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. 2023 Jul 25;80(8):228. doi: 10.1007/s00018-023-04876-8

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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/.

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Fig. 6 — Subnuclear dynamics of the association of Jacob with LaminB1 and CREB are regulated by nuclear [Ca.²⁺]_n transients. Synaptic NMDAR activity leads to an active dynein-dependent transport of Jacob from activated synapses to the nucleus (1; [31, 37]). In the nucleus, Jacob is present in the nucleoplasm and in association with the nuclear lamina via a direct interaction with LaminB1 [38]. Association of Jacob with LaminB1 captures the history of previous NMDAR activity in the sense that the number of docked molecules reflects previous activation of GluN2B-containing NMDAR. (2) Blocking of NMDAR activity with APV and ifenprodil reduced the binding under basal glutamatergic transmission [38]. Concomitantly, an increase in nuclear calcium transients results in liberation of Jacob from the complex with LaminB1 (3, 4) which is followed by binding to the transcription factor CREB (3, 4)