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. 2023 Nov 8;24:43. doi: 10.1186/s12865-023-00582-z

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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. 2 — Time course of p38 mitogen-activated protein kinase (MAPK) and heat shock protein (HSP) 27 activation in HaCaT cells treated with pemphigus vulgaris (PV) sera and AK23 monoclonal antibody. (A, B) (with the exception of 0 h group as blank control ant it is not treated with any reagent), Peaks of phospho-p38 MAPK (p-p38 MAPK) and phospho-HSP27 were detected by western blot. (C, D) Densitometric analysis was derived from the ratios of p-p38 MAPK to p38 MAPK and p-HSP27 to HSP27 expression in each group and normalized to the 0 h group. Peak activation of p38 MAPK and HSP27 by PV sera and AK23 occurred around 0.5–2 h. Levels of total p38 MAPK and HSP27 are shown as loading controls (n = 3)