AKT, anti-ERK1 and anti-ERK2 directly comparing wild type and TTR null mice displayed as a phosphorylated to non-phosphorylated protein ratio, normalised against β-actin. (F) Densitometric analysis of immunoblots (n = 3) following immunoprecipitation comparing the fold change of TTR null to wild type mice of phosphorylated to non-phosphorylated AKT, ERK1 and ERK2. (G) Regions of the lateral corpus callosum in wild type and TTR null mice at ages P21 selected for image analysis to identify localisation of pAKT in mature oligodendrocytes (10 µm formalin fixed paraffin embedded sections, scale bar 1 mm). (H) Immunofluorescent images obtained from the lateral corpus callosum of P21 wild type null mice displaying colocalisation of pAKT around the nuclei of Sox10- CC1-positive oligodendrocytes (yellow arrows). Panels top to bottom: DAPI, CC1, Sox10, pAKT merge; DAPI, pAKT; Sox10, pAKT; CC1, pAKT (scale bar 50 µm). (I) Immunofluorescent images obtained from the lateral corpus callosum of P21 TTR null mice displaying increased colocalisation of pAKT around the nuclei of Sox10- CC1-positive oligodendrocytes (yellow arrows). Panels top to bottom: DAPI, CC1, Sox10, pAKT merge; DAPI, pAKT; Sox10, pAKT; CC1, pAKT (scale bar 50 µm).