ArticleJournal of molecular cell biology2020
TRIM65 E3 ligase targets VCAM-1 degradation to limit LPS-induced lung inflammation.
Article in Journal of molecular cell biology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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Who cites it
29 citing papers in PubMed, 55 citations in OpenAlex.
- Cross-linked actin networks (CLANs) and their role in the trabecular meshwork.Experimental eye research · 2026Review
- TRIM47 drives metabolic reprogramming and tumor progression in Nasopharyngeal Carcinoma via K48-linked ubiquitination and degradation of SDHB.Cellular and molecular life sciences : CMLS · 2026Article
- TRIM47-facilitated PLK1 stabilization promotes the proliferation of liver cancer cells.Cellular oncology (Dordrecht, Netherlands) · 2025Article
- Ubiquitin E3 Ligases and p53 in Doxorubicin-Induced Cardiotoxicity.International journal of molecular sciences · 2025Review
- Understanding Endometriosis: A Broad Review of Its Causes, Management, and Impact.International journal of molecular sciences · 2025Review
- Research and development prospects of TRIM65.Journal of cancer research and clinical oncology · 2025Review
- Article
- Upper airway microcirculation remodeling in obstructive sleep apnea is not driven by endothelial activation.Scientific reports · 2025Article
- New insights into the role of ubiquitination in angiogenesis (Review).International journal of molecular medicine · 2025Review
- The Magic and Mystery of TRIM65 in Diseases.Current medicinal chemistry · 2025Review
- Article
- TRIM65 deficiency alleviates renal fibrosis through NUDT21-mediated alternative polyadenylation.Cell death and differentiation · 2024Article
- Exploring biomarkers for diagnosing and predicting organ dysfunction in patients with perioperative sepsis: a preliminary investigation.Perioperative medicine (London, England) · 2024Article
- Tripartite Motif-Containing Protein 65 (TRIM65) Inhibits Hepatitis B Virus Transcription.Viruses · 2024Article
- TRIM65 promotes renal cell carcinoma through ubiquitination and degradation of BTG3.Cell death & disease · 2024Article
- Adhesion molecule-targeted magnetic particle imaging nanoprobe for visualization of inflammation in acute lung injury.European journal of nuclear medicine and molecular imaging · 2024Article
- E3 ligase TRIM65 alleviates intestinal ischemia/reperfusion injury through inhibition of TOX4-mediated apoptosis.Cell death & disease · 2024Article
- LPS inhibits TRIM65 expression in macrophages and C57BL/6J mouse by activating the ERK1/2 signaling pathway.Experimental and therapeutic medicine · 2023Article
- Machine learning and bioinformatics to identify 8 autophagy-related biomarkers and construct gene regulatory networks in dilated cardiomyopathy.Scientific reports · 2022Article
- TRIM65 determines the fate of a novel subtype of pituitary neuroendocrine tumors via ubiquitination and degradation of TPIT.Neuro-oncology · 2022Article
Corrections and comments
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Authors and funding
9 authors at 4 institutions in 2 countries.
Funding
Abstract
Although the adhesion molecules-mediated leukocyte adherence and infiltration into tissues is an important step of inflammation, the post-translational regulation of these proteins on the endothelial cells is poorly understood. Here, we report that TRIM65, an ubiquitin E3 ligase of tripartite protein family, selectively targets vascular cell adhesion molecule 1 (VCAM-1) and promotes its ubiquitination and degradation, by which it critically controls the duration and magnitude of sepsis-induced pulmonary inflammation. TRIM65 is constitutively expressed in human vascular endothelial cells. During TNFα-induced endothelial activation, the protein levels of TRIM65 and VCAM-1 are inversely correlated. Expression of wild-type TRIM65, but not expression of a TRIM65 mutant that lacks E3 ubiquitin ligase function in endothelial cells, promotes VCAM-1 ubiquitination and degradation, whereas small interference RNA-mediated knockdown of TRIM65 attenuates VCAM-1 protein degradation. Further experiments show that TRIM65 directly interacts with VCAM-1 protein and directs its polyubiquitination, by which TRIM65 controls monocyte adherence and infiltration into tissues during inflammation. Importantly, TRIM65-deficient mice are more sensitive to lipopolysaccharide-induced death, due to sustained and severe pulmonary inflammation. Taken together, our studies suggest that TRIM65-mediated degradation of VCAM-1 represents a potential mechanism that controls the duration and magnitude of inflammation.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.