ArticleBioengineered2022
Src-homology domain 2 containing protein tyrosine phosphatase-1 (SHP-1) directly binds to proto-oncogene tyrosine-protein kinase Src (c-Src) and promotes the transcriptional activation of connexin 43 (Cx43).
Article in Bioengineered, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 2 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
2 citing papers in PubMed, 1 citations in OpenAlex.
- Cx43 modulates malignant phenotypes in bladder cancer cells via the c-Src/PTEN/FAK axis.Journal of molecular histology · 2026Article
- SHP-1 alleviates atrial fibrosis in atrial fibrillation by modulating STAT3 activation.Experimental biology and medicine (Maywood, N.J.) · 2023Article
Corrections and comments
- Retracted
Authors and funding
5 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The prevalence of atrial fibrillation (AF), which is one of the common arrhythmias in clinics, is increasing sharply and has affected millions of patients, which is expected to triple by 2050. The purpose of the study was to explore the regulatory relationship between Src-homology domain 2 containing protein tyrosine phosphatase-1 (SHP-1) and proto-oncogene tyrosine-protein kinase Src (c-Src) and the regulation of Connexins 43 (Cx43), and its effect on AF was also studied. Mouse atrial myocyte line (HL-1 cell line) was used as the research object. After overexpression of SHP-1, the expressions of p-c-Src, Cx43, and SHP-1 were detected by Western blot and cellular immunofluorescence, respectively. The location and interaction of SHP-1 and c-Src in the cells were detected by immunofluorescence co-localization and co-immunoprecipitation (Co-IP). The regulation of c-Src and Cx43 was detected by DNA pull down, chromatin co-immunoprecipitation (CHIP), and dual-luciferase reporter system. The results revealed that overexpression of SHP-1 could inhibit the phosphorylation and activation of c-Src and increase the expression of Cx43. Moreover, there was a direct binding between SHP-1 and c-Src, and c-Src could bind to the promoter region of Cx43 and inhibit the transcription of Cx43. In conclusion, SHP-1 could bind to c-Src and inhibit the activity of c-Src, thus enhancing the transcriptional activation of Cx43 and improving the function of gap junction.
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Registered trials
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