Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

D133 ORF10 immunoprecipitation from WT and TorsinKO cells

ABSTRACT: WT and TorsinKO HeLa cells were transfected with d133-ORF10-FLAG from KSHV. The protein was immunoprecipitated with anti-FLAG beads to investigate proteins contained within nuclear envelope blebs. A control sample with no specific immunoprecipitation was compared to the co-immunoprecipitations. Eluting proteins were ran into an SDS-PAGE gel and extracted for mass spectrometry analysis.

INSTRUMENT(S): LTQ Orbitrap Elite

ORGANISM(S): Homo Sapiens (human)

TISSUE(S): Epithelial Cell, Cell Culture

SUBMITTER: Sarah Prophet

LAB HEAD: Christian Schlieker

PROVIDER: PXD036264 | Pride | 2022-08-25

REPOSITORIES: Pride

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	Prophet_ORF10-F_HA_RE-IP.mzid.gz	Mzid
	Prophet_ORF10-F_HA_RE-IP.mzid_QEp19-5290_Prophet_4tor_pc3_upper_band-_1_.MGF	Mzid
	Prophet_ORF10-F_HA_RE-IP.mzid_QEp19-5291_Prophet_4tor_pc3_lower_band-_1_.MGF	Mzid
	Prophet_ORF10-F_HA_RE-IP.mzid_QEp19-5296_Prophet_4tor_ORF10-F_upper_band-_1_.MGF	Mzid
	Prophet_ORF10-F_HA_RE-IP.mzid_QEp19-5297_Prophet_4tor_ORF10-F_lower_band-_1_.MGF	Mzid

Items per page:

1 - 5 of 22

Similar Datasets

Proximity labeling via MLF2-APEX2 fusion

Project description:Proximity labeling approach to identify protein inside nuclear envelope blebs arising in Torsin-deficient HeLa cells. WT and TorsinKO cells were engineered to express MLF2-APEX2 fusion. APEX reaction was carried out via 1 mM H2O2 for 1 minute in the presence of biotin phenol. Biotinylated protein were captured via streptavidin beads. Each APEX reaction was accompanied by an untreated (no H2O2) control.

2022-08-25 | PXD036262 | Pride

Protein co-purifying with MLF2-MBP from Expi293 cells

Project description:MLF2-MBP was expressed as a fusion protein in Expi293 cells. This was purified and a protein around 70 kDa was found to stoichiometrically co-purify. To verify this protein's identity, the 70 kDa region was extracted from a gel in addition to submitting the entire elution for mass spectrometry analysis.

2022-08-25 | PXD036267 | Pride

25 kDa band from HSPA1A immunoprecipitation

Project description:HSPA1A was immunoprecipitated from WT and TorsinKO HeLa cells. A band around 27 kDa was identified uniquely in TorsinKO samples and for identification, this band was extracted.

2022-08-25 | PXD036266 | Pride

d133 ORF10 IP (Table S2, Prophet et al.)

Project description:The truncated d133-ORF10-FLAG from KSHV was expressed and immunoprecipitated from WT and TorsinKO HeLa cells. The datasets were compared to an untransfected control. As d133-ORF10 localizes to blebs in TorsinKO cells, this approach allows probing of bleb protein contents.

2022-08-23 | MSV000090186 | MassIVE

RIP-seq of NAT10 interacted cellular and KSHV transcripts in iSLK-KSHV cells

Project description:Flag-RIP-seq was performed in NAT10-Flag overexpressing iSLK-KSHV cells.

