Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Identification of ubiquitination sites on protein CSDE1 in SHSY5Y cells.

ABSTRACT: This bottom-up proteomics dataset provides a global map of post-translational modifications (PTMs) on the RNA-binding protein CSDE1 in human neuroblastoma SHSY5Y cells. The data was acquired to survey the modification landscape of CSDE1, with a particular observation that lysine (K) residues displayed the most abundant modification signals among all amino acids. This unbiased survey informed subsequent functional studies investigating the role of specific modification sites. The relationship between CSDE1 and the E3 ligase MKRN2 was established in our prior research.

INSTRUMENT(S):

ORGANISM(S): Homo Sapiens (human)

TISSUE(S): Neuroblastoma Cell

SUBMITTER: Zi Wang

LAB HEAD: Ronggui Hu

PROVIDER: PXD073844 | Pride | 2026-03-02

REPOSITORIES: Pride

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	CSDE-Lys-ub-sites.xlsx	Xlsx
	CSDE1-all-protein-peptides.csv	Csv
	README.docx	Other
	checksum.txt	Txt
	huronggui103.raw	Raw

Items per page:

1 - 5 of 5

Publications

Liquid-liquid phase separation couples MKRN2-mediated ubiquitination of CSDE1 with neurodevelopmental disorders.

Wang Zi Z Han Yaning Y Yang Peng P Jia Caiwei C Li Chuanyin C Yuan Shilin S Wei Pengfei P Hu Ronggui R

Frontiers in cellular neuroscience 20260211

<h4>Background</h4>Makorin-2 (MKRN2) is an E3 ubiquitin ligase involved in multiple biological processes, yet its role in neurological disorders remains poorly understood. This study aims to elucidate how MKRN2 regulates the RNA-binding protein CSDE1-a molecule linked to autism-related genes-and to explore the functional implications of this interaction in neurodevelopment.<h4>Methods</h4>Using mass-spectrometry screening, we identified CSDE1 as a direct substrate of MKRN2. Ubiquitination sites ...[more]

PMID: 41757349

Similar Datasets

Profiling of CSDE1-bound RNAs under MKRN2-mediated ubiquitination

Project description:This study aims to elucidate how MKRN2-mediated ubiquitination regulates the RNA-binding capacity of CSDE1. By overexpressing CSDE1 in MKRN2 knockout (KO) SHSY5Y cells and complementing with MKRN2 for comparison, we systematically analyzed the alterations in the RNA-binding repertoire of CSDE1 upon its interaction with MKRN2.

2026-02-02 | GSE317793 | GEO

Context-dependent phosphorylation of CSDE1 drives interactions with ribosomes

Project description:The RNA-binding protein CSDE1 is a key regulator of mRNA stability and translation in a broad spectrum of biological processes. We have previously shown that CSDE1 functions as an oncoprotein promoting invasion and metastasis in melanoma, whereas it behaves as a tumour suppressor promoting cellular senescence in squamous cell carcinoma. The reasons underlying these context-specific behaviours are unknown. To identify melanoma-specific vulnerabilities, we have compared CSDE1 protein isoforms and post-translational modifications in melanoma cells and keratinocytes, and in melanocytic cells of different tumorigenic potential. By combining long-read Nanopore sequencing with two-dimensional gel electrophoresis and transcriptome analysis, we identify one major isoform expressed in melanoma cells and patient samples. This isoform is phosphorylated early during cellular transformation, correlating with changes in its subcellular localization. We provide extensive interactome analysis of mammalian CSDE1, showing increased interactions with ribosomes in melanoma cells compared to healthy melanocytes. Importantly, interactions of CSDE1 with the ribosome are promoted by CSDE1 phosphorylation. Our data uncover a specific feature of melanoma cells that could be harnessed for therapeutic intervention

2025-09-10 | PXD062774 | Pride

Co-immumnoprecipitation experiments to identify protein bindining partners of CSDE1

Project description:While the transcriptional network of human embryonic stem cells (hESCs) has been extensively studied, relatively little is known about how post-transcriptional modulations determine hESC function. RNA-binding proteins play central roles in RNA regulation, including translation and turnover. Here we show that the RNA-binding protein CSDE1 is highly expressed in hESCs to maintain their undifferentiated state and prevent default neural fate. Notably, loss of CSDE1 accelerates neural differentiation and potentiates neurogenesis. Conversely, ectopic expression of CSDE1 impairs neural differentiation. We find that CSDE1 post-transcriptionally modulates core components of multiple regulatory nodes of hESC identity, neuroectoderm commitment and neurogenesis. Among these key pro-neural/neuronal factors, CSDE1 binds fatty acid binding protein 7 (FABP7) and vimentin (VIM) mRNAs as well as transcripts involved in neuron projection development regulating their stability and translation. Thus, our results uncover CSDE1 as a central post-transcriptional regulator of hESC identity and neurogenesis. This proteomics dataset contains the data from co-immunopreciptation experiments using CSDE1 antibody in hESCs

