ArticleMolecular medicine reports2017
Molecular mechanism of smurf2 in regulating the expression of SnoN in diabetic nephropathy.
Article in Molecular medicine reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 18 citations in OpenAlex.
- FOXO6 inhibits SMURF2-mediated ubiquitination and degradation of NR4A1 to promote retinal pigment epithelial cell ferroptosis in diabetic retinopathy.Journal of cell communication and signaling · 2026Article
- Smurf2 knockdown attenuates the progression of diabetic nephropathy by inhibiting mesangial cell proliferation and fibrosis through suppressing EYA2 ubiquitination.Renal failure · 2025Article
- Capilliposide A attenuates diabetic nephropathy via modulation of NF-κB/TLR4 and apoptotic pathways.Scientific reports · 2025Article
- Regulation of transforming growth factor-β signalling by SUMOylation and its role in fibrosis.Open biology · 2021Article
- The HECT ubiquitin E3 ligase Smurf2 degrades μ-opioid receptor 1 in the ubiquitin-proteasome system in lung epithelial cells.American journal of physiology. Cell physiology · 2019Article
- Transcriptional cofactors Ski and SnoN are major regulators of the TGF-β/Smad signaling pathway in health and disease.Signal transduction and targeted therapyArticle
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The aim of the present study was to examine the regulatory mechanism underlying the depression in Ski‑related novel protein N (SnoN) in diabetic nephrology (DN). NRK‑52E cells, a rat primary renal tubular epithelial cell line, were cultured to clarify the effect of small mothers against decapentaplegic (Smad) ubiquitination regulatory factor 2 (smurf2) on SnoN in a low glucose environment in vitro. NRK‑52E cells and DM rats were injected with adenoviruses AD‑smurf2 and AD‑shsmurf2, respectively, and the protein expression profiles of SnoN, smurf2 and phosphorylated (p)‑Smad2 were then detected. In addition, the protein levels of smurf2, p‑Smad2 and SnoN were analyzed following treatment with transforming growth factor (TGF)‑β1 or TGF‑β1 inhibitor to validate the effect of the TGF‑β1/Smad signaling pathway. The effect of smurf2 on the degradation of SnoN by ubiquitination was found to be a key factor in DN, which was mediated by the TGF‑β1/Smad signaling pathway.
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