Human tear LC-MS/MS on allergy vs healthy controls
Ontology highlight
ABSTRACT:
INSTRUMENT(S):
ORGANISM(S): Homo Sapiens (human)
TISSUE(S): Tear
SUBMITTER: 
Esrin Aydin
LAB HEAD: Cenk Suphioglu
PROVIDER: PXD051204 | Pride | 2024-05-08
REPOSITORIES: Pride
Dataset's files
Items per page: 5 1 - 5 of 60 |
Similar Datasets
Project description:Many proteins undergo glycosylation in the endoplasmic reticulum (ER) and the Golgi apparatus. Altered glycosylation can manifest in serious, sometimes fatal malfunctions. We recently showed that mutations in the cytoplasmic protein GDP-mannose pyrophosphorylase A (GMPPA) cause a syndrome characterized by alacrima, achalasia, mental retardation and myopathic alterations. GMPPA acts as feedback inhibitor of GDP-mannose pyrophosphorylase B (GMPPB), which provides GDP-mannose as a substrate for protein glycosylation. Loss of GMPPA enhances incorporation of mannose into glycochains of various proteins, including α-dystroglycan (α-DG), a protein that links the extracellular matrix with the cytoskeleton. Here, we show that loss of GMPPA affects the functionality of the Golgi apparatus using different approaches. First, we show a fragmentation of the Golgi apparatus in skeletal muscle fibers and in neurons of GMPPA KO mice. A major reorganization is also evident by mass spectrometry of KO tissues with a regulation of several ER- and Golgi-resident proteins. We further show that loss of GMPPA increases the retention of α-DG in the ER. Notably, mannose supplementation can mimic changes in ER and Golgi structure and function in WT cells. In summary, our data underline the importance of a balanced mannose homeostasis for structure and function of the secretory pathway.
2023-03-11 | PXD037129 | Pride
Project description:Mass spectrometry-based whole proteome analysis of parental and RFX7 knock-out U2OS cells treated with 10 µM Nutlin-3a or DMSO solvent control. Ten biological replicates were used.
2023-03-11 | PXD024869 | Pride
Project description:proteome and glycoproteome comparsion of fut8 KO vs Wt mouse NK cells.
2025-07-29 | PXD043834 | Pride
Project description:Many bacteria and archaea use CRISPR-Cas systems, which provide RNA-based, adaptive, and inheritable immune defenses against invading viruses and other foreign genetic elements. The proper processing of CRISPR guide RNAs (crRNAs) is a crucial step in the maturation of the defense complexes and is frequently performed by specialized ribonucleases encoded by cas genes. However, some systems employ enzymes associated with degradosome or housekeeping functions, such as RNase III or the endoribonuclease RNase E. Here, the endo- and 5´-exoribonuclease RNase J was identified as additional enzyme involved in crRNA maturation, acting jointly with RNase E in the crRNA maturation of a type III-Bv CRISPR-Cas system, and possibly together with a further RNase. Co-IP experiments revealed a small set of proteins that were co-enriched with RNase J, among them PNPase. Despite a measured, strong 3’ exonucleolytic activity of the recombinant enzyme, PNPase was not confirmed to contribute to crRNA maturation. However, the co-IP results indicate that PNPase is a component of the cyanobacterial degradosome that can recruit either RNase E or RNase J, together with additional enriched proteins.
2025-10-06 | PXD060866 | Pride
Project description:Objective To establish whether whole-blood MicroRNA (miRNA) profiles differ between postural tachycardia syndrome (POTS) sufferers and control subjects, and to identify the miRNA that regulate plasma H2S. Study design: High-throughput sequencing was used to obtain whole-blood miRNA expression profiles for five POTS sufferers and five normal children. miRNAs with an adjusted P-value of <0.05 (by DESeq) and with a log2 fold change ≥3 were considered to be differentially expressed (DEmiRNAs). The target genes of the DEmiRNAs were identified using RNAhybrid and miRanda, and only those identified by both were considered. The combined effects of the DEmiRNAs were determined using KEGG pathway analysis. Another 40 POTS and 20 normal patients were used as validation subjects. Plasma H2S was determined with a sulfide electrode, and flow-mediated vasodilation (FMD) was performed with a color Doppler ultrasound system. miRNAs were analyzed using QRT-PCR. Results: Thirteen DEmiRNAs were identified. When P values of 0.01 and 0.05 were used, 198 and 481 genes, respectively, were shown to be targeted by the 13 DEmiRNAs. DEmiRNAs were significantly enriched in 36 pathways (P <.05), in which PI3K/Akt signaling was closely related to vascular function. In the validation subjects, the plasma H2S and FMD was higher in the POTS sufferers, as was the expression level of whole-blood miR-21 (P <.05), which identified POTS patients with a sensitivity of 92.5% and a specificity of 100%. Conclusion: Elevated whole-blood miR-21 levels serve as an indicator for POTS and may explain the increased plasma H2S observed in POTS sufferers.
