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. 2024 Feb 8;25(3):1022–1054. doi: 10.1038/s44319-024-00075-z

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© The Author(s) 2024

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/. Creative Commons Public Domain Dedication waiver http://creativecommons.org/publicdomain/zero/1.0/ applies to the data associated with this article, unless otherwise stated in a credit line to the data, but does not extend to the graphical or creative elements of illustrations, charts, or figures. This waiver removes legal barriers to the re-use and mining of research data. According to standard scholarly practice, it is recommended to provide appropriate citation and attribution whenever technically possible.

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Figure EV2 — (A) LINC00313 levels in HuCCT1 or Huh28 treated with MEK, p38, JNK or PI3K inhibitors, with or without TGFβ1 stimulation for 16 h (n = 3 biological replicates). (B) Immunoblotting for detection of phosphorylated p44/42 (Thr202/Tyr204), phosphorylated p-SAPK/JNK (Thr183/Tyr185), phosphorylated AKT (Ser473), phosphorylated p38 (Thr180/Tyr182), phosphorylated MAPKAPK-2 (Thr334), total p44/42, SAPK/JNK and AKT protein levels and β-tubulin (used as a loading control) in HuCCT1 cells treated with MEK, p38, JNK or PI3K inhibitors, with or without TGFβ1 stimulation for 16 h. DMSO was used as a vehicle treatment. (C) Immunoblotting for detection of the p38 isoforms p38α, p38β, p38γ and p38δ in HuCCT1 cells transiently silenced for MAPK11 or MAPK12 or MAPK13 or MAPK14 and treated or not with TGFβ1 for 16 h. β-tubulin was used as a loading control. (D) Real-time qPCR analysis of LINC00313, MAPK11, MAPK12, MAPK13 and MAPK14 expression in HuCCT1 and Huh28 cell lines transiently transfected with siRNAs targeting MAPK11 or MAPK12 or MAPK13 or MAPK14 and treated or not with TGFβ1 for 16 h. Data information: In Panel (A) data are presented as mean ± SD (n = 3 biological replicates). In panel (D) data are presented as single data points (n = 2 biological replicates). *P ≤ 0.05, **P ≤ 0.01, n.s.: not significant (Student’s t-test). Source data are available online for this figure.