1 min read

ID: 1108563

Short Link: https://gregory-ms.com/articles/1108563/

Discovery Date: 24 November 2022, 18:21:01 UTC

Published Date: 2022-11-24 11:00:00

Source: PubMed

Link: https://pubmed.ncbi.nlm.nih.gov/36420826/?fc=20210216052009&ff=20221124132014&v=2.17.8

Manual Selection: none

Machine Learning Gaussian Naive Bayes Model: false

Abstract

Biol Open. 2022 Nov 24:bio.059634. doi: 10.1242/bio.059634. Online ahead of print.

ABSTRACT

The adherens junction component, alpha-T-catenin (aTcat) is an established contributor to cardiomyocyte junction structure and function, but recent genomic studies link CTNNA3 polymorphisms to diseases with no clear cardiac underpinning, including asthma, autism and multiple sclerosis, suggesting causal contributions from a different cell-type. We show Ctnna3 mRNA is highly expressed in peripheral nerves (e.g., vagus and sciatic), where aTcat protein enriches at paranodes and myelin incisure adherens junctions of Schwann cells. We validate aTcat immunodetection specificity using a new Ctnna3-knockout fluorescence reporter mouse line yet find no obvious Schwann cell loss-of-function morphology at the light microscopic level. CTNNA3/Ctnna3 mRNA is also abundantly detected in oligodendrocytes of the central nervous system via public databases, supporting a general role for aTcat in these unique cell-cell junctions. These data suggest that the wide range of diseases linked to CTNNA3 may be through its role in maintaining neuroglial functions of central and peripheral nervous systems.

PMID:36420826 | DOI:10.1242/bio.059634

Noun Phrases in Title

  • Alpha-T-catenin
  • peripheral nerves
  • a constituent
  • Schwann cell adherens junctions
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