Dataset Information

Data for Mass spectrometry analysis of collagen IV

ABSTRACT: Data for PHFR9 7S: 1. Raw file (6 files) 2. IDPicker files (1 file) 3. Database (1 file) Data for EHS mouse collagen IV: 1.Raw file ( 21 files) 2.IDPicker files (7 files) 3.Database (3 files) Mouse_data_CID_1=Trypsin;Mouse_data_CID_2=Glu C; Mouse_data_CID_3=Trypsin +Glu C; Mouse_data_ETD_1=Trypsin (Replicate1); Mouse_data_ETD_2=Trypsin (Replicate2); Mouse_data_ETD_3=Glu C (Replicate1); Mouse_data_ETD_4=Glu C (Replicate2); Mouse_data_ETD_5=Trypsin +Glu C (Replicate1); Mouse_data_ETD_6=Trypsin +Glu C (Replicate2); Mouse_data_HCD_1=Glu C (Replicate1); Mouse_data_HCD_2=Glu C (Replicate2); Mouse_data_HCD_3=Glu C (Replicate3); Mouse_data_HCD_4=Trypsin (Replicate1); Mouse_data_HCD_5=Trypsin (Replicate2); Mouse_data_HCD_6=Trypsin (Replicate3); Mouse_data_HCD_7=Trypsin +Glu C (Replicate1); Mouse_data_HCD_8=Trypsin +Glu C (Replicate2); Mouse_data_HCD_9=Trypsin + Glu C (Replicate3); Mouse_data_HCD_10=Glu C (Replicate1); Mouse_data_HCD_11=Glu C (Replicate2); Mouse_data_HCD_12=LysC + Trypsin. Data for Human collagen IV: 1. Raw file: (106 files from PXD00125) 2. IDPicker files (108 files) 3. Database (3 files)

INSTRUMENT(S): LTQ Orbitrap Velos, Q Exactive

ORGANISM(S): Homo Sapiens (ncbitaxon:9606) Mus Musculus (ncbitaxon:10090)

SUBMITTER: Dr. Roberto M. Vanacore

PROVIDER: MSV000079260 | MassIVE | Mon Aug 17 20:38:00 BST 2015

SECONDARY ACCESSION(S): PXD003237

REPOSITORIES: MassIVE

ACCESS DATA

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Publications

Comprehensive Characterization of Glycosylation and Hydroxylation of Basement Membrane Collagen IV by High-Resolution Mass Spectrometry.

Basak Trayambak T Vega-Montoto Lorenzo L Zimmerman Lisa J LJ Tabb David L DL Hudson Billy G BG Vanacore Roberto M RM

Journal of proteome research 20151209 1

Collagen IV is the main structural protein that provides a scaffold for assembly of basement membrane proteins. Posttranslational modifications such as hydroxylation of proline and lysine and glycosylation of lysine are essential for the functioning of collagen IV triple-helical molecules. These modifications are highly abundant posing a difficult challenge for in-depth characterization of collagen IV using conventional proteomics approaches. Herein, we implemented an integrated pipeline combini ...[more]

