Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

KSHV ORF18 TurboID in human iSLK cell lines

ABSTRACT: Beta- and gamma-herpesviruses transcribe their late genes in a manner distinct from host transcription. This process is directed by a complex of viral transcriptional activator proteins that hijack cellular RNA polymerase II, and an unknown set of additional factors. We employed proximity labeling to identify the ensemble of viral and cellular proteins dynamically associated with the KSHV late gene transcriptional complex late during infection.

INSTRUMENT(S): Q Exactive HF

ORGANISM(S): Homo Sapiens (human)

TISSUE(S): Epithelial Cell, Cell Culture

SUBMITTER: Dawei Liu

LAB HEAD: Ileana Cristea

PROVIDER: PXD039694 | Pride | 2023-04-06

REPOSITORIES: pride

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	20210312_LAM_4mg_NLS_rep2.raw	Raw
	20210312_LAM_4mg_NLS_rep3.raw	Raw
	20210312_LAM_4mg_ORF18_minusbiotin_rep2.raw	Raw
	20210312_LAM_4mg_ORF18_minusbiotin_rep3.raw	Raw
	20210312_LAM_4mg_ORF18_plusbiotin_rep2.raw	Raw

Items per page:

1 - 5 of 11

Similar Datasets

Analyses of Early- and Late-scnRNAs of Tetrahymena

Project description:In this study, we demonstrated that there is a novel, unanticipated mechanism regulating programmed DNA elimination: a genome-wide trans-recognition network for IES identification. In this mechanism, Early-scnRNAs produced from Type-A IESs in the MIC identify not only the IESs from which they are derived but also other IESs in trans to trigger the cis-spreading of Late-scnRNA production in the IESs. This cis-spreading of Late-scnRNA production requires heterochromatin formation . Furthermore, these Late-scnRNAs can recognize other IESs in trans. This “chain reaction” of Late-scnRNA production by the trans-recognition network most likely provides strong robustness in DNA elimination by buffering cell-to-cell variability in the initial Early-scnRNA populations. 26 to 32-nt small RNAs from various mutants or from immuno precipitated with Argonaute proteins were analyzed by high-throughput sequencing

2015-06-15 | E-GEOD-68455 | biostudies-arrayexpress

Proximal proteins of the type I interferon signaling cascade

Project description:Deciphering the intricate dynamic events governing type I interferon (IFN) signaling is critical to unravel key regulatory mechanisms in host antiviral defense. Here, we leveraged TurboID-based proximity labeling coupled with affinity purification-mass spectrometry to comprehensively map temporal changes to the proximal human proteomes of all seven canonical type I IFN signaling cascade members following IFN stimulation. This established a network of 108 proteins in close proximity to the core members IFNAR1, IFNAR2, JAK1, TYK2, STAT1, STAT2, and IRF9, and validated several known protein assemblies, while also revealing novel, transient associations between key signaling molecules.

2024-05-28 | PXD045482 | Pride

PTPN23 downregulation by WDR4 Determines the Exosome Secretion Fate of MVB to Promote Cancer Metastasis and Immune Evasion

Project description:Exosomes play pleiotropic tumor-promoting functions and are originated from a diversion of endocytic pathway. In late endocytic trafficking, multivesicular bodies (MVBs) are directed to lysosomes for degradation or secreted as exosomes. However, the mechanism controlling different fates of MVBs remains elusive. Here, we show that WDR4 promotes exosome secretion through the degradation of PTPN23, an ESCRT-associated Bro1-family protein. Mechanistically, PTPN23 competes with ALIX, another Bro1-family protein, for binding syntenin, thus enabling PTPN23 and ALIX for promoting MVBs towards degradation and secretion, respectively. Furthermore, ALIX uniquely recruits actin-capping/severing proteins to prevent F-actin accumulation around MVBs, thereby facilitating MVBs trafficking to cell periphery for secretion. Functionally, the WDR4/ALIX-dependent exosomes preferentially load pro-tumor proteins including PTK2, MCAM and NRP1, thereby enhancing metastasis and immune evasion. This study highlights a previously unprecedented mechanism for regulating MVBs fates and exosome cargos, which have potential broad impacts on tuning exosome production and devising cancer therapeutic strategy.

2025-01-24 | PXD050029 | Pride

Project description:Hutchinson-Gilford progeria syndrome (HGPS) is a premature aging disease that is frequently caused by a de novo point mutation at position 1824 in LMNA. This mutation activates a cryptic splice donor site in exon 11, and leads to an in-frame deletion within the prelamin A mRNA and the production of a dominant negative lamin A protein, known as progerin. Here we show that HGPS cells experience genome-wide alterations in patterns of H3K27me3 deposition, changes in the associations of genomic loci with nuclear lamin A/C, and, at late passages, genome-wide loss of spatial compartmentalization of active and inactive chromatin domains that characterizes chromosome folding in normal cells. We further demonstrate that the H3K27me3 changes associate with gene expression alterations in HGPS cells. Our results support a model that the accumulation of progerin in the nuclear lamina leads to altered H3K27me3 marks in heterochromatin, possibly through the down-regulation of EZH2, and disrupts heterochromatin-lamina interactions. These changes may then lead to the genomic disorganization and changes in transcriptional regulation we observe in HGPS fibroblasts. ChIP-Seq was performed for H3K27me3 and lamin A/C in the human genome in three primary fibroblast cell lines: an HGPS patient (HGPS), normal cells from the father of the HGPS patient (Father), and age-matched normal cells (Age Control). Two biological replicates were performed.

