Impaired Cx43 gap junction endocytosis causes morphological and functional defects in zebrafish | Zendy

Caitlin Hyland | Zendy; Michael G. Mfarej | Zendy; Giorgos Hiotis | Zendy; Sabrina Lancaster | Zendy; Noelle Novak | Zendy; M. Kathryn Iovine | Zendy; Matthias M. Falk | Zendy

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Impaired Cx43 gap junction endocytosis causes morphological and functional defects in zebrafish

Author(s) -

Caitlin Hyland,

Michael G. Mfarej,

Giorgos Hiotis,

Sabrina Lancaster,

Noelle Novak,

M. Kathryn Iovine,

Matthias M. Falk

Publication year - 2021

Publication title -

molecular biology of the cell

Language(s) - English

Resource type - Journals

SCImago Journal Rank - 2.463

H-Index - 225

eISSN - 1939-4586

pISSN - 1059-1524

DOI - 10.1091/mbc.e20-12-0797

Subject(s) - gap junction , connexin , endocytosis , biology , microbiology and biotechnology , zebrafish , cytoplasm , cell junction , intracellular , cell signaling , cell , signal transduction , biochemistry , gene

It is shown for the first time that impaired gap junction turnover achieved by CRISPR/Cas9-mediated deletion of critical amino acid residues (256-289) in zebrafish causes a suite of developmental defects that include pronounced cardiovascular morphology and function.

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