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. 2023 Nov 13;16:1241420. doi: 10.3389/fnmol.2023.1241420

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Copyright © 2023 Kropf, Shekari, Jaberi, Puri, Wu and Fahnestock.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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ProNGF-KKE at axon terminals induces greater neurotrophic activity at cell bodies than proNGF-Δ9-13. ProNGF-Δ9-13, proNGF-KKE, or inactivated proNGF were applied to rat BFCN axon terminals for 15 min, followed by quantification of signaling factor activation at BFCN cell bodies. ProNGF-KKE (B) caused greater activation (phosphorylation) of the neurotrophic signaling factor, ERK, compared to proNGF-Δ9-13 (A) and inactivated proNGF (C). pERK is shown in green, total ERK in red, and DAPI in blue. DIV: days in vitro. (D) Quantification of the images shown in A–C. Error bars represent SEM. N = 30 images/group taken from three chambers in three independent experiments. ***p < 0.001, ****p < 0.0001. Scale bars: 10 μm.