2012-10-30 | E-GEOD-41757 | biostudies-arrayexpress

Gene expression analysis of monokaryotic and dikaryotic mycelia from Coprinopsis cinerea

Project description:Sexual reproduction is an ancient trait that evolved shortly after the appearance of the first eukaryotic cell. In order to identify the set of genes differentially expressed in monokaryotic and dikaryotic mycelia, the poly(A)-positive transcriptomes of C. cinerea Okayama7 and C. cinerea A43mutB43mut were sequenced.

2014-06-01 | E-MTAB-1993 | biostudies-arrayexpress

Dm Lmd 6-8hrs Affymetrix ChIP

Project description:Genomewide mapping of D. melanogaster Lame duck protein binding at 6-8hrs after egg laying. Two different rabbit antibodies were used to precipitate the Lmd protein isoform in biological replicates. Additionally a rabbit preimmune-serum was used as a control. The enriched DNA was hybridized to high density Affymetrix GeneChip Drosophila Tiling 1.0R array.

2014-03-01 | E-MTAB-1283 | biostudies-arrayexpress

Dm Snail Affymetrix ChIP

Project description:Genomewide mapping of D. melanogaster Snail protein binding during embryonic development at 2-4 hrs after egg-laying. Two independent repeats were assayed and preimmune-serum was used as a control. The enriched DNA was hybridized to high density Affymetrix GeneChip Drosophila Tiling 1.0R array

2014-01-10 | E-MTAB-1589 | biostudies-arrayexpress

HNF1A, H3K4me3 and H3K27ac ChIP-seq in control and Haster-deficient mouse livers

Project description:The HASTER promoter region is a cis-regulatory element that stabilizes the transcription of HNF1A, preventing silencing or overexpression. We have generated a mouse model where the promoter of Haster has been specifically deleted in liver (Haster loxP/loxP; AlbCre). In liver the prevailing consequence is upregulation of HNF1A. We performed HNF1A, H3K4me3 and H3K27ac ChIP-seq to assess the impact of HNF1A upregulation on the chromatin landscape of Haster KO liver.

2022-05-01 | E-MTAB-11471 | biostudies-arrayexpress

Identification of interaction partners of the Toxoplasma gondii Cysteine Repeat Modular Proteins TGGT1_292020 and TGGT1_261080

Project description:Apicomplexa are obligate intracellular parasites. While most species are restricted to specific hosts and cell types, Toxoplasma gondii can invade every nucleated cell derived from warm-blooded animals. This broad host range suggests that this parasite can recognize multiple host cell ligands or structures, leading to the activation of a central protein complex, which should be conserved in all apicomplexans. Cysteine Repeat Modular Proteins (CRMPs) are a family of apicomplexan specific proteins. In Toxoplasma gondii, two CRMPs are present in the genome. We performed pulldown of 3xHA tagged CRMPA and CRMPB. In a second dataset we performed biotinylation of TurboID tagged CRMPB on extracellular parasites to identify transient interaction partners. In a third dataset, we performed biotinylation of TurboID tagged CRMPA or B during invasion or in an invasion blocking buffer.

2022-12-13 | PXD031649 | Pride

BRCA1 functions independently of homologous recombination in DNA interstrand crosslink repair

Project description:Brca1 is required for DNA repair by homologous recombination (HR) and normal embryonic development. Here we report that deletion of the DNA damage responsefactor 53BP1 overcomes embryonic lethality in Brca1-nullizygous mice, and rescues HR deficiency, as measured by hypersensitivity to PARP (polyADPribose polymerase) inhibition. However, Brca1,53BP1 double-deficient cells are hypersensitive to DNA interstrand crosslinks (ICLs), indicating that BRCA1 has an additional role in DNA cross-link repair that is distinct from HR. Disruption of the non-homologous end-joining (NHEJ) factor, Ku, promotes DNA repair in Brca1-deficient cells; however deletion of either Ku or 53BP1 exacerbates genomic instability in cells lacking FANCD2, a mediator of the Fanconi Anemia pathway for ICL repair. Brca1 therefore has two separate roles in ICL repair, whereas FANCD2 provides a key activity that can not be bypassed by ablation of 53BP1 or Ku. B cells were stimulated to undergo class switch recombination in vitro. Chromatin from B cells was harvested 72 hours post-stimulation and used for RPA ChIP to study the extent of resection of DNA DSBs.

2012-09-30 | E-GEOD-35698 | biostudies-arrayexpress

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