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Order 30968 - Carla Miro Vinyals 2023-02-23, Order 35373 - Carla Miro Vinyals 2024-05-29

ABSTRACT: HeLa or HEK293 cells transiently transfected with Galt1-sCGrx1p-HA redox sensor protein. Cells were treated with 0.1 mM IAA for 20 min on ice. The samples are anti-HA magnetic beads with the sensor protein captured from whole cell lysate.

INSTRUMENT(S):

ORGANISM(S): Homo Sapiens (human)

SUBMITTER: Tobias Kockmann

LAB HEAD: Pablo Rivera

PROVIDER: PXD060874 | Pride | 2025-02-19

REPOSITORIES: Pride

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			Action	DRS
	20230224_C30968_002_S474941_HeLa_Galt1sCGrx1pHA_01IAA_B_Cell_extracts.raw	Raw
	20230224_C30968_003_S474940_HeLa_Galt1sCGrx1pHA_01IAA_A_Cell_extracts.raw	Raw
	20230224_C30968_004_S474942_HeLa_Galt1sCGrx1pHA_01IAA_C_Cell_extracts.raw	Raw
	20240606_C35373_002_S698656_HEK293_Galt1sCGrx1pHA_01IAA_rep3_Cell_extracts.raw	Raw
	20240606_C35373_003_S698654_HEK293_Galt1sCGrx1pHA_01IAA_rep1_Cell_extracts.raw	Raw

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Publications

Characterization of the glutathione redox state in the Golgi apparatus.

Miró-Vinyals Carla C Emmert Sarah S Grammbitter Gina G Jud Alex A Kockmann Tobias T Rivera-Fuentes Pablo P

Redox biology 20250219

Redox homeostasis is crucial for cell function, and, in eukaryotic cells, studying it in a compartmentalized way is essential due to the redox variations between different organelles. The redox state of organelles is largely determined by the redox potential of glutathione, EGSH, and the concentration of its reduced and oxidized species, [GS]. The Golgi apparatus is an essential component of the secretory pathway, yet little is known about the concentration or redox state of GSH in th ...[more]

PMID: 39986117

Similar Datasets

Order 28341 - Carla Miro Vinyals 2022-05-09

Project description:HeLa treated with IAA or NEM (Figure S3). Stable cell line expressing GALT1-HA-sCGrx1p sensor protein were treated with 20 mM NEM (A) or IAA (B) for 30 min at 37°C. The processed samples are anti-HA magnetic beads with the sensor protein captured from whole cell lysate.

2025-02-17 | PXD060873 | Pride

Auxin-induced gene expression in mesocotyl elongation of maize inbred line 3681-4 tolerant to deep-sowing

Project description:In order to elucidate the molecular mechanism of auxin-induced mesocotyl elongation, gene expression profiling analyses were performed in a deep-sowing tolerant maize inbred line 3681-4. Gene expression studies combing Affymetrix GeneChip analysis and Real-time PCR were employed to determine the molecular mechanism underlying IAA promotion of maize mesocotyl elongation. Under deep-sowing condition, IAA is transported by auxin transporter-like protein 1 and binds to auxin binding protein ABP20, which results in degradation of Aux/IAA and de-repressing of auxin-inducible genes. Then, transcriptional factor such as MYB, kinase such as LRR, fructose and mannose metabolism and so on are activated. Finally, genes involved in cell wall synthesis and modification are expressed so that mesocotyl elongation of 3681-4 is promoted. Furthermore, gene expression of a key enzyme ACO in ethylene biosynthesis and ethylene receptor ETR2 were up-regulated after the treatment with 10-4 M IAA, which suggested that mesocotyl elongation of 3681-4 inclined to be inhibited when the concentration of applied IAA was increased from 10-4 M to 10-3 M. In two independent experiments, we generate 10-day-old maize mesocotyl-specific gene expression profiles through comparing genome-wide expression patterns of IAA treatment and TIBA (an auxin transportation inhibitor) treatment under 20 cm deep-sowing condition in darkness by using 17,555 Affymetrix maize whole genome array.

2009-03-26 | E-GEOD-15371 | biostudies-arrayexpress

Transcription profiling of Saccharomyces cerevisiae pGAL1-MKS1, pGAL1-NNK1, and pGAL1-FMP48 overexpression

Project description:Analysis of the transcriptional effects of pGAL1-MKS1, pGAL1-NNK1, and pGAL1-FMP48 overexpression. BY4700 gal1::NAT ura3delta0 S. cerevisiae cells carrying a [pGAL1-MKS1-HA, URA3, CEN], [pGAL1-NNK1-HA, URA3, CEN], or [pGAL1-FMP48-HA, URA3, CEN] plasmid, or empty vector BG1805, were grown to early log phase, induced with 0.2% galactose, and harvested after 1.5 h and 6 h. RNA from a strain overexpressing MKS1, NNK1, or FMP48 was competitively hybridized with RNA from an identically treated strain carrying empty vector. FMP48 = YGR052W. MKS1 = YNL076W. NNK1 = YKL171W.

