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Updated: Jan 18, 2026

Measurement of Differentially Methylated INS DNA Species in Human Serum Samples as a Biomarker of Islet β Cell Death
Published on: December 21, 2016
Association Between Proteasome 26S Subunit, Non-ATPase 3 Methylation and Insulin β Cell Apoptosis in Type 2 Diabetic
Guiping Huang1,2, Guodong He1,2, Shaoxian Chen1
1Medical Research Institute, Guangdong Provincial People's Hospital (Guangdong Academy of Medical Sciences), Southern Medical University, Guangzhou, People's Republic of China.
Background:
The methylation of PSMD3 and its influence on protein stability and degradation could play a crucial role in the pathogenesis of type 2 diabetes mellitus (T2DM), although the underlying molecular mechanisms are not yet fully understood. This study investigates the molecular and bioinformatic features of PSMD3 methylation in T2DM.
Methods:
Bioinformatics analyses were conducted on the T2DM database chip. A model of T2DM was established in rat RIN-m5F cells induced by high glucose (HG) concentration. The function of the PSMD3 gene in T2DM was examined through its overexpression. Western blotting was used to detect the expression of PSMD3 and USP14 proteins. Flow cytometry was used to detect cell apoptosis and proliferation.
Results:
Methylation of PSMD3 was upregulated in the T2DM tissue microarray data and associated with USP14. PSMD3 overexpression reduced apoptosis and enhanced proliferation in HG-treated RIN-m5F cells. In HG-treated RIN-m5F cells, PSMD3 was linked to USP14 inactivation.
Conclusion:
PSMD3 methylation might potentially influences cell apoptosis and proliferation in T2DM development which might be associated with activating USP14. This study offers an in-depth examination of PSMD3 methylation's molecular and bioinformatic traits in T2DM, advancing our comprehension of the molecular mechanisms leading to T2DM.
Insights
Methylation of PSMD3 (proteasome subunit 3) is upregulated in type 2 diabetes mellitus (T2DM) and may influence cell apoptosis and proliferation by affecting USP14 activity. This research explores PSMD3 methylation
Area of Science:
- Molecular Biology
- Biochemistry
- Genetics
Background:
- The role of PSMD3 methylation in type 2 diabetes mellitus (T2DM) pathogenesis is not fully understood.
- PSMD3 methylation's impact on protein stability and degradation may be significant in T2DM development.
Purpose of the Study:
- To investigate the molecular and bioinformatic characteristics of PSMD3 methylation in T2DM.
- To explore the association between PSMD3 methylation and T2DM pathogenesis.
Main Methods:
- Bioinformatics analyses on T2DM database chip.
- Establishment of a high glucose-induced T2DM cell model (RIN-m5F cells).
- Assessment of PSMD3 gene function via overexpression, Western blotting, and flow cytometry.
Main Results:
- PSMD3 methylation was upregulated in T2DM tissues and correlated with USP14.
- PSMD3 overexpression decreased apoptosis and increased proliferation in high glucose-treated cells.
- PSMD3 was linked to USP14 inactivation in high glucose-treated cells.
Conclusions:
- PSMD3 methylation may influence T2DM development by affecting cell apoptosis and proliferation, potentially through USP14 activation.
- This study enhances understanding of the molecular mechanisms underlying T2DM pathogenesis related to PSMD3 methylation.
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