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ILDR1 deficiency causes degeneration of cochlear outer hair cells and disrupts the structure of the organ of Corti: a mouse model for human DFNB42.

Sang Q, Li W, Xu Y, Qu R, Xu Z, Feng R, Jin L, He L, Li H, Wang L - Biol Open (2015)

Bottom Line: ILDR1 deficiency affects expression of tricellulin in vivo, and this provides a possible explanation to hearing loss.Gene ontology classification indicated that a number of differentially expressed proteins are involved in cell adhesion, protein and vesicle-mediated transport, cell death, membrane organization, and cellular homeostasis.A few of these proteins are closely related to hearing development.

View Article: PubMed Central - PubMed

Affiliation: State Key Laboratory of Genetic Engineering and MOE Key Laboratory of Contemporary Anthropology, School of Life Sciences, Fudan University, Shanghai, 200032, PR China Institute of Biomedical Sciences, Fudan University, No 138 Yixueyuan Road, Shanghai, 200032, PR China.

No MeSH data available.


Related in: MedlinePlus

Gene ontology analysis of differentially expressed proteins in the cochleae of Ildr1+/− and Ildr1−/− P21 mice using the online DAVID software.The x-axis shows the number of proteins in each category.
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f08: Gene ontology analysis of differentially expressed proteins in the cochleae of Ildr1+/− and Ildr1−/− P21 mice using the online DAVID software.The x-axis shows the number of proteins in each category.

Mentions: To further elucidate the mechanism of deafness related to ILDR1 deficiency, we used a differential proteomic approach (LC-MS/MS) to comprehensively assess differential protein expression in the cochleae of Ildr1+/− and Ildr1−/− mice at P21. We used 70 µg of mouse cochlear protein for LC-MS/MS analysis, and three replicates were run for each individual sample. Only proteins detected in at least two replicates were used in further analysis. Altogether, 708 proteins were up-regulated (fold change >1.5) and 114 proteins were down-regulated (fold change <0.5) in Ildr1−/− mice (supplementary material Tables S1, S2). To interpret the likely roles of differentially expressed proteins in the pathology of deafness, we analyzed and built the biological pathways related to these proteins. Identified GO processes were divided into several categories, including cell adhesion, protein and vesicle-mediated transport, cell death, immune response, membrane organization, and cellular homeostasis (Fig. 8).


ILDR1 deficiency causes degeneration of cochlear outer hair cells and disrupts the structure of the organ of Corti: a mouse model for human DFNB42.

Sang Q, Li W, Xu Y, Qu R, Xu Z, Feng R, Jin L, He L, Li H, Wang L - Biol Open (2015)

Gene ontology analysis of differentially expressed proteins in the cochleae of Ildr1+/− and Ildr1−/− P21 mice using the online DAVID software.The x-axis shows the number of proteins in each category.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4400585&req=5

f08: Gene ontology analysis of differentially expressed proteins in the cochleae of Ildr1+/− and Ildr1−/− P21 mice using the online DAVID software.The x-axis shows the number of proteins in each category.
Mentions: To further elucidate the mechanism of deafness related to ILDR1 deficiency, we used a differential proteomic approach (LC-MS/MS) to comprehensively assess differential protein expression in the cochleae of Ildr1+/− and Ildr1−/− mice at P21. We used 70 µg of mouse cochlear protein for LC-MS/MS analysis, and three replicates were run for each individual sample. Only proteins detected in at least two replicates were used in further analysis. Altogether, 708 proteins were up-regulated (fold change >1.5) and 114 proteins were down-regulated (fold change <0.5) in Ildr1−/− mice (supplementary material Tables S1, S2). To interpret the likely roles of differentially expressed proteins in the pathology of deafness, we analyzed and built the biological pathways related to these proteins. Identified GO processes were divided into several categories, including cell adhesion, protein and vesicle-mediated transport, cell death, immune response, membrane organization, and cellular homeostasis (Fig. 8).

Bottom Line: ILDR1 deficiency affects expression of tricellulin in vivo, and this provides a possible explanation to hearing loss.Gene ontology classification indicated that a number of differentially expressed proteins are involved in cell adhesion, protein and vesicle-mediated transport, cell death, membrane organization, and cellular homeostasis.A few of these proteins are closely related to hearing development.

View Article: PubMed Central - PubMed

Affiliation: State Key Laboratory of Genetic Engineering and MOE Key Laboratory of Contemporary Anthropology, School of Life Sciences, Fudan University, Shanghai, 200032, PR China Institute of Biomedical Sciences, Fudan University, No 138 Yixueyuan Road, Shanghai, 200032, PR China.

No MeSH data available.


Related in: MedlinePlus