Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Cell surface nucleolin is a novel ADAMTS5 receptor mediating endothelial cell apoptosis

ABSTRACT: This study demonstrates that TS5-p45 induces endothelial cell (EC) apoptosis in a caspase-dependent manner via its cell surface receptor Nucleolin (NCL). To unravel how this apoptosis mechanism is induced in ECs, we performed RNA-seq using TS5-p45-treated ECs. Transcriptional changes under TS5-p45 treatment was further evaluated to highlight some of the caspase-dependent apoptosis-inducing and -suppressing genes which are altered in favor of apoptosis.

ORGANISM(S): Homo sapiens

PROVIDER: GSE191049 | GEO | 2022/03/02

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Nucleolin-aptamer therapy in retinoblastoma: molecular changes and mass spectrometry–based imaging

Project description:Retinoblastoma (RB) is an intraocular childhood tumor which, if left untreated, leads to blindness and mortality. Nucleolin (NCL) protein which is differentially expressed on the tumor cell surface, binds ligands and regulates carcinogenesis and angiogenesis. We found that NCL is over expressed in RB tumor tissues and cell lines compared to normal retina. We studied the effect of nucleolin-aptamer (NCL-APT) to reduce proliferation in RB tumor cells. Aptamer treatment on the RB cell lines (Y79 and WERI-Rb1) led to significant inhibition of cell proliferation. Locked nucleic acid (LNA) modified NCL-APT administered subcutaneously (s.c.) near tumor or intraperitoneally (i.p.) in Y79 xenografted nude mice resulted in 26 and 65% of tumor growth inhibition, respectively. Downregulation of inhibitor of apoptosis proteins, tumor miRNA-18a, altered serum cytokines, and serum miRNA-18a levels were observed upon NCL-APT treatment. Desorption electrospray ionization mass spectrometry (DESI MS)-based imaging of cell lines and tumor tissues revealed changes in phosphatidylcholines levels upon treatment. Thus, our study provides proof of concept illustrating NCL-APT-based targeted therapeutic strategy and use of DESI MS-based lipid imaging in monitoring therapeutic responses in RB.

2016-11-15 | GSE89818 | GEO

Binding of Nucleolin to HBV cccDNA

Project description:Covalently closed circular DNA (cccDNA) forms the basis for replication and persistence of hepatitis B virus (HBV) in the chronically infected liver. In this study we sought to identify host factors interacting with the HBV genome. Nucleolin (Ncl) was identified as a potential interactor of HBV cccDNA. This interaction was veriefied using an established ChIPseq protocol. The data show that Ncl binds cccDNA albeit at lower levels than HBcAg. Ncl deposition occurs across the genome without a clear localization and a variable pattern of deposition between experiments. This verifies the interaction of Ncl with HBV-cccDNA.

2021-12-31 | GSE123715 | GEO

Nuclear nucleolin interactome analysis

Project description:Nucleolin (NCL) is a major component of the cell nucleolus, which has the ability to rapidly shuttle to several other cell’s compartments. NCL has been shown to play important roles in a variety of essential functions among which ribosome biogenesis, gene expression and cell growth. However, the precise mechanisms underlying NCL functions are still unclear. Our study aimed to provide new information on NCL functions via the identification of its nuclear interacting partners. Using an interactomics approach, we identified 140 binding partners of NCL, among which, a 100 of them, were specifically found associated to NCL independently of the presence of RNA.

2016-04-11 | PXD003554 | Pride

Cell surface nucleolin is a novel ADAMTS5 receptor mediating endothelial cell apoptosis

Project description:Cell surface nucleolin is a novel ADAMTS5 receptor mediating endothelial cell apoptosis

| PRJNA789689 | ENA

A Novel Role for Nucleolin in Splice Site Selection

Project description:In search for nuclear partners of initiator-tRNA, previously shown to be involved in a quality control of splice site selection, we identified nucleolin (NCL) as specifically and directly bound to it in the nucleus and not in the cytoplasm (using affinity purification of UV crosslinked nuclear initiator-tRNA followed by mass spectrometry). To further explore the role of NCL in splice site selection, we knocked down NCL. We report the activation of 399 latent splice sites upon NCL knockdown, as revealed by RNA deep sequencing of siRNA treated NCL compared to control siRNA. Our study identifies NCL as the first protein component of this quality control mechanism of splice site selection. Our study thus establishes an experimental strategy and computational pipeline that could be used to identify other components of this quality control mechanism.

2022-03-08 | GSE142836 | GEO

iCLIP Analysis of WT, phospho-defective, and phospho-mimicking mutants of mouse Nucleolin in iKras PDAC cells

Project description:This experiment aimed to identify Nucleolin (Ncl) binding sites on a transcriptome-wide scale, by performing iCLIP in mouse iKras PDAC cells (Ying et al., 2012) transiently transfected with a mammalian expression construct encoding a wild-type (WT) myc-Ncl, a phospho-defective mutant in which S28, S34, S40, and S41 residues were mutated to A, or a phospho-mimicking mutant with these residues mutated to D. Cells transfected with an empty vector (myc-pRK5-DEST) were used as controls in the experiment.

