ArticleActa biochimica et biophysica Sinica2022
PHD3 inhibits cell proliferation through hydroxylation of PAX2 at proline 9.
Article in Acta biochimica et biophysica Sinica, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed, 4 citations in OpenAlex.
- miR-373-3p promotes aerobic glycolysis in colon cancer cells by targeting MFN2.Acta biochimica et biophysica Sinica · 2024Article
- The P124A mutation of SRP14 alters its migration on SDS-PAGE without impacting its function.Acta biochimica et biophysica Sinica · 2024Article
- PHD3 inhibits colon cancer cell metastasis through the occludin-p38 pathway.Acta biochimica et biophysica Sinica · 2023Article
- Co-Expression of MultipleInternational journal of molecular sciences · 2023Article
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The oncoprotein transcription factor paired box 2 (PAX2) is aberrantly expressed in cancers, but the underlying mechanism remains elusive. Prolyl hydroxylase 3 (PHD3) hydroxylates the proline residue of HIFα, mediating HIFα degradation. The von Hippel-Lindau protein (pVHL) is an E3 ligase which mediates ubiquitination and degradation of hydroxylated HIFα. PHD3 and pVHL are found to inhibit the expression of PAX2, however, the molecular mechanism is unclear. Here we demonstrate that PHD3 hydroxylates PAX2 at proline 9, which is required for pVHL to mediate PAX2 ubiquitination and degradation. Overexpression of PHD3 enhances prolyl hydroxylation, ubiquitination and degradation of PAX2 with little effect on those of PAX2(P9A). PHD3 does not influence PAX2 expression in
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