Project description:N-terminomics of mitochondrial proteins using subtiligase
Additional variable modifications:
Abu (L-aminobutyric acid) (+85.05276 Da)
Project description:N-terminomics of mitochondrial proteins using subtiligase
Additional variable modifications:
Abu (L-aminobutyric acid) (+85.05276 Da)
Project description:N-terminomics of mitochondrial proteins using subtiligase
Additional variable modifications:
Abu (L-aminobutyric acid) (+85.05276 Da)
Project description:Subtiligase based reverse N-terminomics (Abu N-terminal tagging) of two Jurkat cell lysate replicates incubated with SARS-CoV-2 PLpro.
Project description:Subtiligase-based N-terminomics (Abu N-terminal tagging) of whole mouse brain and immunoprecipitated prion protein. Mouse expressing either WT or mutant (S3) form of PrP were used in this study. Five replicates for single brain experiments and one replicate for combined brains approach are included. For labeling of PrP, 2 biological replicates are part of the study.
Project description:We surveyed the heterogeneity of the mitochondrial proteome and its function during a typical night and day cycle in Arabidopsis shoots. This used a staged, quantitative analysis of the proteome across 10 time points covering 24 h of the life of 3-week-old Arabidopsis shoots grown under 12-h dark and 12-h light conditions. Results were queried against an in-house Arabidopsis database comprising ATH1.pep (release 7) from The Arabidopsis Information Resource and the Arabidopsis mitochondrial and plastid protein sets (the combined database contained a total of 30,700 protein sequences with 12,656,682 residues) using the Mascot search engine version 2.2 and utilizing error tolerances of +-1.2 Da for MS and +-0.6 Da for MS/MS, 'enzyme' set to trypsin, 'maximum missed cleavages' set to 1, variable modifications of oxidation (Met) and carbamidomethyl (Cys), instrument set to ESI-TRAP, and peptide charge set at 2+ and 3+. ATH1.pep is a non-redundant database with systematically named protein sequences based on Arabidopsis genome sequencing and annotation. PRIDE XML files with accession numbers 10471–10525 and without peptide/protein identifications have already been made public.
Project description:<p> Human disorders of mitochondrial oxidative phosphorylation (OXPHOS) represent a devastating collection of inherited diseases. These disorders impact at least 1:5000 live births, and are characterized by multi-organ system involvement. They are characterized by remarkable locus heterogeneity, with mutations in the mtDNA as well as in over 77 nuclear genes identified to date. It is estimated that additional genes may be mutated in these disorders. </p> <p>To discover the genetic causes of mitochondrial OXPHOS diseases, we performed targeted, deep sequencing of the entire mitochondrial genome (mtDNA) and the coding exons of over 1000 nuclear genes encoding the mitochondrial proteome. We applied this 'MitoExome' sequencing to 124 unrelated patients with a wide range of OXPHOS disease presentations from the Massachusetts General Hospital Mitochondrial Disorders Clinic. </p> <p>The 2.3Mb targeted region was captured by hybrid selection and Illumina sequenced with paired 76bp reads. The total set of 1605 targeted nuclear genes included 1013 genes with strong evidence of mitochondrial localization from the MitoCarta database, 377 genes with weaker evidence of mitochondrial localization from the MitoP2 database and other sources, and 215 genes known to cause other inborn errors of metabolism. Approximately 88% of targeted bases were well-covered (>20X), with mean 200X coverage per targeted base. </p>
Project description:Extremely variable clinic and genetic features characterize Mitochondrial Encephalomyopathy Disorders (MED). Pathogenic mitochondrial DNA (mtDNA) defects can be divided into large-scale rearrangements and single point mutations. Clinical manifestations become evident when a threshold percentage of the total mtDNA is mutated. In some MED, the "mutant load" in an affected tissue is directly related to the severity of the phenotype. However, the clinical phenotype is not simply a direct consequence of the relative abundance of mutated mtDNA. Other factors, such as nuclear background, can contribute to the disease process, resulting in a wide range of phenotypes caused by the same mutation. Using Affymetrix oligonucleotide cDNA microarrays (HG-U133A), we studied the gene expression profile of muscle tissue biopsies obtained from 12 MED patients (4 common 4977-bp deleted mtDNA and 8 A3243G: 4 PEO and 4 MELAS phenotypes) compared with age-matched healthy individuals. Keywords = mtDNA mutation Keywords = muscle biopsy Keywords = human Keywords = mitochondrial disease Keywords: other
Project description:Extremely variable clinic and genetic features characterize Mitochondrial Encephalomyopathy Disorders (MED). Pathogenic mitochondrial DNA (mtDNA) defects can be divided into large-scale rearrangements and single point mutations. Clinical manifestations become evident when a threshold percentage of the total mtDNA is mutated. In some MED, the "mutant load" in an affected tissue is directly related to the severity of the phenotype. However, the clinical phenotype is not simply a direct consequence of the relative abundance of mutated mtDNA. Other factors, such as nuclear background, can contribute to the disease process, resulting in a wide range of phenotypes caused by the same mutation. Using Affymetrix oligonucleotide cDNA microarrays (HG-U133A), we studied the gene expression profile of muscle tissue biopsies obtained from 12 MED patients (4 common 4977-bp deleted mtDNA and 8 A3243G: 4 PEO and 4 MELAS phenotypes) compared with age-matched healthy individuals.