Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Profile the composition of reconstituted nuclear speckles

ABSTRACT: Nuclear extract from Hela Cells are incubated with recombinant SON IDR2 protein, resulting condensates are spun down and the compostion profiled by mass spectrometry.

INSTRUMENT(S): Q Exactive

ORGANISM(S): Homo Sapiens (human)

TISSUE(S): Permanent Cell Line Cell, Cell Culture

DISEASE(S): Cervix Carcinoma

SUBMITTER: Bokai Zhu

LAB HEAD: Bokai Zhu

PROVIDER: PXD050371 | Pride | 2024-11-25

REPOSITORIES: pride

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	Nuclear_extract_input_rep1.pepXML	Pepxml
	Nuclear_extract_input_rep1.raw	Raw
	Nuclear_extract_input_rep2.pepXML	Pepxml
	Nuclear_extract_input_rep2.raw	Raw
	SON_IDR2_seed-rep1.pepXML	Pepxml

Items per page:

1 - 5 of 8

Publications

SON-dependent nuclear speckle rejuvenation alleviates proteinopathies.

Dion William W Tao Yuren Y Chambers Maci M Zhao Shanshan S Arbuckle Riley K RK Sun Michelle M Kubra Syeda S Jamal Imran I Nie Yuhang Y Ye Megan M Larsen Mads B MB Camarco Daniel D Ickes Eleanor E DuPont Claire C Wang Haokun H Wang Bingjie B Liu Silvia S Pi Shaohua S Chen Bill B BB Chen Yuanyuan Y Chen Xu X Zhu Bokai B

bioRxiv : the preprint server for biology 20241017

Current treatments targeting individual protein quality control have limited efficacy in alleviating proteinopathies, highlighting the prerequisite for a common upstream druggable target capable of global proteostasis modulation. Building on our prior research establishing nuclear speckles as a pivotal membrane-less organelle responsible for global proteostasis transcriptional control, we aim to alleviate proteinopathies through nuclear speckle rejuvenation. We identified pyrvinium pamoate as a ...[more]

PMID: 38659924

Similar Datasets

RNA-seq of human plasma microRNAs in Alzheimer Disease

Project description:MicroRNAs (miRNAs) could play an important role as potential Alzheimer Disease (AD) biomarkers. Plasma samples were collected from participants: Mild cognitive impairment (MCI) due to AD patients (n= 20), preclinical AD patients (n= 8) and healthy controls (n= 20). Then, small RNA sequencing analysis, followed by miRNA differential expression analysis comparing different methods (DESeq2, edgeR, NOISeq) were carried out.

2022-05-08 | E-MTAB-11103 | biostudies-arrayexpress

SON and its alternatively spliced isoforms control MLL complex-mediated H3K4me3 and transcription of leukemia-associated genes (ChIP-seq data)

Project description:Dysregulation of MLL complex-mediated histone methylation plays a pivotal role in gene expression associated with diseases, but little is known about cellular factors modulating MLL complex activity. Here, we report that SON, previously known as an RNA splicing factor, controls MLL complex-mediated transcriptional initiation. SON binds to DNA near transcription start sites, interacts with menin, and inhibits MLL complex assembly, resulting in decreased H3K4me3 and transcriptional repression. Importantly, alternatively spliced short isoforms of SON are markedly upregulated in acute myeloid leukemia. The short isoforms compete with full-length SON for chromatin occupancy, but lack the menin-binding ability, thereby antagonizing full-length SON function in transcriptional repression while not impairing full-length SON-mediated RNA splicing. Furthermore, overexpression of a short isoform of SON enhances replating potential of hematopoietic progenitors. Our findings define SON as a fine-tuner of the MLL-menin interaction and reveal short SON overexpression as a marker indicating aberrant transcriptional initiation in leukemia.

2016-03-24 | GSE76910 | GEO

Expression data from HeLa cells transiently transfected with control siRNA or SON siRNA

2011-04-01 | GSE26888 | GEO

Son Maintains Accurate Splicing of Pre-mRNAs Encoding Chromatin Modifiers

Project description:Exon and expression analysis of HeLa cells after knockdown of SON Serine-arginine-rich (SR) proteins play a key role in alternative pre-mRNA splicing in eukaryotes. Our laboratory recently showed that a large SR protein called Son has unique repeat motifs that are essential for maintaining the subnuclear organization of pre-mRNA processing factors in nuclear speckles. Motif analysis of Son highlights putative RNA interaction domains that suggest a direct role for Son in pre-mRNA splicing. A genome-wide screen was performed to identify putative human transcription and splicing targets of Son.

2011-12-22 | GSE28672 | GEO

SON inhibits megakaryocytic differentiation via repressing the megakaryocytic gene expression program in acute megakaryoblastic leukemia

Project description:A high incidence of acute megakaryoblastic leukemia (AMKL) in Down syndrome patients implies that chromosome 21 genes have a pivotal role in AMKL development, but the functional contribution of individual genes remains elusive. Here, we report that SON, a chromosome 21-encoded DNA- and RNA-binding protein, inhibits megakaryocytic differentiation by suppressing RUNX1 and the megakaryocytic gene expression program. As megakaryocytic progenitors differentiate, SON expression is drastically reduced, with mature megakaryocytes having the lowest levels. In contrast, AMKL cells express an aberrantly high level of SON, and knockdown of SON induced the onset of megakaryocytic differentiation in AMKL cell lines. Genome-wide transcriptome analyses revealed that SON knockdown turns on the expression of pro-megakaryocytic genes while reducing erythroid gene expression. Mechanistically, SON represses RUNX1 expression by directly binding to the proximal promoter and two enhancer regions, the known +23 kb enhancer and the novel +139 kb enhancer, at the RUNX1 locus to suppress H3K4 methylation. In addition, SON represses the expression of the AP-1 complex subunits JUN, JUNB and FOSB which are required for late megakaryocytic gene expression. Our findings define SON as a negative regulator of RUNX1 and megakaryocytic differentiation, implicating SON overexpression in impaired differentiation during AMKL development.

