Ubiquitin‐Proteasome System in Periodontitis: Mechanisms and Clinical Implications DOI Creative Commons
Yilin Ma, Ru Jia, Shuhong Chen

et al.

Cell Proliferation, Journal Year: 2024, Volume and Issue: unknown

Published: Dec. 3, 2024

ABSTRACT The progression of periodontitis, a bacteria‐driven inflammatory and bone‐destructive disease, involves myriad cellular molecular mechanisms. Protein regulation significantly influences the pathogenesis management periodontitis. However, research regarding its regulatory role in periodontitis remains relatively limited. ubiquitin‐proteasome system (UPS), which mainly ubiquitination by E3 ubiquitin ligases (E3s) deubiquitination deubiquitinating enzymes (DUBs), is primary intracellular non‐lysosomal mechanism protein degradation. Recent studies have provided compelling evidence to support involvement UPS progression. Increasing indicated that E3s, such as CUL3, Nedd4‐2, Synoviolin, FBXL19, PDLIM2, TRIMs TRAFs, modulate responses bone resorption through multiple classical signalling pathways, including NLRP3, GSDMD, NF‐κB, Wnt/β‐catenin Nrf2. Meanwhile, DUBs, OTUD1, A20, CYLD, UCH‐L1 USPs, also broadly regulating pathways Wnt/β‐catenin, BMP2. Therefore, modulation E3s DUBs has proven be an effective therapy against This review provides comprehensive overview ubiquitinating underlying Finally, we summarise several chemical genetic methods regulate pave way for development targeted therapies

Language: Английский

Proteasomes and Ubiquitin C-Terminal Hydrolase L1 as Biomarkers of Tissue Damage and Inflammatory Response to Different Types of Injury—A Short Review DOI Creative Commons
Marzena Tylicka, Ewa Matuszczak, Joanna Kamińska

et al.

Life, Journal Year: 2025, Volume and Issue: 15(3), P. 413 - 413

Published: March 6, 2025

The proteasomal system of protein degradation is crucial for various cellular processes, including transduction signals and differentiation cells. Proteasome activity rises after traumatic stressors such as hyperoxia, radiation, or oxidative damage. Removal damaged proteins essential to provide the necessary conditions cell repair. Several studies report activation thermal injury, CNS abdominal trauma, ischemia-reperfusion possible clinical implications use proteasome inhibitors. It important highlight distinct roles UCHL1, 26S, 20S subunits biomarkers. UCHL1 appears be particularly relevant identifying brain neuronal damage in advancing diagnosis prognosis injury (TBI) other neurological conditions. Meanwhile, 26S proteasomes may serve markers peripheral tissue This enhances our understanding ability target specific types settings.

Language: Английский

Citations

0
The ELF3-TRIM22-MAVS signaling axis regulates type I interferon and antiviral responses DOI Creative Commons
Qixin Zhao, Pan Pan, Mo Li

et al.

Journal of Virology, Journal Year: 2025, Volume and Issue: unknown

Published: March 31, 2025

ABSTRACT Activation of the innate immune response is essential for host cells to restrict dissemination invading viruses and other pathogens. Proteins belonging tripartite motif (TRIM) family are key effectors in antiviral immunity. Among these, TRIM22, a RING-type E3 ubiquitin ligase, has been recognized as significant regulator pathogenesis various diseases. In present study, we identified TRIM22 critical modulator mitochondrial signaling protein (MAVS) activation. Loss function led reduced production type I interferons (IFNs) viral infection such influenza A virus (IAV) or vesicular stomatitis (VSV), thereby facilitating replication. Mechanistically, was found enhance retinoic acid-inducible gene (RIG-I)-mediated through catalysis Lys63-linked polyubiquitination MAVS, which, turn, activated TANK-binding kinase 1 (TBK1)/interferon regulatory factor 3 (IRF3) pathway, driving IFN-β production. Additionally, shown inhibit assembly MAVS-NLRX1 inhibitory complex, further amplifying responses. Our findings also demonstrated that RNA upregulated expression via nuclear translocation ELF3, transcription activates expression. This loop underscores role modulating IFN providing insights into host’s defense mechanisms. research highlights potential targeting ELF3-TRIM22-MAVS axis therapeutic strategy enhancing immunity preventing infections. IMPORTANCE Interferon (IFN)-mediated responses crucial against foreign pathogens regulated by pathways. The family, its multifaceted roles regulation defense, plays part this process. our explored important helped regulate We enhances (MAVS), which producing interferons. Interestingly, discovered increases after an infection, due moved nucleus activate transcription. created feedback strengthens pathway. By uncovering these mechanisms, aimed understanding how system works provide could lead innovative therapies.

Language: Английский

Citations

0
Loss of Trim31 Worsens Cardiac Remodeling in a Mouse Model of Heart Failure by Enhancing the Activation of the NLRP3 Inflammasome DOI
Fengqi Duan, H. Li, Bo Lu

et al.

Inflammation, Journal Year: 2024, Volume and Issue: unknown

Published: Dec. 13, 2024

Language: Английский

Citations

1
Ubiquitin‐Proteasome System in Periodontitis: Mechanisms and Clinical Implications DOI Creative Commons
Yilin Ma, Ru Jia, Shuhong Chen

et al.

Cell Proliferation, Journal Year: 2024, Volume and Issue: unknown

Published: Dec. 3, 2024

ABSTRACT The progression of periodontitis, a bacteria‐driven inflammatory and bone‐destructive disease, involves myriad cellular molecular mechanisms. Protein regulation significantly influences the pathogenesis management periodontitis. However, research regarding its regulatory role in periodontitis remains relatively limited. ubiquitin‐proteasome system (UPS), which mainly ubiquitination by E3 ubiquitin ligases (E3s) deubiquitination deubiquitinating enzymes (DUBs), is primary intracellular non‐lysosomal mechanism protein degradation. Recent studies have provided compelling evidence to support involvement UPS progression. Increasing indicated that E3s, such as CUL3, Nedd4‐2, Synoviolin, FBXL19, PDLIM2, TRIMs TRAFs, modulate responses bone resorption through multiple classical signalling pathways, including NLRP3, GSDMD, NF‐κB, Wnt/β‐catenin Nrf2. Meanwhile, DUBs, OTUD1, A20, CYLD, UCH‐L1 USPs, also broadly regulating pathways Wnt/β‐catenin, BMP2. Therefore, modulation E3s DUBs has proven be an effective therapy against This review provides comprehensive overview ubiquitinating underlying Finally, we summarise several chemical genetic methods regulate pave way for development targeted therapies

Language: Английский

Citations

0