Connexin 43 drives glioblastoma cancer stem cell phenotypes through a WNK lysine-deficient protein kinase 1-c-MYC signaling axis.

doi:10.1016/j.celrep.2025.116303

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Article

Connexin 43 drives glioblastoma cancer stem cell phenotypes through a WNK lysine-deficient protein kinase 1-c-MYC signaling axis.

Cell reports - 23 Sept 2025

Mulkearns-Hubert Erin E, Hajdari Nicole, Hong Ellen S, Jacobs Ashley P, Gaboriau Aymerick, Giltner Sophia, Tannish Gavin, Kay Kristen E, Wang Sabrina Z, LaViolette Peter S, Silver Daniel J, Hubert Christopher G, Dhawan Andrew, Lathia Justin D

Abstract excerpt

The coordination of cellular processes such as growth and survival relies on communication between cells through gap junctions. Connexin proteins comprise gap junctions and also function to mediate protein-protein interactions and communication with the extracellular space via hemichannels. Despite their essential roles, connexin function in cancer is context dependent, with connexin 43 (Cx43) reported to both...

Read the complete abstract on PubMed

Topics

Connexin 43
Glioblastoma
Neoplastic Stem Cells
Humans
Signal Transduction

Methodology Data sources Editorial policy Privacy Delete account & data About Contact Helena Bioinformatics

Proto-Oncogene Proteins c-myc

Animals

Cell Line, Tumor

WNK Lysine-Deficient Protein Kinase 1

Mice

Brain Neoplasms

Phenotype

Cell Proliferation

Gap Junctions

Source

Open in PubMed Open full text

Identifiers

PMID: 40946315
DOI: 10.1016/j.celrep.2025.116303
PMCID: PMC12443334

Genes

MYC
WNK1

Provenance

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