Related Experiment Video
Updated: Aug 11, 2026
Assessment of Kidney Function in Mouse Models of Glomerular Disease
Published on: June 30, 2018
Proteomic analysis revealed the altered kidney protein profile of a Cyld knockout mouse model
1Center for Stem Cell & Regenerative Medicine, The Second Hospital of Shandong University, Jinan, China.
Abstract:
The aim of this study was to compare the proteomics pattern of the kidneys from Cyld knockout mice with that from normal mouse kidneys and establish a preliminary understanding of the role of Cyld in the kidney. Proteins from the kidneys of knockout Cyld mice and wild-type mice were extracted, isobaric tags for relative and absolute quantitation (iTRAQ) was performed, and the proteomics patterns of the two groups were compared. The genotypes of the mice were verified by polymerase chain reaction. A total of 1748 proteins with a local false discovery rate of ≤5% were identified, among which 1437 proteins were reliably recognized and quantified. The expression of two dysregulated proteins was confirmed by Western blotting. Gene ontology and pathway analyses indicated that the proteins identified were involved in biological processes, cell components, and molecular functions, and participated in different pathways. Some of the proteins identified were relevant to renal function or kidney diseases. The difference between the proteomics profiles of kidneys from Cyld knockout mice and wild-type mice was prominent, which correlates to kidney dysfunction and the development of renal diseases.
Insights
Cyld knockout mice exhibit distinct kidney proteomic patterns compared to normal mice, suggesting Cyld
Area of Science:
- Nephrology
- Proteomics
- Genetics
Background:
- The Cylchilin (Cyld) gene's role in kidney function and disease is not well understood.
- Investigating Cyld's impact on renal proteomic profiles can elucidate its physiological and pathological significance.
Purpose of the Study:
- To compare the kidney proteomic patterns between Cyld knockout and wild-type mice.
- To identify proteins and pathways affected by Cyld deficiency in the kidney.
- To establish a preliminary understanding of Cyld's role in renal health and disease.
Main Methods:
- Kidney protein extraction from Cyld knockout and wild-type mice.
- Proteomic analysis using isobaric tags for relative and absolute quantitation (iTRAQ).
- Genotype verification by polymerase chain reaction (PCR) and protein validation by Western blotting.
Main Results:
- Identified and quantified 1748 proteins (1437 reliably) with a local false discovery rate ≤5%.
- Observed prominent differences in proteomic profiles between Cyld knockout and wild-type kidneys.
- Gene Ontology and pathway analyses revealed involvement in renal function and kidney disease-related pathways.
Conclusions:
- Cyld deficiency significantly alters the kidney proteome.
- Proteomic changes are associated with kidney dysfunction and the potential development of renal diseases.
- Further research into Cyld's specific mechanisms in kidney pathology is warranted.
