ArticleBiochimica et biophysica acta2014
C-Src-mediated phosphorylation of δ-catenin increases its protein stability and the ability of inducing nuclear distribution of β-catenin.
Article in Biochimica et biophysica acta, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 8 citations in OpenAlex.
- δ-catenin controls layer-specific transcriptional maturation of astrocytes via Zbtb20.bioRxiv : the preprint server for biology · 2026Article
- Effects of the carcinogen TCDD on δ-catenin stability and tumorigenic potential in prostate cancer cells.American journal of cancer research · 2025Article
- δ-catenin promotes Twist1 stabilization in prostate cancer through ubiquitination modification.American journal of cancer research · 2024Article
- δ-Catenin promotes cell migration and invasion via Bcl-2-regulated suppression of autophagy in prostate cancer cells.American journal of cancer research · 2022Article
- bFGF-mediated phosphorylation of δ-catenin increases its protein stability and the ability to induce the nuclear redistribution of β-catenin.American journal of cancer research · 2021Article
- Article
- Genetic alterations of δ-catenin/NPRAP/Neurojungin (CTNND2): functional implications in complex human diseases.Human genetics · 2016Review
- Early signaling dynamics of the epidermal growth factor receptor.Proceedings of the National Academy of Sciences of the United States of America · 2016Article
- Interaction of EGFR to δ-catenin leads to δ-catenin phosphorylation and enhances EGFR signaling.Scientific reports · 2016Article
Corrections and comments
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Authors and funding
12 authors at 4 institutions in 2 countries.
Funding
Abstract
Although δ-catenin was first considered as a brain specific protein, strong evidence of δ-catenin overexpression in various cancers, including prostate cancer, has been accumulated. Phosphorylation of δ-catenin by Akt and GSK3β has been studied in various cell lines. However, tyrosine phosphorylation of δ-catenin in prostate cancer cells remains unknown. In the current study, we demonstrated that Src kinase itself phosphorylates δ-catenin on its tyrosine residues in prostate cancer cells and further illustrated that Y1073, Y1112 and Y1176 of δ-catenin are predominant sites responsible for tyrosine phosphorylation mediated by c-Src. Apart from c-Src, other Src family kinases, including Fgr, Fyn and Lyn, can also phosphorylate δ-catenin. We also found that c-Src-mediated Tyr-phosphorylation of δ-catenin increases its stability via decreasing its affinity to GSK3β and enhances its ability of inducing nuclear distribution of β-catenin through interrupting the integrity of the E-cadherin. Taken together, these results indicate that c-Src can enhance the oncogenic function of δ-catenin in prostate cancer cells.
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