Correction: Corrigendum: Ubiquitin ligase RNF20/40 facilitates spindle assembly and promotes breast carcinogenesis through stabilizing motor protein Eg5

Duan, Yang; Huo, Dawei; Gao, Jie; Wu, Heng; Zheng, Yi; Liu, Zhe; Zhang, Kai; Lin, Shan; Zhou, Xing; Wang, Yue; Su, Dongxue; Ding, Xiang; Shi, Lei; Wang, Yan; Shang, Yongfeng; Xuan, Chenghao

doi:10.1038/ncomms13462

Cited by 6 publications

(1 citation statement)

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“…For example, ubiquitin ligase RNF20/RNF40 stabilizes motor protein Eg5 to accelerate spindle assembly, and facilitates breast cancer tumorigenesis. 17 Additionally, the RNF20/RNF40 complex affects mRNA splicing and gene transcription by regulating tumor protein p53. 18 Besides, RNF20/RNF40 triggers the transcription of heat shock-responsive genes by modulating eEF1BδL monoubiquitylation.…”

Section: Discussionmentioning

confidence: 99%

RNF20/RNF40 ameliorates streptozotocin-induced type 1 diabetes by activating vitamin D receptors in vivo

Liu¹,

Wu²,

H³

et al. 2023

Allergol Immunopathol

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Background: Type 1 diabetes is one of the chronic autoimmune diseases. Its features include the immune-triggered pancreatic beta-cells destruction. Ubiquitin ligases RNF20 and RNF40 have been discovered to participate into beta cells gene expression, insulin secretion, and expression of vitamin D receptors (VDRs). However, no reports about the role of RNF20/ RNF40 in type 1 diabetes are known till now. The aim of this study was to clarify the role of RNF20/RNF40 in type 1 diabetes and explore the mechanism. Methods: In this study, streptozotocin (STZ)-induced mice type 1 diabetes model was used. The protein expressions of genes were examined through Western blot analysis. Fasting blood glucose was detected through glucose meter. The plasma insulin was tested through the commercial kit. Hematoxylin and eosin staining was utilized to observe pathological changes of pancreatic tissues. Immunofluorescence assay was performed to evaluate the level of insulin. The levels of pro-inflammatory cytokines in serum were assessed by enzyme-linked-immuno-sorbent serologic assay. The cell apoptosis was measured through terminal deoxynucleotidyl transferase dUTP nick end labelling assay. Results: STZ was used to stimulate mice model for type 1 diabetes. At first, both RNF20 and RNF40 expressions were down-regulated in STZ-mediated type 1 diabetes. Additionally, RNF20/RNF40 improved hyperglycemia in STZ-stimulated mice. Moreover, RNF20/RNF40 relieved pancreatic tissue injury in STZ-induced mice. Further experiments found that RNF20/ RNF40 rescued the strengthened inflammation mediated by STZ treatment. The cell apoptosis was enhanced in the pancreatic tissues of STZ-triggered mice, but this effect was weakened by overexpression of RNF20/RNF40. Besides, the VDR expression was positively regulated by RNF20/RNF40. Finally, VDR knockdown reversed improved hyperglycemia, inflammation, and cell apoptosis stimulated by overexpression of RNF20/RNF40. Conclusion: Our findings proved that RNF20/RNF40 activated VDR to relieve type 1 diabetes. This work might highlight the functioning of RNF20/RNF40 in the treatment of type 1 diabetes.

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Section: Discussionmentioning

confidence: 99%