ArticleCell stress & chaperones2019
Protective effects of UFL1 against endoplasmic reticulum stress-induced autophagy in bovine mammary epithelial cells.
Article in Cell stress & chaperones, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed, 15 citations in OpenAlex.
- The UFM1 Conjugation System: A Master Regulator of Cellular Stress Surveillance in Human Disease.Biology · 2026Review
- UFMylation of NLRP3 Prevents Its Autophagic Degradation and Facilitates Inflammasome Activation.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- A guide to UFMylation, an emerging posttranslational modification.The FEBS journal · 2023Review
- Ubiquitin-like modifier 1 ligating enzyme 1 relieves cisplatin-induced premature ovarian failure by reducing endoplasmic reticulum stress in granulosa cells.Reproductive biology and endocrinology : RB&E · 2022Article
- The Role of Tea Tree Oil in Alleviating Palmitic Acid-Induced Lipid Accumulation in Bovine Hepatocytes.Frontiers in veterinary science · 2021Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Ubiquitin-fold modifier 1 (UFM1)-specific ligase 1 (UFL1) is an important component of the UFM1 conjugation system, which is required for various cellular processes including protein translation, apoptosis, autophagy, and signal transduction. However, both, the expression of UFL1 in mammary cells and its role in endoplasmic reticulum (ER) stress in bovine mammary epithelial cells (BMECs) remain to be fully elucidated. Here, we characterized the potential roles of UFL1 in BMECs. Amino acid sequence comparison indicated that bovine UFL1 shares a high level of sequence identity with the UFL1 of other ruminant species. Notably, UFL1 expression in BMECs was increased by endoplasmic reticulum (ER) stress induced by treatment with tunicamycin (TM). ER stress-related gene expression was further increased in UFL1 knockdown cells upon TM treatment. Moreover, UFL1 overexpression inhibited TM-stimulated ER stress and alleviated ER stress-induced autophagy. Together, our results indicated that UFL1 is a novel ER stress-responsive protein in BMECs. Thus, our study provides a basis for further research into ER stress-related processes in bovine mammary tissues and potential targets for alleviating ER stress in these cells.
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