2023-09-27 | GSE173889 | GEO

CD109 is novel KSHV entry receptor in human endothelial cells and enhances infection during cellular senescence

Project description:The aging process is characterized by cellular functional decline and increased susceptibility to infections. Understanding the association between virus infection and aging is crucial for developing effective strategies against viral infections in older individuals. Kaposi's sarcoma-associated herpesvirus (KSHV) infection increases the risk of Kaposi's sarcoma, a vascular cancer prevalent among the elderly without HIV infection. However, the relationship between KSHV pathogenesis and cellular senescence remains unknown. Here, we demonstrate that KSHV infectivity is significantly increased in senescent human endothelial cells due to enhanced binding of virions to cell surface. Proteomic analysis identified caveolin-1 and CD109 that promote KSHV infection and were significantly upregulated in senescent cells. In particular, CD109 is expressed on cell surface and directly interacts with KSHV virions to enhance KSHV infection. Knockout of CD109 abolished while overexpression of CD109 promote KSHV binding to cell surface, and infectivity. These results identify CD109 as a novel KSHV entry receptor that enhances KSHV infection in senescent cells, which might in part explain the higher sensitivity of elder subjects to KSHV infection and Kaposi's sarcoma.

2024-04-17 | PXD048212 | Pride

Pleomorphic Variants of Borreliella (syn. Borrelia) burgdorferi Express Evolutionary Distinct Transcriptomes

Project description:The objective of the study was to uncover the transcriptional differences between B. burgdorferi pleomorphic forms (spirochetes, round bodies, blebs and biofilms).

2023-03-17 | GSE199941 | GEO

Quantitative proteomics analysis of lytic KSHV infection in human endothelial cells reveals novel targets of viral immune modulation

Project description:Kaposi’s Sarcoma associated herpesvirus (KSHV) is an oncogenic human virus and leading cause of mortality in HIV infection. Reactivation of KSHV from latent to lytic stage infection initiates a cascade of viral gene expression, and here we show how these changes remodel the host cell proteome to enable viral replication. By undertaking a systematic and unbiased analysis of changes to the endothelial cell proteome following lytic KSHV reactivation, we quantify >7000 cellular and 71 viral proteins. Lytic KSHV infection resulted in >2-fold downregulation of 291 cellular proteins, including PKR, the key cellular sensor of double-stranded RNA. A complementary KSHV genome-wide CRISPR genetic screen identified K5 as the viral gene responsible for the downregulation of two novel KSHV targets, Nectin-2 and CD155, both ligands of the NK cell DNAM-1 receptor. Despite the high episome copy number, we show that CRISPR Cas9 provides a remarkably efficient way to target KSHV genomes.

2021-08-23 | PXD021387 | Pride

Quantitative proteomics analysis of lytic KSHV infection in human endothelial cells reveals novel targets of viral immune modulation

2022-05-26 | PXD017365 | Pride

Site-Specific Association with Host and Viral Chromatin by KSHV LANA and its Reversal during Lytic Reactivation

Project description:Latency-associated nuclear antigen (LANA), a multifunctional protein expressed by the Kaposi sarcoma-associated herpesvirus (KSHV) in latently-infected cells, is required for stable maintenance of the viral episome. This is mediated by two interactions: LANA binds to specific sequences (LBS1 and 2) on viral DNA, and also engages host histones, tethering the viral genome to host chromosomes in mitosis. LANA has also been suggested to affect host gene expression, but both the mechanism(s) and role of this dysregulation in KSHV biology remain unclear. Here we have examined LANA interactions with host chromatin on a genome-wide scale using ChIP-seq, and show that LANA predominantly targets human genes near their transcriptional start sites (TSSs). These host LANA-binding sites are generally found within transcriptionally active promoters and display striking overrepresentation of a consensus DNA sequence virtually identical to the LBS1 motif in KSHV DNA. Comparison of the ChIP-seq profile with whole transcriptome (RNA-seq) data reveals that few of the genes that are differentially regulated in latent infection are occupied by LANA at their promoters. This suggests that direct LANA binding to promoters is not the prime determinant of altered host transcription in KSHV-infected cells. Most surprisingly, the association of LANA to both host and viral DNA is strongly disrupted during the lytic cycle of KSHV. This disruption can be prevented by the inhibition of viral DNA synthesis, suggesting the existence of novel and potent regulatory mechanisms linked to either viral DNA replication or late gene expression. Profiling of KSHV LANA positioning on the host genome and examination of gene expression from promoters bound by KSHV LANA.

2014-04-01 | E-GEOD-56144 | 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