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. 2022 Dec 22;8:137. doi: 10.1038/s41421-022-00502-2

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© The Author(s) 2022

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/.

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Fig. 7 — Left, active PAPP-A dimer is able to bind the IGFBP–IGF at the exosites and cleaves IGFBP at the active sites, releasing the bioactive IGF to promote cell proliferation, cell invasion, cell migration, etc. Right, PAPP-A is inactive when complexed with either proMBP or STC2 at the exosites. Higher proMBP concentration leads to compromised PAPP-A activity and restricts fetal growth. STC2 could also modulate PAPP-A activity and block the downstream IGF receptor (IR)-mediated signaling.