Dataset Information

OVA N-glycans PGC-LC-MSMS - Large-scale identification and visualization of N-glycans with primary structures using GlySeeker

ABSTRACT: With PNGase F digestion, PGC enrichment,OVA N-glycans were analyzed using PGC nanoLC-ESI-MS/MS.Datasets were analyzed by the N-glycan database search engine called GlycanGoggle developed in our group.

INSTRUMENT(S): Q Exactive

ORGANISM(S): Gallus Gallus (chicken)

SUBMITTER: Kaijie Xiao

LAB HEAD: Zhixin Tian

PROVIDER: PXD006400 | Pride | 2019-01-17

REPOSITORIES: Pride

ACCESS DATA

Publications

Large-scale identification and visualization of N-glycans with primary structures using GlySeeker.

Xiao Kaijie K Wang Yue Y Shen Yun Y Han Yuyin Y Tian Zhixin Z

Rapid communications in mass spectrometry : RCM 20180101 2

<h4>Rationale</h4>Most of the current popular tandem mass spectrometers have the capability of resolving the primary structures (monosaccharide composition, sequence and linkage) of N-glycans; however, compositions or putative structures have mostly been reported so far. Identification and visualization tools of N-glycans are needed.<h4>Methods</h4>The isotopic mass-to-charge ratio and envelope fingerprinting algorithm, which has been successfully used for intact protein database search and iden ...[more]

PMID: 29105226

Similar Datasets

Project description:Mitochondrial oxidative function is tightly controlled to maintain energy homeostasis in response to nutrient and hormonal signals. An important cellular component in the energy sensing response is the target of rapamycin (TOR) kinase pathway; however whether and how mTOR controls mitochondrial oxidative activity is unknown. Here, we show that mTOR kinase activity stimulates mitochondrial gene expression and oxidative function. In skeletal muscle cells and TSC2-/- MEFs, the mTOR inhibitor rapamycin largely decreased gene expression of mitochondrial transcriptional regulators such as PGC-1alpha and the transcription factors ERRalpha and NRFs. As a consequence, mitochondrial gene expression and oxygen consumption were reduced upon mTOR inhibition. Using computational genomics, we identified the transcription factor YY1 as a common target of mTOR and PGC-1alpha that controls mitochondrial gene expression. Inhibition of mTOR resulted in a failure of YY1 to interact and be coactivated by PGC-1alpha. Notably, knock-down of YY1 in skeletal muscle cells caused a significant decrease in mRNAs of mitochondrial regulators and mitochondrial genes that resulted in a decrease in respiration. Moreover, YY1 was required for rapamycin-dependent repression of mitochondrial genes. Thus, we have identified a novel mechanism in which a nutrient sensor (mTOR) balances energy metabolism via transcriptional control of mitochondrial oxidative function. These results have important implications for our understanding of how these pathways might be altered in metabolic diseases and cancer. Experiment Overall Design: Using Affymetrix MOE430 v2 gene chips, biological triplicates of each condition were analyzed: vehicle-treated, rapamycin-treated, gfp-infected, and pgc-1alpha-infected resulting in a total of 12 samples. Experiment Overall Design: Data were analyzed by RMA (with default settings) in BioConductor 1.2 -- one batch for the Rapamycin vs. Vehicle, and another batch for the PGC vs GFP.

Project description:The transcriptional coactivator peroxisome proliferator-activated receptor-gamma coactivator 1 alpha (PGC-1Î±) is a chief activator of the mitochondrial and metatolic program in skeletal muscle (skm) and prevents atrophy. Here we tested whether PGC-1Î± overexpression could restructure the transcriptome and metabolism of cultured human skeletal myotubes, which display an athropic phenotype. An oligonucleotide microarray analysis was used to reveal PGC-1Î± effects on the whole transcriptome, and the possible impact on fuel metabolism reprogramming was examined. Fifty-three different genes displayed changed expression levels in response to PGC-1Î±: 42 upregulated and 11 downregulated. Main associations of gene ontologies (GO) for the upregulated genes were mitochondrial components and processes and this correlated with an increase in COX activity, an indicator of mitochondrial content. Palmitate and lactate oxidation to CO2 was enhanced, but not glucose oxidation. The other most significant GO associations of upregulated genes were chemotaxis and cytokine activity, and accordingly, several cytokines, including IL8, CXCL6, CCL5 and CCL8, were within top induced genes. Among the most regulated genes were also potential metabolic regulators of fatty acid and glucose storage. FITM1/FIT1 induction was associated with an increased number of lipid droplets with smaller area, while triglyceride levels were modestly increased in oleate-incubated cells. Downregulation of CALM1, the calcium-modulated Î´ subunit of phosphorylase kinase, was linked to inactivation of glycogen phosphorylase and greater accumulation of glycogen. The most upregulated gene was PVALB, which is also related to calcium signaling. In conclusion, only the deficient mitochondrial transcriptional program of cultured myotubes is rescued by PGC-1Î±. New PGC-1Î± gene targets and pathways arise, some of which may mediate its activating effects in processes such as lipid and carbohydrate storage and angiogenesis. 6 samples from 3 different skeletal muscle cell cultures were used: 3 were transfected with adenovirus containing PGC-1aplha and 3 with adenovirus containing GFP (control). The 3 PGC-1alpha samples were compared against the control samples.

Dataset Information

OVA N-glycans PGC-LC-MSMS - Large-scale identification and visualization of N-glycans with primary structures using GlySeeker

Publications

Large-scale identification and visualization of N-glycans with primary structures using GlySeeker.

Similar Datasets

OmicsDI is part of the ELIXIR infrastructure