2022-06-07 | E-MTAB-10961 | biostudies-arrayexpress
Project description:Proteomics analysis of iWAT-EVs to identify EV related markers in young and aged mice
2025-09-05 | PXD066710 | Pride
Project description:In this study we looked for the main protein pathway regulators which were responsible for the therapeutic impact on colon cancers when combining magnetic hyperthermia with the chemo-therapeutic agent 5-fluorouracil (5FU). In this context, chitosan-coated magnetic nanoparticles (MNP) functionalized with 5FU were intratumorally injected into subcutaneous human colon cancer xenografts (HT-29) in mice and exposed to an alternating magnetic field. A decreased tu-mor growth was found particularly for the combined thermo-chemotherapy vs. the correspond-ing monotherapies. By using computational analysis of the tumor proteome, we found upregu-lated functional pathway categories termed “cellular stress and injury”, “intracellular second messenger and nuclear receptor signaling”, “immune responses”, and “growth proliferation and development”. We predict TGF-beta, and other mediators, as important upstream regulators. In conclusion our findings show that the combined thermo-chemotherapy induces thrombogenic collagen fibers which are able to impair tumor nutrient supply. Further on, we associate several responses to the recognition of damage associated molecular patterns (DAMPs) by phagocytic cells, which immigrate into the tumor area. The activation of some pathways associated with cell survival implies the necessity to conduct multiple therapy sessions in connection with a corre-sponding monitoring, which could possibly be conducted on the base of the identified protein regulators.
2021-11-10 | PXD027656 | Pride
Project description:Hematopoietic stem cell transplantation (HSCT) is successfully applied since the late 1950s, however, its efficacy still needs to be improved. A promising strategy is to transplant high numbers of pluripotent hematopoietic stem cells (HSCs). Therefore, an advanced ex vivo culture system is needed that supports the proliferation and maintains the pluripotency of HSC to override possible limitations in cell numbers gained from donors. To model the natural HSC niche in vitro and thus, to amplify high numbers of undifferentiated HSCs, we used an optimized HSC cell culture medium in combination with artificial 3D bone marrow-like scaffolds made of polydimethylsiloxane (PDMS). After 14 days in vitro (DIV) cell culture, we performed transcriptome and proteome analysis of the whole cell populations. Ingenuity pathway analysis (IPA) indicated that our 3D PDMS cell culture scaffolds activated interleukin, SREBP, mTOR and FOXO signaling pathways as well as the HSC metabolism, which we confirmed by ELISA, Western blot and metabolic flux analysis. These molecular signaling pathways and HSC metabolism are well known to promote the expansion HSCs and are involved in their pluripotency maintenance. After selection and enrichment of immature CD34-positive/CD38-negative HSCs using FACS sorting, we could confirm our findings by another proteome analysis followed by IPA. Thus, we could show that our 3D bone marrow-like PDMS scaffolds activate key molecular signaling pathways to amplify the numbers of undifferentiated HSC efficiently ex vivo.
2021-11-10 | PXD025849 | Pride
Project description:Purpose: Chemotherapy is pivotal in the multimodal treatment of pancreatic cancer patients. In recent years, technical advances have developed experimental methods that unveiled a high degree of inter- and intratumoral heterogeneity in pancreatic cancer. We hypothesized that intratumoral heterogeneity (ITH) impacts response to gemcitabine treatment and demands specific targeting of resistant subclones. Experimental Design: We addressed the effect of ITH on response to gemcitabine treatment using single cell-derived cell lines (SCDCL) from the classical-like cell line BxPC3 and the basal-like cell line Panc-1 which were analyzed by mRNA-seq and mass spectrometry. Results: Individual SCDCLs of the parental tumor cell populations of BxPC3 and Panc-1 showed considerable heterogeneity in response to gemcitabine. Unsupervised principal component analysis (PCA) including the 1,000 most variably expressed genes showed a clustering of the SCDCLs according to their respective sensitivity to gemcitabine treatment for BxPC3, while this clustering was less clear for Panc-1. In BxPC3 SCDCLs, enriched signaling pathways EMT, TNF signaling via NfKB, and IL2STAT5 signaling correlated with more resistant behavior to gemcitabine. In Panc-1 SCDCLs MYC targets V1 and V2 as well as E2F targets were associated with stronger resistance to gemcitabine. Feature extraction of proteomes again identified less proteins whose expression was associated with the response of individual SCDCLs in Panc-1 compared to BxPC3. Based on molecular profiles, we could show that the gemcitabine-resistant SCDCLs of both BxPC3 and Panc-1 are more sensitive to the BET inhibitor JQ1 compared to the respective gemcitabine-sensitive SCDCLs. Conclusions: Our model system of SCDCLs identified gemcitabine-resistant subclones within a parental tumor population and provides evidence for the critical role of ITH for treatment response in pancreatic cancer. Through molecular profiling, we identified specific signaling pathways and protein signatures that might help to explain the differential response to treatment among clones. We exploited these molecular differences for an improved and more targeted therapy of resistant subclones of a heterogeneous tumor.
2023-09-19 | PXD042256 | Pride
Project description:Increasing evidence suggests that in Amyotrophic Lateral Sclerosis (ALS) mutated RNA binding proteins acquire aberrant functions, leading to altered RNA metabolism with significant impact on encoded protein levels. Here, by taking advantage of a human induced Pluripotent Stem Cell (hiPSC)-based model, we aimed to gain insights on the impact of ALS mutant FUS on the motoneuron proteome. Label-free proteomics analysis by mass-spectrometry revealed upregulation of proteins involved in catabolic processes and oxidation-reduction, and downregulation of cytoskeletal proteins and factors directing neuron projection. Mechanistically, proteome alteration does not correlate with transcriptome changes. Rather, we observed a strong correlation with selective binding of mutant FUS to target mRNAs in their 3’UTR. Novel validated targets, selectively bound by mutant FUS only, include genes previously involved in familial or sporadic ALS, such as VCP, and regulators of membrane trafficking and cytoskeleton remodeling, such as ASAP1. These findings unveil a novel mechanism by which mutant FUS might intersect other pathogenic pathways in ALS patients’ motoneurons.
2020-10-27 | PXD019596 | Pride