2010-05-25 | E-MEXP-2171 | biostudies-arrayexpress

Exserohilum rostratum isolate:F01-23-02

Project description:Exserohilum rostratum

| PRJNA990688 | ENA

Pharmacokinetics and safety of a single intravenous dose of myo-inositol in preterm infants of 23-29 wk.

Project description:BackgroundMyo-inositol given to preterm infants with respiratory distress has reduced death, increased survival without bronchopulmonary dysplasia, and reduced severe retinopathy of prematurity in two randomized trials. Pharmacokinetic (PK) studies in extremely preterm infants are needed before efficacy trials.MethodsInfants born in 23-29 wk of gestation were randomized to a single intravenous (i.v.) dose of inositol at 60 or 120 mg/kg or placebo. Over 96 h, serum levels (sparse sampling population PK) and urine inositol excretion were determined. Population PK models were fit using a nonlinear mixed-effects approach. Safety outcomes were recorded.ResultsA single-compartment model that included factors for endogenous inositol production, allometric size based on weight, gestational age strata, and creatinine clearance fit the data best. The central volume of distribution was 0.5115 l/kg, the clearance was 0.0679 l/kg/h, endogenous production was 2.67 mg/kg/h, and the half-life was 5.22 h when modeled without the covariates. During the first 12 h, renal inositol excretion quadrupled in the 120 mg/kg group, returning to near-baseline value after 48 h. There was no diuretic side effect. No significant differences in adverse events occurred among the three groups (P > 0.05).ConclusionA single-compartment model accounting for endogenous production satisfactorily described the PK of i.v. inositol.

| S-EPMC3962781 | biostudies-literature

Identification of proteins binding "ubiquitin like" activity based probes

Project description:HA antibody beads were used to pulldown HA proteins in a cell lysate. The HA protein is an activty based probe (consisting of a small protein and a warhead) and was spiked into the cell lysate. 35, 156, 149 and 61 are different probes. Experiments were performed with and without pretreatment of the cell lysate with IAA an alkylating agent which should reduce the binding between the probe and its targets in cell lysate (cysteine based proteases).

2022-11-29 | MSV000090802 | MassIVE

Endoplasmic Reticulum Aminopeptidase 1 (ERAP1) Polymorphism Relevant to Inflammatory Disease Shapes the Peptidome of the Birdshot Chorioretinopathy-Associated HLA-A*29:02 Antigen.

Project description:Birdshot chorioretinopathy is a rare ocular inflammation whose genetic association with HLA-A*29:02 is the highest between a disease and a major histocompatibility complex (MHC) molecule. It belongs to a group of MHC-I-associated inflammatory disorders, also including ankylosing spondylitis, psoriasis, and Behçet's disease, for which endoplasmic reticulum aminopeptidases (ERAP) 1 and/or 2 have been identified as genetic risk factors. Since both enzymes are involved in the processing of MHC-I ligands, it seems reasonable that common peptide-mediated mechanisms may underlie the pathogenesis of these diseases. In this study, comparative immunopeptidomics was used to characterize >5000 A*29:02 ligands and quantify the effects of ERAP1 polymorphism and expression on the A*29:02 peptidome in human cells. The peptides predominant in an active ERAP1 context showed a higher frequency of nonamers and bulkier amino acid side chains at multiple positions, compared with the peptides predominant in a less active ERAP1 background. Thus, ERAP1 polymorphism has a large influence, shaping the A*29:02 peptidome through length-dependent and length-independent effects. These changes resulted in increased affinity and hydrophobicity of A*29:02 ligands in an active ERAP1 context. The results reveal the nature of the functional interaction between A*29:02 and ERAP1 and suggest that this enzyme may affect the susceptibility to birdshot chorioretinopathy by altering the A*29:02 peptidome. The complexity of these alterations is such that not only peptide presentation but also other potentially pathogenic features could be affected.

| S-EPMC4587329 | biostudies-literature

Effect of TMAO and Urea on Dimers and Tetramers of Amyloidogenic Heptapeptides (23FGAILSS29).

