Published June 24, 2025 | Version 1.0
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Image: Paracingulin controls the junctional accumulation of nonmuscle myosin-2 in endothelial cells in vivo

  • 1. Department of Molecular and Cellular Biology, University of Geneva

Contributors

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  • 1. Department of Molecular and Cellular Biology, University of Geneva

Description

Extended Data Figure Legend: A) Validation of Crispr/Cas9-mediated deletion of CGNL1 in two distinct clonal lines of bEnd.3 cells by genomic sequencing. The WT sequence is shown on top. B) Validation of KO by immunoblotting analysis of the expression of CGNL1, NM2A, NM2B and ZO-1 in WT and CGNL1-KO bEnd.3 cells. Beta-tubulin was used as a loading control. Numbers on the left refer to migration of molecular weight standards.

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Additional details

Related works

Is part of
Journal article: 10.17912/micropub.biology.001602 (DOI)

Funding

We thank the Swiss National Science Foundation (Grants N. 31003A_135730, 31003A_152899, 31003A_172809, 310030_200681 to S.C.) and the State of Geneva for generous and continuous support.

Dates

Accepted
2025-06-23