{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Cummins TD"],"funding":["NIDDK NIH HHS","NIEHS NIH HHS"],"pagination":["653-61"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC2829334"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["1804(4)"],"pubmed_abstract":["The aim of this study was to define novel mediators of tubule injury in diabetic kidney disease. For this, we used state-of-the-art proteomic methods combined with a label-free quantitative strategy to define protein expression differences in kidney tubules from transgenic OVE26 type 1 diabetic and control mice. The analysis was performed with diabetic samples that displayed a pro-fibrotic phenotype. We have identified 476 differentially expressed proteins. Bioinformatic analysis indicated several clusters of regulated proteins in relevant functional groups such as TGF-beta signaling, tight junction maintenance, oxidative stress, and glucose metabolism. Mass spectrometry detected expression changes of four physiologically relevant proteins were confirmed by immunoblot analysis. Of these, the Grb2-related adaptor protein (GRAP) was up-regulated in kidney tubules from diabetic mice and fibrotic kidneys from diabetic patients, and subsequently confirmed as a novel component of TGF-beta signaling in cultured human renal tubule cells. Thus, indicating a potential novel role for GRAP in TGF-beta-induced tubule injury in diabetic kidney disease. Although we targeted a specific disease, this approach offers a robust, high-sensitivity methodology that can be applied to the discovery of novel mediators for any experimental or disease condition."],"journal":["Biochimica et biophysica acta"],"pubmed_title":["Quantitative mass spectrometry of diabetic kidney tubules identifies GRAP as a novel regulator of TGF-beta signaling."],"pmcid":["PMC2829334"],"funding_grant_id":["P30 ES014443","P30ES014443","K01 DK076743","DK176743"],"pubmed_authors":["Barati MT","Powell DW","Cummins TD","Klein JB","Salyer SA","Coventry SC"],"additional_accession":[]},"is_claimable":false,"name":"Quantitative mass spectrometry of diabetic kidney tubules identifies GRAP as a novel regulator of TGF-beta signaling.","description":"The aim of this study was to define novel mediators of tubule injury in diabetic kidney disease. For this, we used state-of-the-art proteomic methods combined with a label-free quantitative strategy to define protein expression differences in kidney tubules from transgenic OVE26 type 1 diabetic and control mice. The analysis was performed with diabetic samples that displayed a pro-fibrotic phenotype. We have identified 476 differentially expressed proteins. Bioinformatic analysis indicated several clusters of regulated proteins in relevant functional groups such as TGF-beta signaling, tight junction maintenance, oxidative stress, and glucose metabolism. Mass spectrometry detected expression changes of four physiologically relevant proteins were confirmed by immunoblot analysis. Of these, the Grb2-related adaptor protein (GRAP) was up-regulated in kidney tubules from diabetic mice and fibrotic kidneys from diabetic patients, and subsequently confirmed as a novel component of TGF-beta signaling in cultured human renal tubule cells. Thus, indicating a potential novel role for GRAP in TGF-beta-induced tubule injury in diabetic kidney disease. Although we targeted a specific disease, this approach offers a robust, high-sensitivity methodology that can be applied to the discovery of novel mediators for any experimental or disease condition.","dates":{"release":"2010-01-01T00:00:00Z","publication":"2010 Apr","modification":"2026-03-16T16:53:22.504Z","creation":"2025-09-01T03:06:22.369Z"},"accession":"S-EPMC2829334","cross_references":{"pubmed":["19836472"],"doi":["10.1016/j.bbapap.2009.09.029"]}}