Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Tamm-Horsfall protein augments neutrophil NETosis

ABSTRACT: Proteome profiles of isolated peripheral human neutrophils pretreated with purified Tamm-Horsfall protein and stimulated to undergo NETosis with PMA.

INSTRUMENT(S): Orbitrap Exploris 480

ORGANISM(S): Homo Sapiens (human)

SUBMITTER: Antrix Jain

LAB HEAD: Kathryn Patras

PROVIDER: PXD045468 | Pride | 2024-09-23

REPOSITORIES: pride

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	51066_1_EXP_914_hs_TMT16_prof_250ng_F01.mokapot.psms.txt	Txt
	51066_1_EXP_914_hs_TMT16_prof_250ng_F01.pepXML	Pepxml
	51066_1_EXP_914_hs_TMT16_prof_250ng_F01.raw	Raw
	51066_1_EXP_914_hs_TMT16_prof_250ng_F02.mokapot.psms.txt	Txt
	51066_1_EXP_914_hs_TMT16_prof_250ng_F02.pepXML	Pepxml

Items per page:

1 - 5 of 75

Similar Datasets

Project title: Effect of FHD-286 or BRG1/BRM degrader AU15330 on protein expressions in MLL1-rearranged AML cells

Project description:MOLM13 cells and patient-derived de novo AML cells with MLL1 rearrangement were treated with 100 nM of FHD-286 or 100 nM of AU15330, a dual BRG1/BRM protein degrader for 48 hours. The goal was to determine the global protein expression alterations that correlate with the cell cycle, growth inhibitory and/or lethal effects of treatment with a chromatin remodeling inhibitor, FHD-286, or a BRG1/BRM protein degrader in MLL1-rearranged AML cells.

2025-04-28 | PXD055994 | Pride

Determination of protein expression changes due to treatment with chromatin remodeling inhibitor FHD-286 in MLL1-rearranged AML cells

Project description:We treated MLL1-rearranged AML MOLM13 cells with a chromatin remodeling inhibitor, FHD-286, at a dose of 100 nM, for different time intervals (up to 48 hours) to measure the time-dependent changes to the AML proteome

2025-05-26 | PXD047965 | Pride

Determination of protein expression changes due to treatment with chromatin remodeling inhibitor FHD-286 in patient-derived mutant NPM1 and FLT-ITD-expressing AML cells

Project description:We treated patient-derived mutant NPM1-and FLT3-ITD expressing AML cells with a chromatin remodeling inhibitor, FHD-286, at a dose of 100 nM, for 48 hours to determine FHD-286-mediated changes to the AML proteome.

2025-05-06 | PXD047967 | Pride

Transcriptome sequencing of human neutrophil

Project description:TcpC is a multifunctional virulence factor of uropathogenic E. coli (UPEC). Neutrophil extracellular trap formation (NETosis) is a crucial anti-infection mechanism of neutrophils. Here we show the influence of TcpC on NETosis and related mechanisms. In situ NETosis of kidneys from pyelonephritis mouse model induced by TcpC-secreting wild-type CFT073 (CFT073wt) and LPS-induced in vitro NETosis in CFT073wt- or recombinant TcpC (rTcpC)-treated neutrophils are inhibited. rTcpC enters neutrophils through caveolin-mediated endocytosis and inhibits LPS-induced production of ROS, proinflammatory cytokines and protein but not mRNA levels of peptidylarginine deiminase 4 (PAD4). rTcpC treatment enhances PAD4 ubiquitination and accumulation in proteasomes. Moreover, in vitro ubiquitination kit analyses suggest that TcpC is a PAD4-targetd E3 ubiquitin-ligase. These data suggest that TcpC inhibits NETosis primarily by serving as an E3 ligase that promotes degradation of PAD4. Our findings provide a novel mechanism underlying TcpC-mediated innate immune evasion.

2021-05-05 | GSE173807 | GEO

Phospho-proteomic Analyses Provide Insight into Underlying Molecular Mechanisms of NETosis

Project description:NETosis, a novel cell death leads to neutrophil extracellular trap (NET) formation, is involved in both infectious and noninfectious disease. However, mechanisms underlying NETosis remain unclear. To explore the underlying molecular mechanisms and common factors associated with both NOX-dependent and NOX-independent NETosis, we conducted global proteomics and phospho-proteomics analyses of phorbol 12-myristate 13-acetate (PMA)-, ionomycin-, and monosodium urate (MSU) - induced early stage NETosis. Global proteomic analyses identified 64, 97, and 141 proteins differentially regulated in the PMA, ionomycin, and MSU comparisons with the control, respectively. Next, phospho-proteomic analyses identified: 931, 565 and 201 phosphorylation sites differentially regulated in the PMA, ionomycin, and MSU comparisons with the control, respectively. Furthermore, overlap analysis of the three comparisons identified 9 proteins and 49 phosphorylation sites derived from 41 phosphoproteins. Among the 41 differentially regulated phosphoproteins, 23 were associated with the nucleus, 5 with chromatin binding and 13 with poly(A) RNA binding according to GO annotation. Of which, DEK, Methyl-CpG-binding protein 2 (MECP2) and structure-specific recognition protein 1 (SSRP1) involved in both chromatin and poly(A) RNA binding. In conclusion, our study provides insight into molecular mechanisms of NETosis and this dataset will be benefit for further elucidation.