2018-05-16 | PXD007271 | Pride

A post-transcriptional program coordinated by CSDE1 prevents intrinsic neural differentiation of human embryonic stem cells

2018-05-16 | PXD007270 | Pride

Ribosome profiling of UNR (CSDE1) KD

Project description:Investigation of the effects of UNR (CSDE1) knock-down on translation in Melanoma Cells using Ribosome Profiling

2016-11-07 | E-MTAB-3815 | biostudies-arrayexpress

Phosphorylation of CSDE1 drives ribosome interactions with implications for cancer malignancy

Project description:The RNA-binding protein CSDE1 is a key regulator of mRNA stability and translation in a broad spectrum of biological processes. We have previously shown that CSDE1 functions as an oncoprotein in melanoma, where it promotes invasion and metastasis, whereas it behaves as a tumour suppressor in squamous cell carcinoma, a tumor derived from keratinocytes. The reasons underlying these context-specific behaviours are unknown. To identify melanoma-specific vulnerabilities, we have compared CSDE1 protein isoforms and post-translational modifications in melanoma cells and keratinocytes, as well as in cells of different tumorigenic potential. Combining Nanopore sequencing with two-dimensional gel electrophoresis and proteomics, we identify one major CSDE1 isoform expressed in melanoma cells and patient samples and find that CSDE1 phosphorylation and interactions with ribosomes represent an early event in cellular transformation, correlating with changes in the subcellular localization of CSDE1. Our data show that CSDE1 phosphorylation promotes de novo interactions of CSDE1 with ribosomes, uncovering a specific vulnerability of melanoma cells that might be harnessed for therapeutic intervention.

2025-08-13 | GSE292019 | GEO

iCLIP transcriptome-wide mapping of UNR (CSDE1) binding sites

Project description:Analysis of UNR (CSDE1) binding to RNA targets by iCLIP transcriptome-wide mapping.

2016-11-07 | E-MTAB-3818 | biostudies-arrayexpress

Sciatic nerve injury-responsive differential CSDE1 association efficiency of ribosomal protein coding mRNAs

Project description:Gpr151 is an injury-responsive gene that promotes axon regeneration through its interaction with the 5'UTR region of its mRNA transcripts and the RNA-binding protein CSDE1. We found that knocking down or overexpressing the 5'UTR of Gpr151 changes the ribosomal protein mRNA regulon regulated by CSDE1. After the sciatic nerve injury, the association between the ribosomal protein mRNA regulon and CSDE1 was enhanced at dorsal root ganglions(DRGs), but this enhancement was not observed in the AAV-shGpr151 injected mice. Overexpression of 5'UTRmut, which has increased binding affinity to CSDE1, enhanced the ribosomal protein mRNA regulon and its association with CSDE1 in embryonic DRG neurons.

2023-08-18 | GSE236910 | GEO

DRG tissue CSDE1-IP sequencing using sciatic nerve injured and uninjured mice.

Project description:To determine CSDE1 associated RNAs after injury in sensory neurons, we conducted CSDE1-IP sequencing analysis using dorsal root ganglion (DRG) tissues of wild type mice.

2025-09-01 | GSE301321 | GEO

Effect of CSDE1 knockout in RAW264.7 cells on gene expression following SARS CoV-2 RNA stimulation

Project description:RIG-I-like receptors (RLRs)-mediated antiviral innate immunity is critical for restricting RNA viral infection. The liquid-liquid phase separation (LLPS) is crucial for fine-tuning cellular signaling transduction, but whether RLR signaling is under the regulation of LLPS remains largely enigmatic. In this study, we identify the RNA-binding protein cold shock domain containing E1 (CSDE1) as a novel negative regulator of RLR signaling to promote viral immune evasion. The deficiency of CSDE1 in macrophages results in increased expression of type I interferon and ISGs following RNA viral infection. Mice with macrophage conditional knockout of CSDE1 are less susceptible to RNA viral infection. CSDE1, with multivalent CSD motifs, forms bio-molecular condensates with long single stranded RNA (ssRNA). The LLPS of CSDE1 sequesters viral RNA from recognition by RLRs to inhibit RLR signaling. Notably, virus-activated TBK1 kinase mediates the phosphorylation of CSDE1 to disturb its LLPS. Consequently, phosphorylation of CSDE1 relieves its suppression of RLR signaling. Intriguingly, LLPS of CSDE1 promotes the condensation of the SARS-CoV-2 nucleocapsid (N) protein and is critical for the anti-interferon activity of the N protein. Repression of CSDE1 condensation with screened compound abrogates the CSDE1 LLPS and subsequent replication of SARS-CoV-2. Overall, our study delineates a novel regulatory mechanism of RLR signaling transduction by phosphorylation-modulated LLPS of CSDE1, indicating that targeting the LLPS of CSDE1 is a promising strategy for RNA viral infection treatment.

2026-04-07 | GSE299410 | GEO