Project description:Human islet amyloid polypeptide (hIAPP) (1-37) is an intrinsically disordered protein that is released with insulin by β-cells found in the pancreas. Under certain environmental conditions, hIAPP can aggregate, which leads to β-cell death. FGAILSS (23-29) residues of the hIAPP protein form β sheets, which may be toxic species in type 2 diabetes (T2D) patients. All-atom molecular dynamics (MD) simulations have been used to analyze the effect of two distinct types of osmolytes trimethylamine N-oxide (TMAO) and urea on two and four FGAILSS heptapeptides. TMAO leads the individual peptide toward an extended conformation with a higher radius of gyration and favors the formation of antiparallel β-sheets with an increase in its concentration. However, urea mostly shows compaction of individual peptides except at 4.0 M in the case of a tetramer but does not show aggregation behavior as a whole. TMAO leads both the dimer and tetramer toward the native state with an increase in its concentration. Moreover, both the dimer and tetramer show irregular behavior in urea. The tetramer in 4.0 M urea shows the maximum fraction of native contacts due to the formation of antiparallel β-sheets. This formation of antiparallel β-sheets favors the aggregation of peptides. TMAO forms a smaller number of hydrogen bonds with peptides as compared to urea as the exclusion of TMAO and accumulation of urea around the peptides have occurred in the first solvation shell (FSS). Principal component analysis (PCA) results suggest that the minima in the free energy landscape (FEL) plot are homogeneous for a particular conformation in TMAO with smaller basins, while in urea, the dimer shows minima mostly for extended conformations. For a 4.0 M urea concentration, the tetramer shows the minimum for antiparallel β-sheets, which indicates the aggregation behavior of the tetramer, and for a higher concentration, it shows minima with wider basins of extended conformations.

| S-EPMC7593999 | biostudies-literature

Variation in auxin sensing guides AUX/IAA repressor ubiquitylation and destruction

Project description:Auxin is a drug-like small molecule and morphogen that triggers the formation of SCFTIR1/AFB-AUX/IAA co-receptor complexes leading to ubiquitylation and proteasome-dependent degradation of AUX/IAA transcriptional repressors in plants. Here, we systematically dissect auxin sensing by SCFTIR1-IAA6 and SCFTIR1-IAA19 co-receptor complexes, and assess IAA6/IAA19 ubiquitylation in vitro and IAA6/IAA19 degradation in vivo. TIR1-IAA19 and TIR1-IAA6 interactions form co-receptors with different affinities, which specify ubiquitylation and turnover rate of the AUX/IAA. We demonstrate lysine ubiquitylation in IAA6/IAA19 and propose this ubiquitylation signature to be a consequence of auxin-mediated SCFTIR1-AUX/IAA interactions. We present evidence for an evolving AUX/IAA repertoire, typified by the IAA6/IAA19 ohnologs, that contributes differentially to auxin sensing. We postulate that AUX/IAAs have emerged as a versatility toolbox for auxin-modulated transcriptional control, as the gamut of AUX/IAA destruction kinetics enables fine-tuning of transcriptional auxin response and contributes to the complexity of hormone signaling.

2017-06-14 | PXD004027 | Pride

Allele-specific Alterations in the Peptidome Underlie the Joint Association of HLA-A*29:02 and Endoplasmic Reticulum Aminopeptidase 2 (ERAP2) with Birdshot Chorioretinopathy.

Project description:Virtually all patients of the rare inflammatory eye disease birdshot chorioretinopathy (BSCR) carry the HLA-A*29:02 allele. BSCR is also associated with endoplasmic reticulum aminopeptidase 2 (ERAP2), an enzyme involved in processing HLA class I ligands, thus implicating the A*29:02 peptidome in this disease. To investigate the relationship between both risk factors we employed label-free quantitative mass spectrometry to characterize the effects of ERAP2 on the A*29:02-bound peptidome. An ERAP2-negative cell line was transduced with lentiviral constructs containing GFP-ERAP2 or GFP alone, and the A*29:02 peptidomes from both transduced cells were compared. A similar analysis was performed with two additional A*29:02-positive, ERAP1-concordant, cell lines expressing or not ERAP2. In both comparisons the presence of ERAP2 affected the following features of the A*29:02 peptidome: 1) Length, with increased amounts of peptides >9-mers, and 2) N-terminal residues, with less ERAP2-susceptible and more hydrophobic ones. The paradoxical effects on peptide length suggest that unproductive binding to ERAP2 might protect some peptides from ERAP1 over-trimming. The influence on N-terminal residues can be explained by a direct effect of ERAP2 on trimming, without ruling out and improved processing in concert with ERAP1. The alterations in the A*29:02 peptidome suggest that the association of ERAP2 with BSCR is through its effects on peptide processing. These differ from those on the ankylosing spondylitis-associated HLA-B*27. Thus, ERAP2 alters the peptidome of distinct HLA molecules as a function of their specific binding preferences, influencing different pathological outcomes in an allele-dependent way.

| S-EPMC6072538 | biostudies-literature

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