Correction: CHIP induces ubiquitination and degradation of HMGB1 to regulate glycolysis in ovarian endometriosis
This correction identifies the co-corresponding authors for a paper investigating how CHIP induces HMGB1 ubiquitination and degradation to regulate glycolysis in ovarian endometriosis.
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This document is a formal correction notice published in Cellular and Molecular Life Sciences, issued to rectify an omission in the authorship details of a previously published article. The authors identified that the co-corresponding authors, Chune Ren and Zhenhai Yu, were incorrectly listed in the original version and have now been added to the official record. The text contains no new scientific data or experimental findings, serving solely to update the metadata associated with the prior publication regarding CHIP-induced ubiquitination of HMGB1. Relevance to endometriosis: This paper is centrally about ovarian endometriosis, as it corrects the authorship of a study investigating the molecular mechanisms regulating glycolysis within this specific condition.
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Cited by (5)
- PRMT3-mediated FOXO1 arginine methylation exacerbates oxidative stress-induced decidualization defects in the eutopic endometrium of endometriosis 2025
- Ubiquitination of PFKFB4 by CHIP regulates glycolysis and progression in endometriosis† 2025
- PRMT3-mediated FOXO1 arginine methylation exacerbates oxidative stress-induced decidualization defects in the eutopic endometrium of endometriosis 2025
- Ubiquitination of PFKFB4 by CHIP regulates glycolysis and progression in endometriosis† 2025
- Ubiquitination of PFKFB4 by CHIP Regulates Glycolysis and Progression in Endometriosis 2024
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