Cell signalling
Can connexin43 work inside the nucleus?
Open access · cc by · source: Europe PMC
Cx43 sits at the nuclear envelope, enters via Importin-β, forms active nuclear channels in HEK293 cells and cardiomyocytes, and can change gene expression during myogenic differentiation.
How this study connects
Role on claims
Each row is a claim on a concept or method page where this paper supports, challenges, or qualifies the statement. Roles are hand-checked — not a model guess.
Not yet placed on a claim. This paper has study layers, but no concept page yet cites it as support, challenge, or qualifier.
Study at a glance
- Design
- Animal / in-vitro — Cell, tissue, and patch-clamp work showing Cx43 at the nuclear envelope of cultured cells and cardiac tissue
- N
- N=1 · Mechanistic study in HEK293 Cx43+ cells, adult primary cardiomyocytes, cardiomyoblasts, and cardiac tissue (not a clinical cohort)
- Population
- Cultured HEK293 cells, adult primary cardiomyocytes, cardiomyoblasts, and cardiac tissue
- Outcome
- Nuclear-envelope localization of Cx43, Importin-β-dependent translocation, nuclear channels, and transcriptome effects
Structured fields used in claim comparison tables when every cited study has a complete layer.
Inspect source passages
Can connexin43 work inside the nucleus?
These passages occur verbatim in the stored paper text. They support the points listed below; they do not verify every statement in the explanation.
Cx43 localizes to the nuclear envelope of different cell types and cardiac tissue.
we demonstrate that Cx43 localizes to the nuclear envelope of different cell types and in cardiac tissue.
Nuclear translocation of Cx43 relies on Importin-β.
We show that translocation of Cx43 to the nucleus relies on Importin-β, and that Cx43 significantly impacts the cellular transcriptome, likely by interacting with transcriptional regulators.
Key findings
Full-length Cx43 localizes to the nuclear envelope in multiple cell types and cardiac tissue. Nuclear entry needs Importin-β. Patch-clamp showed active nuclear-envelope channels, consistent with small-molecule nucleocytoplasmic shuttling. Nuclear Cx43 accumulates during cardiomyoblast differentiation.
Methodology
Used biochemistry, super-resolution and immunogold EM, Importin-β dependence tests, transcriptome readouts, and nuclear patch-clamp in HEK293 cells and adult primary cardiomyocytes.
Limitations
This is not a patient trial of a Cx43 drug; nuclear channel function in vivo human heart disease remains to be proven.
Related papers in this topic
Same topic cluster — not a recommendation engine.