Nectins and Nectin-like molecules drive vascular development and barrier function.

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      Publisher: Springer Country of Publication: Germany NLM ID: 9814575 Publication Model: Print-Electronic Cited Medium: Internet ISSN: 1573-7209 (Electronic) Linking ISSN: 09696970 NLM ISO Abbreviation: Angiogenesis Subsets: MEDLINE
    • Publication Information:
      Publication: Dec. 2004- : Berlin : Springer
      Original Publication: London ; Philadelphia : Rapid Science Publishers,
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    • Abstract:
      Angiogenesis, barriergenesis, and immune cell migration are all key physiological events that are dependent on the functional characteristics of the vascular endothelium. The protein family of Nectins and Nectin-like molecules (Necls) is a group of cell adhesion molecules that are widely expressed by different endothelial cell types. The family includes four Nectins (Nectin-1 to -4) and five Necls (Necl-1 to -5) that either interact with each other by forming homo- and heterotypical interactions or bind to ligands expressed within the immune system. Nectin and Necl proteins are mainly described to play a role in cancer immunology and in the development of the nervous system. However, Nectins and Necls are underestimated players in the formation of blood vessels, their barrier properties, and in guiding transendothelial migration of leukocytes. This review summarizes their role in supporting the endothelial barrier through their function in angiogenesis, cell-cell junction formation, and immune cell migration. In addition, this review provides a detailed overview of the expression patterns of Nectins and Necls in the vascular endothelium.
      (© 2023. The Author(s), under exclusive licence to Springer Nature B.V.)
    • Comments:
      Erratum in: Angiogenesis. 2023 Apr 29;:. (PMID: 37119333)
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    • Contributed Indexing:
      Keywords: Adherens junction; Angiogenesis; Endothelial cells; Migration; Nectin; Nectin-like molecule
    • Accession Number:
      0 (Nectins)
      0 (Cell Adhesion Molecules)
    • Publication Date:
      Date Created: 20230303 Date Completed: 20230710 Latest Revision: 20231218
    • Publication Date:
      20231218
    • Accession Number:
      10.1007/s10456-023-09871-y
    • Accession Number:
      36867287