Human colorectal cancer and wildtype LC-MSMS
Ontology highlight
ABSTRACT:
INSTRUMENT(S):
ORGANISM(S): Homo Sapiens (human)
TISSUE(S): Epithelial Cell, Colon
DISEASE(S): Colon Cancer
SUBMITTER: 
Chia-Yu Sung
LAB HEAD: Chien-Yueh Lee
PROVIDER: PXD057687 | Pride | 2026-01-28
REPOSITORIES: Pride
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| 10N_raw_peptides.txt | Txt | |||
| 10T_raw_peptides.txt | Txt | |||
| 11N_raw_peptides.txt | Txt | |||
| 11T_raw_peptides.txt | Txt | |||
| 12N_raw_peptides.txt | Txt |
Items per page: 5 1 - 5 of 65 |
Similar Datasets
Project description:SUMO modification of proteins (sumoylation) is essential for mitotic progression from yeast to humans, but only a limited number of sumoylated proteins with functions in mitosis have been discovered. Vertebrates express three SUMO paralogs, SUMO-1, SUMO-2 and SUMO-3, but only SUMO-2 and -3 are chromosome-associated in mitosis. In this study, we used chromosome spreads to more precisely define the localization of endogenous SUMO-2 and -3 to the centromere as well as the chromosome protein scaffold. Furthermore, we developed methodologies for the immunopurification of endogenous SUMO-2 and -3 modified proteins from cell extracts. Using LC-MS/MS, we analyzed proteins immunopurified from mitotic chromosome fractions and G0 nuclear fractions. We identified 296 putative sumoylated proteins, with 138 being modified specifically in mitosis. We identified proteins known to localize to the centromere and kinetochore and the chromosome protein scaffold, consistent with SUMO-2/3 localization. Furthermore, we demonstrate that utilizing cell synchronization and fractionation allowed for the discovery of low abundance sumoylated proteins that are not detected in large asynchronous analyses. Our results provide a foundation for further characterization of the roles of sumoylation in regulating diverse aspects of chromosome segregation in mitosis. Thermo .raw files were uploaded to the ProHits (Liu et al, 2010) analytical suite and converted to .mzXML format using ReAdW software. Data were searched using X!Tandem (Craig & Beavis, 2004) against human ORFs (RefSeq v45). Search parameters specified a parent MS tolerance of +/- 15ppm, and an MS/MS tolerance of 0.4 Da, with up to two missed cleavages for trypsin. Oxidation of methionine and tryptophan, ubiquitylation of lysine, and alkylation of cysteine (by NEM) were allowed as variable modifications. Statistical validation of the results was performed using Peptide Prophet and Protein Prophet (Keller et al, 2002; Nesvizhskii et al, 2003) as part of the trans-proteomic pipeline. For each search, the Protein Prophet probability at a 1% false discovery rate was used as a cutoff value to generate SAINT-compatible input files. SAINT parameters were as follows: 5000 iterations, low mode Off (0), minFold 1 and normalization (1) (Choi et al, 2011). SAINT cutoff values of 0.75 were used to generate a high-confidence list of protein identifications.
2019-11-25 | PXD000381 | Pride
Project description:The abundance of noncanonical open reading frames present in long noncoding RNAs (lncRNAs) indicates the potential for translational capacity, thereby enabling the generation of multiple functional peptides or proteins. Nevertheless, the existence of peptide or protein products derived from lncRNAs and their specific roles in gastric cancer remain largely unexplored. In this study, we identified HOXA10-HOXA9-derived small protein (HDSP) in gastric cancer by conducting a comprehensive analysis and experimental validation with mass spectrometry and western blotting. HDSP is highly expressed and has oncogenic roles in gastric cancer. Mechanistically, HDSP blocked TRIM25-mediated ubiquitination and degradation by interacting with MECOM. This led to the accumulation of MECOM, which further enhanced the transcription of SPINK1, a gene that promotes cancer through the EGFR signaling pathway. In addition, MECOM promoted the transcription of HOXA10-HOXA9, creating a feedback regulatory loop that activated downstream SPINK1-EGFR signaling. Finally, we found that HDSP knockdown inhibited tumor growth in a patient-derived xenograft (PDX) model, and the infusion of an artificially synthesized HDSP peptide as a neoantigen improved the anti-tumor efficacy of immune cells against gastric cancer in vitro and in vivo. Our findings provide a potential therapeutic target or neoantigen candidate for the treatment of gastric cancer.