2019-06-27 | PXD014418 |

NET proteome of neutrophils from people with long-standing type 1 diabetes and healthy control

Project description:Type 1 diabetes (T1D) is a chronic T-cell-mediated autoimmune disease, leading to the destruction of the pancreatic insulin-producing beta cells. Little is known about the involvement of neutrophils that exert multifaceted functions like phagocytosis, degranulation, production of cytokines and the formation of neutrophil extracellular traps (NETosis), in the pathogenesis of T1D. Our aim was to gain insight into the proteome of neutrophils undergoing NETosis from patients with long-standing T1D compared to age- and sex-matched healthy controls under both resting and stimulated conditions (phorbol-myristate acetate, PMA, 100nM; ionomycin, 20µM; 3hours) by LC/MS-MS.

2023-05-15 | PXD033599 | Pride

Targeting kinome reprogramming in ESR1 fusion-driven breast cancer

Project description:Multiplexed, deep-scale LC-MSMS analysis for proteome and phosphoproteome expression profile and the targeted LC-MSMS analysis for kinases in enriched kinome of the ER+ breast cancer patient-derived xenograft tumors.

2023-10-24 | PXD036644 | Pride

Neutrophil-derived PAD4 induces citrullination of CKMT1 in epithelial cells to exacerbate mucosal inflammation

Project description:Objective Increased neutrophil extracellular trap-osis (NETosis) is a hallmark of inflammatory bowel disease (IBD). However, the mechanisms of NETosis formation and its detrimental effect on the intestinal epithelium remain poorly understood. Design Dextran sulfate sodium (DSS) induce colitis in peptidyl-arginine deiminase-4 deficient (PAD4-/-) and wild-type (WT) mice. PAD4, NETosis and citrullination levels were detected in mice and human volunteers. Citrullination analysis and single-cell RNA-sequencing (scRNA-seq) were performed to explore the target of PAD4 during NETosis formation. The effect of this citrullinated target in the intestinal epithelium during the pathogenesis of IBD was validated both in vivo and in vitro. Results The levels of NETosis and citrullination were improved in IBD patients, which was positively associated with endoscopic inflammation scores. Deleting PAD4 alleviated colonic inflammation and intestinal barrier dysfunctions. In citrullination analysis, R243 of mitochondrial creatine kinase 1 (CKMT1) was identified as the potential target of PAD4 during NETosis. The scRNA-seq data further indicated that PAD4 in neutrophils contributed to the increase of epithelia (Nos2+ Clca3b+) and the decrease of distal immature epithelia. PAD4-mediated NETosis contributed to the destruction of intestinal barriers and increase of apoptosis as well as lower level of CKMT1 protein in vitro. Finally, mice with intestinal epithelial-specific ablation of CKMT1 were used to verify its detrimental role in the development of IBD, which was also validated by the moderate correlation between CKMT1 and endoscopic scores in IBD patients.

2025-06-09 | PXD041504 | Pride

Project description:Understanding Complex Chromatin Dynamics of Primary Human Neutrophils During PMA Induced NETosis

| PRJNA1120432 | ENA

Effect of CDK7 inhibitor, FHD-286, SNDX-50469, or Tasquinimod on protein expression alterations in patient-derived secondary AML or de novo MLL1-rearranged AML cells

Project description:Patient-derived secondary AML cells were treated with 100 nM of SY-5609 for 24 hours, 100 nM of FHD-286 for 48 hours, or 20 µM of Tasquinimod for 48 hours to determine the global protein expression alterations that correlate with the cell cycle, growth inhibitory and lethal effects of treatment with a CDK7 inhibitor, chromatin remodeling inhibitor, or S100A8/S100A9 inhibitor or in secondary AML cells. Patient-derived de novo AML cells with MLL1 rearrangement and Menin T349M mutation were treated with 100 nM of FHD-286 or 500 nM SNDX-50469 for 48 hours to determine the global protein expression alterations that correlate with the cell cycle, growth inhibitory and/or lethal effects of treatment with a chromatin remodeling inhibitor, FHD-286, or a Menin inhibitor SNDX-50469 in MLL1 rearranged AML cells

2025-04-28 | PXD053548 | Pride

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data