Activation of TRAF1 induced by USP7/SP1 exacerbates the severity of infantile pneumonia DOI Creative Commons
Ying Liu, Yilun Ji, Yu Zhang

et al.

Hereditas, Journal Year: 2025, Volume and Issue: 162(1)

Published: March 22, 2025

Abstract Background Infantile pneumonia (IP) is a leading cause of morbidity and mortality in children worldwide, with limited treatment options. Tumor necrosis factor receptor-associated 1 (TRAF1) has been implicated the pathogenesis various inflammatory diseases. Given lack effective therapies IP, understanding role TRAF1 regulating IP crucial for developing new therapeutic strategies. Methods This study utilized vitro vivo models to investigate IP. WI-38 cells were stimulated lipopolysaccharide (LPS), rats administered LPS mimic The mRNA expression Sp1 transcription (SP1) was analyzed using quantitative real-time polymerase chain reaction. protein TRAF1, ubiquitin-specific peptidase 7 (USP7), SP1 detected by western blotting. Cell viability apoptosis assessed cell counting kit-8 assay flow cytometry/TUNEL assays, respectively. Interleukin-6 tumor factor-α levels measured enzyme-linked immunosorbent assays. Reactive oxygen species malondialdehyde fluorescence microscopy colorimetric interactions among USP7, identified co-immunoprecipitation assay, immunofluorescence dual-luciferase reporter assay. silencing-induced effects validated rat model. Lung tissue pathology haematoxylin eosin Massion Results induced apoptosis, inflammation, oxidative stress cells, however, silencing ameliorated these effects. USP7 stabilized through its deubiquitinating activity, while overexpression reversed LPS-treated cells. In addition, transcriptionally activated Further, improved lung injury LPS-induced mice. Conclusion Activation USP7/SP1 exacerbated severity suggesting that targeting may have significant clinical implications

Language: Английский

USP7 contributes to cisplatin resistance in non-small cell lung cancer by deubiquitination of BCL2 DOI
Zhihao Chen, Wenjun Shang, Gang Huang

et al.

Molecular & Cellular Toxicology, Journal Year: 2025, Volume and Issue: unknown

Published: April 9, 2025

Language: Английский

Citations

0
Activation of TRAF1 induced by USP7/SP1 exacerbates the severity of infantile pneumonia DOI Creative Commons
Ying Liu, Yilun Ji, Yu Zhang

et al.

Hereditas, Journal Year: 2025, Volume and Issue: 162(1)

Published: March 22, 2025

Abstract Background Infantile pneumonia (IP) is a leading cause of morbidity and mortality in children worldwide, with limited treatment options. Tumor necrosis factor receptor-associated 1 (TRAF1) has been implicated the pathogenesis various inflammatory diseases. Given lack effective therapies IP, understanding role TRAF1 regulating IP crucial for developing new therapeutic strategies. Methods This study utilized vitro vivo models to investigate IP. WI-38 cells were stimulated lipopolysaccharide (LPS), rats administered LPS mimic The mRNA expression Sp1 transcription (SP1) was analyzed using quantitative real-time polymerase chain reaction. protein TRAF1, ubiquitin-specific peptidase 7 (USP7), SP1 detected by western blotting. Cell viability apoptosis assessed cell counting kit-8 assay flow cytometry/TUNEL assays, respectively. Interleukin-6 tumor factor-α levels measured enzyme-linked immunosorbent assays. Reactive oxygen species malondialdehyde fluorescence microscopy colorimetric interactions among USP7, identified co-immunoprecipitation assay, immunofluorescence dual-luciferase reporter assay. silencing-induced effects validated rat model. Lung tissue pathology haematoxylin eosin Massion Results induced apoptosis, inflammation, oxidative stress cells, however, silencing ameliorated these effects. USP7 stabilized through its deubiquitinating activity, while overexpression reversed LPS-treated cells. In addition, transcriptionally activated Further, improved lung injury LPS-induced mice. Conclusion Activation USP7/SP1 exacerbated severity suggesting that targeting may have significant clinical implications

Language: Английский

Citations

0