2023-03-01 | E-MTAB-12481 | biostudies-arrayexpress

Nucleolin HITS-CLIP, RNA-Seq and Ribo-Seq upon inhibition of 5'-tRFCys

Project description:Expression of 5'-tRFCys is significantly upregulated during breast cancer metastasis and suppression of 5'-tRFCys significantly reduced metastatic lung colonization of breast cancer. We identified Nucleolin (Ncl) as the direct binding partner of 5'-tRFCys. To identify the molecular mechanism underlying 5'-tRFCys promotion of breast cancer, we performed Ncl HITS-CLIP, RNA-Seq, Ribosome profiling (Ribo-Seq) upon inhibition of 5'-tRFCys. These analyses reveal that 5'-tRFCys enhances Ncl binding to a subset of transcripts, resulting in increased transcript stability of those transcripts and expression.

2022-06-03 | GSE173373 | GEO

Convergence of Cockayne Syndrome Group A and B Proteins at rRNA Transcription through Nucleolin Regulation

Project description:Cockayne Syndrome (CS) is a rare neurodegenerative disease characterized by short stature, cachexia, sun-sensitivity, accelerated aging, and short lifespan. Mutations in two human genes, ERCC8/CSA and ERCC6/CSB, are causative for CS and the protein products of these genes, CSA and CSB, while structurally unrelated, play roles in DNA repair and other aspects of DNA metabolism in human cells. Many clinical and molecular features of CS remain poorly understood, and it has been suggested that CSA and CSB regulate transcription of rDNA genes and ribosome biogenesis. The goal of this study was to investigate the dysregulation of rRNA synthesis in CS. Here, we report that Nucleolin (Ncl), a nucleolar protein that regulates rRNA synthesis and ribosome biogenesis, interacts specifically with CSA and CSB. In addition, CSA induces ubiquitination of Ncl, enhances binding of CSB to Ncl, and CSA and CSB both stimulate binding of Ncl to rDNA and subsequent rRNA synthesis. These findings suggest that CSA and CSB are positive regulators of rRNA synthesis via Ncl regulation. A majority of CS patients carry mutations in CSA and CSB and present with similar clinical features, thus our findings may provide novel insights into disease mechanism and the neuropathological features of CS.

2020-03-16 | GSE122736 | GEO

Analysis of the impact of Nucleolin phospho-mutants on the proteome of pancreatic ductal adenocarcinoma cells.

Project description:To reveal the impact of Nucleolin (Ncl) phosphorylation on oncogenic KRAS-induced changes in the proteome of Pancreatic Ductal Adenocarcinoma (PDAC) cells, we carried out a quantitative proteomic analysis on tumour cells isolated from an inducible mouse model of PDAC (iKras PDAC) (Ying et al., 2012), which were ectopically expressing wild-type or different phospho-mutants of Ncl. In this mouse model, oncogenic Kras (G12D) expression can be controlled by administration of doxycycline (Dox). Tandem Mass Tagging (TMT) was employed for quantitative analysis of Dox induced (24hrs) vs. non-induced iKras-PDAC cells, which were privously transfected with three different expression constructs of mouse myc-tagged Ncl. These constructs encoded for wild-type Ncl (WT Ncl), a phospho-defective mutant with four Serine to Alanine mutations on S28, S34, S41, and S42 sites (S4A Ncl), and a phospho-mimicking mutant with the same Serines mutated to Aspartic Acid (S4D Ncl). Cells were subjected to whole cell lysis, followed by Trypsin digestion, TMT barcoding with TMT 6plex kit (Thermo), and peptide fractionation, before analysis by LC-MS/MS.

2023-02-12 | PXD038496 | Pride

Nucleolin is a cell surface receptor of C1QTNF4

Project description:C1QTNF4 is a secreted protein that is structurally unique within the C1QTNF family, a family of proteins that have structural homology with both complement C1q and the tumor necrosis factor superfamily. The role of C1QTNF4 in immunity and inflammation remains poorly defined and a cell surface receptor has yet to be identified. Here we performed co-immunoprecipitation with subsequent mass spectrometric analysis in order to identify a cell surface receptor of C1QTNF4. We report identification of nucleolin as a cell surface binding partner of C1QTNF4. Nucleolin may serve as a docking molecule for C1QTNF4 and act in a context-dependent manner through co-receptors. Having identified nucleolin as a cell surface receptor is a further step to understanding C1QTNF4’s function in the healthy immune system.

2021-03-21 | PXD023088 | 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