2024-05-07 | PXD043737 | Pride
Project description:Traditional surgery plus radiotherapy or chemotherapy, existing targeted therapies failed to significantly improve the survival rate of recurrent endometrial cancer, so suggesting that mechanism of recurrence and progression that modulates in endometrial cancer is clinically important. Here, we show that GPER(G protein-coupled estrogen receptor 1) was binded to AMF, and the complex were translocation form plasma to cytoplasmic. Mechanistic investigations elucidated that interaction of AMF with GPER triggers phosphoinositide-3-kinase (PI3K) signaling activating and accelerating the ability of endometrial cancer cells growth. Furthermore, we found that AMF may contribute to GPER-mediated endometrial cancer progression using animal experiments and human histological experiments which be consistent with the above conclusions. On the basis of these evidences including invivo and invitro, our findings suggest that AMF–GPER interaction might be novel key molecular targets for therapeutic management of patients with endometrial cancer, whose disease were progression and recurrence.
2019-03-12 | PXD009780 | Pride
Project description:Deceased kidney donation after brain death (DBD) is the main source of transplants, yet these grafts yield inferior transplant outcomes when compared to living donation. In brain death, cerebral injury contributes to systemic biological dysregulation, causing significant cellular stress in donor kidneys that adversely impacts the quality of grafts. Here, we hypothesized that proteolytic processes in DBD kidneys might lead to podocyte damage with subsequent development of post-transplant dysfunction. Using protein topography and migration analysis platform (PROTOMAP), we mapped degradation profiles of cytoskeletal proteins in DBD kidneys. Cytoskeletal proteolytic degradation was further studied by Immunoblotting on a separate cohort of deceased and living donor kidney biopsies. To investigate potential mechanism of kidney cytoskeletal protein degradation, in-vitro human podocytes and ex-vivo precision-cut human kidney slices were employed. We found novel proteolytic profiles of key podocyte cytoskeletal proteins in donor kidneys associated with suboptimal posttransplant function. These were unique to brain-death and were not observed in circulatory-death or living-donor kidneys. Talin-specific protein degradation in DBD kidneys indicated Calpain-1 activation may have a key role in proteolytic processes observed in the dysfunctional kidneys. Investigation of the underlying mechanism suggests that Transforming-Growth Factor-β (TGFβ) induces Calpain-1 activation, leading to brain-death specific podocyte degradation patterns and dysregulation of actin cytoskeleton; events that were prevented, in-vitro, by Calpain inhibition. Conclusion Our data demonstrate that podocyte protein degradation impacts the quality of DBD kidneys, propose a role of TGFβ mediated Calpain-1 proteolytic processing of cytoskeletal Talin-1, suggesting therapeutic opportunities to prevent kidney dysfunction.
2022-08-12 | PXD022074 | Pride
Project description:This study aims to investigate differentially expressed proteins in tumor pericytes with or without TCAF2-ovexpression. Tumor pericytes were isolated from tumor of patients with colorectal cancer. Then, tumor pericytes were cultured, transfected with vector or TCAF2 overexpressing plasmid. Top ten cytokines were screened and Wnt5a was the most significant one.
2024-01-26 | PXD032935 | Pride
Project description:Drought restricts plant growth and agricultural production. As an important medicinal plant, Blumea balsamifera is sensitive to water, but there is still a lack of systematic research on its drought response mechanism.
2025-07-14 | PXD063289 | Pride
Project description:To delve deeper into the underlying mechanism of Argl’s involvement in lipid metabolism, weconducted co-immunoprecipitation (Co-IP) and mass spectrometry analysis to identify proteins thinteract with Argl.