PMID: 26593852

Similar Datasets

Project description:Obesity-induced inflammation causes metabolic dysfunction, but the mechanisms remain elusive. Here we show that the innate immune transcription factor interferon regulatory factor (IRF3) adversely affects glucose homeostasis through induction of the endogenous FAHFA hydrolase androgen induced gene 1 (AIG1) in adipocytes. Adipocyte-specific knockout of IRF3 protects mice against high-fat diet-induced insulin resistance, whereas overexpression of IRF3 or AIG1 in adipocytes promotes insulin resistance on a high-fat diet. Furthermore, pharmacological inhibition of AIG1 reversed obesity-induced insulin resistance and restored glucose homeostasis in the setting of adipocyte IRF3 overexpression. We, therefore, identify the adipocyte IRF3/AIG1 axis as a crucial link between obesity-induced inflammation and insulin resistance and suggest an approach for limiting the metabolic dysfunction accompanying obesity. ## File Key ### MS-ABPP The following raw files were acquired on an Eclipse instrument in triplicate with two concentrations of inhibitor in both brain and kidney. These variables are encoded in the file names. Associated analysis pipeline files from CIMAGE are provided for each raw file (same file name, with a .raw_output_rt_10_sn_2.5.to_excel extension). - brain_conc1.0_rep1.raw - brain_conc1.0_rep2.raw - brain_conc1.0_rep3.raw - brain_conc10.0_rep1.raw - brain_conc10.0_rep2.raw - brain_conc10.0_rep3.raw - kidney_conc1.0_rep1.raw - kidney_conc1.0_rep2.raw - kidney_conc1.0_rep3.raw - kidney_conc10.0_rep1.raw - kidney_conc10.0_rep2.raw - kidney_conc10.0_rep3.raw ### TMT Dose Response The following raw files were acquired on an Eclipse instrument instrument in both brain and white adipose tissues: - brain_dose_response.raw - wat_dose_response.raw The TMT channels were organized as follows: - DMSO channels: 1, 3, 5 - ABD-110 @ 0.001 μM: 7, 9, 11 - ABD-110 @ 0.01 μM: 2, 4, 6 - ABD-110 @ 0.1 μM: 13, 15, 17 - ABD-110 @ 1 μM: 8, 10, 12 - ABD-110 @ 10 μM: 14, 16, 18 Associated analysis pipeline files after IDFilter run are provided for each file (same file name, with a _filtered_matches suffix and an .idXML extension). ### PRM AIG1 In Vivo Target Engagement The A prefix before the replicate number refers to treatment with ABD-110, whereas the V prefix refers to vehicle treatment. Diet and tissue type are also encoded in the filename. The following files were acquired on a Lumos instrument, with 5 replicates for each condition (as noted in square brackets). Associated pipeline analysis files are Skyline exports and are provided as two .csv files having names beginning with Skyline_PRM_export and ending with the tissue types contained. - Brain_Chow_A[1-5].raw - Brain_Chow_V[1-5].raw - Brain_HVD_A[1-5].raw - Brain_HVD_V[1-5].raw - eWAT_Chow_A[1-5].raw - eWAT_Chow_V[1-5].raw - eWAT_HVD_A[1-5].raw - eWAT_HVD_V[1-5].raw - iWAT_Chow_A[1-5].raw - iWAT_Chow_V[1-5].raw - iWAT_HVD_A[1-5].raw - iWAT_HVD_V[1-5].raw - Kindey_Chow_A[1-5].raw - Kindey_Chow_V[1-5].raw - Kindey_HVD_A[1-5].raw - Kindey_HVD_V[1-5].raw

Project description:It is well known that rennin-angiotensin-aldosterone system (RAAS) plays a critical role in the development of diabetic cardiomyopathy. The present study was aimed to clarify the role of a novel member of RAAS, angiotensin IV (Ang IV) and its downstream mediator forkhead box protein O1 (FoxO1), in the pathogenesis of diabetic cardiomyopathy. In vivo, diabetic mice were treated with low-, medium- and high-dose Ang IV, AT4R antagonist divalinal, FoxO1 inhibitor AS1842856 (AS), or their combinations. In vitro, cardiomyocytes and cardiofibroblasts were treated with different concentrations of glucose, low-, medium- and high-dose Ang IV, divalinal, FoxO1-overexpression plasmid (FoxO1-OE), AS or their combinations. The results showed that Ang IV treatment dose-dependently attenuated left ventricular dysfunction, fibrosis, and myocyte apoptosis in diabetic mice. Besides, enhanced autophagy and FoxO1 protein expression by diabetes were dose-dependently suppressed by Ang IV treatment. However, these cardioprotective effects of Ang IV were completely abolished by divalinal administration. Bioinformatics analysis revealed that the differentially expressed genes were enriched in autophagy, apoptosis, and FoxO signaling pathways among control, diabetes, and diabetes+high-dose Ang IV groups. Similar to Ang IV, AS treatment ameliorated diabetic cardiomyopathy in mice. In vitro, high glucose stimulation increased collagen expression, apoptosis, overactive autophagy flux and FoxO1 nuclear translocation in cardiomyocytes, and upregulated collagen and FoxO1 expression in cardiofibroblasts, which were substantially attenuated by Ang IV treatment. However, these protective effects of Ang IV were completely blocked by the use of divalinal or FoxO1-OE, and these detrimental effects were reversed by the additional administration of AS. In summary, Ang IV treatment dose-dependently attenuated left ventricular dysfunction and remodeling in a mouse model of diabetic cardiomyopathy, and the mechanisms involved stimulation of AT4R and suppression of FoxO1-mediated fibrosis, apoptosis, and overactive autophagy.