2020-09-01 | GSE157178 | GEO

General anaesthesia leads to phosphoproteome changes in proteins involved in cytoskeleton remodelling and synaptic processes in the supraoptic nucleus of the hypothalamus

Project description:Despite the widespread use of general anaesthetics, the mechanisms mediating their effects are still not understood. Although suppressed in most parts of the brain, neuronal activity, as measured by FOS activation, is increased in the hypothalamic supraoptic nucleus (SON) by numerous general anaesthetics, and evidence points to this brain region being involved in the induction of general anaesthesia and natural sleep. Posttranslational modifications of proteins, including changes in phosphorylation, enable fast modulation of protein function which could be underlying the rapid effects of general anaesthesia. In order to identify potential phosphorylation events in the brain mediating general anaesthesia effects, we have explored the phosphoproteome responses in the rat SON, and compared these to cingulate cortex (CC) which displays no FOS activation is response to general anaesthetics. We found many changes in the phosphoproteomes of both the CC and SON in response to 15 minutes of isoflurane exposure. Pathway analysis indicated that proteins undergoing phosphorylation adaptations are involved in cytoskeleton remodelling and synaptic signalling events. Importantly, changes in protein phosphorylation appeared to be brain region-specific suggesting that differential phosphorylation adaptations might underlie the different neuronal activity responses to general anaesthesia between the CC and SON. In summary, these data suggest that rapid posttranslational modifications in proteins involved in cytoskeleton remodelling and synaptic signalling events might mediate the central mechanisms mediating general anaesthesia.

2024-01-23 | PXD039391 | Pride

Son Maintains Accurate Splicing of Pre-mRNAs Encoding Chromatin Modifiers

2011-12-22 | E-GEOD-28672 | biostudies-arrayexpress

DARTseq identifies m6A targets in mouse primary cells

Project description:The goal of this study is to identify m6A targets in mouse HSC and MPP1-4 cells Stem cells regulate their self-renewal and differentiation fate outcomes through both symmetric and asymmetric divisions. When exposed to stress such as inflammation, stem cells can rapidly undergo symmetric commitment divisions to generate differentiated progenitors for tissue regeneration and immune maintenance. m6A RNA methylation controls symmetric commitment and inflammation of hematopoietic stem cells (HSCs) through unknown mechanisms. Here, we demonstrate that the nuclear speckle protein SON is an essential m6A target required for murine HSC self-renewal, symmetric commitment, and inflammation control. Global profiling of m6A identified that m6A mRNA methylation of Son increases during HSC commitment. Upon m6A depletion, Son mRNA increases, but its protein is depleted. Reintroduction of SON rescues defects in HSC symmetric commitment divisions and engraftment. Conversely, Son deletion results in a loss of HSC fitness, while overexpression of SON improves mouse and human HSC engraftment potential by increasing quiescence. Additionally, SON nuclear speckles asymmetrically and symmetrically segregate during HSC division, correlating with hematopoietic differentiation. Mechanistically, we found that SON rescues MYC and suppresses the METTL3-HSC inflammatory gene expression program by indirectly reducing double-stranded RNAs and directly suppressing nascent transcription of proinflammatory chemokine CCL5. Depletion of CCL5 partially rescues the functional defect of m6A-deficient HSCs. Thus, our findings define a m6A-SON-CCL5 axis that controls inflammation and HSC fate.

2023-12-07 | GSE231862 | GEO

Expression data from HeLa cells transiently transfected with control siRNA or SON siRNA

Project description:SON is a large Ser/Arg (SR)-related protein localized in nuclear speckles. SON siRNA causes defects in mitotic progression and genome instability. We used microarrays to detail the pattern of gene expression after SON knockdown. HeLa cells were grown in 100 mm dishes and transfected with negative control siRNA or SON siRNA (400 pmol). Then, cells were harvested after 66 hours and RNAs were isolated. Microarrays were performed using GeneChip Human Genome U133A 2.0 (Affymetrix).

2011-04-01 | E-GEOD-26888 | biostudies-arrayexpress

Total RNA-seq and long-read RNAseq (Nanopore) upon Son KD in mouse embryonic stem cells

Project description:Gene-expression noise can influence cell-fate choices across pathology and physiology. However, a crucial question persists: do regulatory proteins or pathways exist that control noise independently of mean expression levels? Resulting from a previous screen, the protein SON was identified as a potential noise regulator. We perform Son KD and utilize (1) total RNA sequencing (RNA-seq) to analyze differences in splicing efficiency of introns upon Son KD; and (2) Nanopore sequencing to analyze changes in isoform usage. These datasets correspond to the aforementioned total RNA-seq and long-read polyA+ cDNA Nanopore sequencing upon Son KD.

2024-08-05 | GSE271659 | GEO

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