2026-02-03 | PXD059821 | Pride
Project description:Magnetosomes are membranous organelles than contain crystals of magnetic minerals and enable magnetotactic bacteria to orientate in magnetic fields. The enveloping magnetosome membrane was found to contain a subset of specific proteins that are encoded within a genomic island. However, along with proteins that are bona fide and confirmed magnetosome proteins, proteomic studies repetitively revealed the presence of numerous other and partially highly abundant proteins within the magnetosome membrane fraction, which could not yet clearly be discriminated as contaminants, acquired during purification from other cellular compartments, or as genuine integral magnetosome membrane proteins. In order to clearly identify all proteins from the magnetotactic Alphaproteobacterium Magnetospirillum gryphiswaldense that are specifically targeted to the magnetosome membrane and to estimate their abundancy, we analyzed the protein composition of several cellular fractions by semi-quantitative mass spectrometry. Although spectra from over 1000 proteins were found within the magnetosome membrane fraction, our comparative approach could exclude most of them as contaminants. We found that almost all specifically magnetosome membrane-integral proteins belong to a well-defined subgroup of previously identified magnetosome-associated proteins, indicating that the protein composition of the compartment is strongly controlled. Furthermore, the correlation of our semi-quantitative proteome data with recently published quantitative Western blot and cryo-electron tomography results revealed that the magnetosome membrane is tightly packed with transmembrane domains of integral proteins, indicating a very high protein composition of the membrane. Our findings will help to further define the structure of the organelle and contribute to the elucidation of the processes involved in biogenesis of magnetosomes.
2017-10-24 | PXD006166 | Pride
Project description:Innate immunity serves as the primary defense against viral and microbial infections in humans. Among its components, retinoic acid-inducible gene I (RIG-I)-like receptors (RLRs) are well-characterized intracellular pattern-recognition proteins that trigger innate immune responses upon viral infection. However, the precise influence of cellular metabolites, especially fatty acids, on the regulation of RLR-mediated antiviral innate immunity remains largely elusive. Here, through screening a metabolite library, palmitic acid (PA) has been identified as a crucial metabolite responsible for modulating antiviral infections. Mechanistically, PA induces the palmitoylation of MAVS, leading to MAVS aggregation and subsequent activation, thereby enhancing the innate immune response against viral infections. Functionally, the enzyme palmitoyl-transferase ZDHHC24 plays a key role in catalyzing the palmitoylation of MAVS at both C46 and C79 residues, thereby facilitating the transduction of RLR-mediated TBK1-IRF3-IFN signaling pathway, particularly under conditions of PA stimulation or high-fat diet feeding. Conversely, the absence of ZDHHC24 significantly attenuates virus-induced innate immune responses in both cells and mice. Moreover, APT2 counteracts with ZDHHC24 to de-palmitoylate MAVS, thus inhibiting the antiviral response. Consequently, inhibition of APT2 using compounds like ML349 effectively reverses MAVS palmitoylation and activation in response to antiviral infections. These findings underscore the critical role of PA and ZDHHC24 in regulating antiviral innate immunity through MAVS palmitoylation, and suggest potential therapeutic strategies for combating viral infections, such as enhancing PA intake or specifically targeting APT2.
2024-09-10 | PXD054077 | Pride
Project description:Tieguanyin (TGY) and Shuixian (SX) cultivars of Camellia sinensis were selected to explore the mechanism underlying the accumulation of the rare earth element lanthanum through proteomics. Roots and fresh leaves of TGY and SX with low- and high-accumulation potential for lanthanum, respectively, were studied; 845 differentially expressed proteins (DEPs) were identified. Gene ontology analysis showed that the DEPs are involved in redox processes and related to molecular functions, such as defense and oxidative stress reactions, catalytic activity, and metal ion binding. Kyoto Encyclopedia of Genes and Genomes metabolic pathway analysis showed that DEPs were associated with glutathione (GSH) and α-linolenic acid metabolism, plant pathogen interaction, and oxidative phosphorylation. Thirty-seven proteins in the GSH metabolism pathway showed significant differences, of which 18 GSH S-transferases show differential expression patterns in the root system.The expression multiples of GST (TEA004130.1) and GST (TEA032216.1) in T1L and T0L were 6.84 and 4.06, respectively, which were significantly higher than those in S1L and S0L. The lanthanum-induced activation of the GSH-related antioxidant defense system may cause the difference in TGY and SX. The LOX2.1 (TEA011765.1) and LOX2.1 (TEA011776.1 expression ratios) in the α-linolenic acid metabolic pathway were 2.44 and 6.43 in T1R and T0R, respectively, which were significantly higher than those in S1R snd S0R. The other differential proteins were also sig-nificantly upregulated in TGY leaves.The synthesis of specific substances induces lantha-num-associated defense responses in TGY, which is of great significance for the stability of its yield.
2023-03-11 | PXD039195 | Pride