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 Oct 22;11(10):891. doi: 10.1038/s41419-020-03112-6

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

Fig. 4 — A, B Celf1 protein level was repressed by miR-322/-503 overexpression (OE) in C2C12-CUG200 cells. C, D Celf1 protein level was repressed by miR-322/-503 OE in HEK293T cells. E A mutual binding site of miR-322/-503 on Celf1-3′UTR was predicted by RNA22. F miR-322/-503 significantly repressed the relative luciferase activity of luciferase reporter that contained wild-type Celf1-3′UTR. However, the repression was abolished if the predicted binding sites of miR-322/-503 was mutated (Celf1-3′UTR-mut). G, H The knockdown of Celf1 in C2C12-CUG200 cells was verified by western blot. I Celf1 knockdown significantly upregulated the expressions of myogenic markers (MyoD, MyoG, and Mef2C) and downregulated Celf1 expression during C2C12-CUG200 differentiation. All expression levels were normalized to the control group at day 0. J Celf1 knockdown promoted myotube formation during C2C12-CUG200 differentiation. Myotube formation was displayed by immunostaining of MF20 on day 6. K Celf1 knockdown increased myotube areas (left) and fusion index (right) of C2C12-CUG200 differentiation. L, M Celf1 knockdown did not repress ribonuclear foci formation in C212-CUG200 cells. The ribonuclear foci were detected with CAG probe RNA FISH. Control, pLL4.0 vector stable transfection; miR-322/-503, pLL4.0-miR-322/-503 stable transfection; pLL4.0, pLL4.0 vector transient transfection; pLL4.0-miR-322/-503, pLL4.0-miR-322/-503 transient transfection; scramble, C2C12-CUG200/scramble cells; shCelf1, C2C12-CUG200/shCelf1 cells; * statistically significant (p < 0.05); ns not statistically significant.