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. 2019 Sep 14;25:44. doi: 10.1186/s10020-019-0111-4

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© The Author(s) 2019

Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided 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 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.

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Fig. 3 — PRSS1_R116C enhances malignant phenotypes in pancreatic cancer via the JAK1/STAT5 pathway. a. Trypsin was co-localized with PAR2; b. Effect of PRSS1_R116C mutant/PRSS1 wild type overexpression on trypsin and PAR2 expression levels. c. RNA-seq was performed to assess the mRNA expression levels of critical proteins in the JAK-STAT pathway; d. qRT-PCR was applied to confirm the mRNA levels of critical proteins in the JAK1-STAT5 pathway; e. Western blot measurement of tumor relevant proteins