Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Human ESCO2-interacting proteins in response to DNA damage

ABSTRACT: We used IP-MS to detected the proteins that interact with ESCO2 in response to DNA damage.

INSTRUMENT(S): LTQ Orbitrap

ORGANISM(S): Homo Sapiens (human)

TISSUE(S): Epithelial Cell, Kidney

SUBMITTER: Jianfeng Fu

LAB HEAD: Xiaofeng Zheng

PROVIDER: PXD039072 | Pride | 2023-10-24

REPOSITORIES: Pride

ACCESS DATA

Json Xml

Publications

ATM-ESCO2-SMC3 axis promotes 53BP1 recruitment in response to DNA damage and safeguards genome integrity by stabilizing cohesin complex.

Fu Jianfeng J Zhou Siru S Xu Huilin H Liao Liming L Shen Hui H Du Peng P Zheng Xiaofeng X

Nucleic acids research 20230801 14

53BP1 is primarily known as a key regulator in DNA double-strand break (DSB) repair. However, the mechanism of DSB-triggered cohesin modification-modulated chromatin structure on the recruitment of 53BP1 remains largely elusive. Here, we identified acetyltransferase ESCO2 as a regulator for DSB-induced cohesin-dependent chromatin structure dynamics, which promotes 53BP1 recruitment. Mechanistically, in response to DNA damage, ATM phosphorylates ESCO2 S196 and T233. MDC1 recognizes phosphorylated ...[more]

PMID: 37377435

Similar Datasets

MicroRNA-dependent transposable element transcriptional silencing in Drosophila somatic ovarian cells [RIP-Seq]

Project description:RNAi-related silencing mechanisms concern as diverse biological processes as gene regulation, mostly via the miRNA pathway, and defense against molecular parasites, mainly controlled by the siRNA and the piRNA pathways. In Drosophila somatic ovarian cells, transposable elements (TEs) are repressed by chromatin changes induced by Piwi-interacting RNAs (piRNAs). We show here that a functional miRNA pathway is required for this piRNA-mediated TE transcriptional silencing to operate in this tissue. A general miRNA depletion, caused by tissue- and stage-specific knock-down of either drosha (involved in miRNA biogenesis) or AG01 and gawky (both responsible for miRNA activity) resulted in chromatin-mediated TE transcriptional desilencing and piRNA loss. For unknown reasons, the amount of piRNA produced by the traffic jam 3' UTR was apparently unaffected in miRNA-defective somatic ovarian cells. Although weaker, similar phenotypes could also be observed upon individual titration (by expression of the complementary miR-sponge) of at least three miRNAs, miR-14, miR-34 and miR-989. This work adds the maintenance of genome stability, via the piRNA-mediated TE repression, to the list of the already reported miRNA-controlled biological functions. Analyses of RNA present in 3 different genetic backgounds with or without Drosha-IP: a control, a second one expressing the wild-type Drosha protein and a third one expressing the trans-dominant negative Drosha protein in the somatic cells.

2015-04-08 | E-GEOD-60973 | biostudies-arrayexpress

Interacting proteins of SnRK2.4 by IP-MS

Project description:This project is designed to identify the interacting protein of SnRK2.4 through IP-MS.

2020-07-02 | PXD017499 | Pride

SgK269 Interactome - Homo- and Heterotypic Association Regulates Signalling by the SgK269/PEAK1 and SgK223 Pseudokinases

Project description:Anti Flag IP of Flag-SgK269 and control IP from MCF10A EcoR cells.

2016-08-24 | PXD004250 | Pride

Entamoeba histolytica splicing/mRNP proteome

Project description:First, the snRNP component U1A was HA-tagged and the intron of the RabX13 gene was MS2-tagged and amoeba transformats were established with such constructs. Next, amoeba transformants were UV cross-linked and their nucler extracts were immunoprecipitated (IP) with anti-HA agarose or MS2-spharose beads. Precipitates were subjected to tandem mass spectrometry (MS/MS) analyses. MS2-IP helped to discriminate the nuclear roles (chromatin-, co-transcriptional-, splicing-related), of the proteins probed.

2014-09-11 | PXD001080 | Pride

MicroRNA-dependent transposable element transcriptional silencing in Drosophila somatic ovarian cells

Project description:This SuperSeries is composed of the SubSeries listed below. Refer to individual Series

2015-04-08 | E-GEOD-60974 | biostudies-arrayexpress

Next-generation sequencing for the fat mass and obesity-associated protein (FTO) binding mRNA

Project description:Purpose: The goals of this study are to investigate the mRNAs that bind to the FTO protein in the white fat tissue from mice. Methods: 1. White fat from CAG promoter driven transgenic Flag-tagged FTO mice were extracted with RNA protected. 2. Flag-FTO proteins were immunoprecipitated with control IP using IgG. 3. The immunoprecipitated RNAs were deep sequenced and analyzed. Results: We focused on the mRNAs which have functions related to lipid metabolism and homeostasis. Immunoprecipitated RNAs profiles from Flag-FTO IP and IgG IP were generated by deep sequencing.

2016-01-05 | E-GEOD-74255 | biostudies-arrayexpress

Regulatory role of E3 ubiquitin ligase Smurf2 on transcriptional corepressor KAP1

Project description:An E3 ubiquitin ligase Smurf2 and transcriptional co-repressor KAP1 have been documented to play crucial roles in similar cellular pathways including cell cycle, DNA damage response, chromatin compaction, senescence and cell death. Smurf2 and KAP1, through regulation of these cellular processes either drive or suppress tumorigenesis. Studies till date confer Smurf2 with a dual role in carcinogenesis, an oncogene and a tumor suppressor, depending on the cellular context. However, the molecular mechanisms governing Smurf2 functions remain unclear. Furthermore, studies have demonstrated significantly altered KAP1 protein levels in many human malignancies, despite which, the mechanisms operating in and regulating KAP1 stability and activity are obscure. In this study, we obtained evidence which indicates a strong and dynamic association between Smurf2 and KAP1. We found that Smurf2 directly binds KAP1 through its C2, WW1 and HECT domains. Further mechanistic studies also revealed that Smurf2 multi(mono)ubiquitinates KAP1 in E3 ligase-dependent manner. Moreover, Smurf2 differentially alters KAP1 protein levels in different types of mammalian and cancer cells and tissues, and significantly alters KAP1 interactome. Based on these findings, we propose a mechanism to explain the dual role and differential regulation of Smurf2 on KAP1 in a cell-context dependent manner. Further investigations of the identified Smurf2/KAP1 module could potentially lead to development of new, more efficient diagnostics tools and treatment paradigms.

2022-04-07 | PXD029642 | Pride

The Functions of Serine 687 Phosphorylation of Human DNA Polymerase eta in UV Damage Tolerance

Project description:DNA polymerase (pol) is a Y-family translesion synthesis polymerase that plays a key role in the cellular tolerance toward UV irradiation-induced DNA damage. Here, we identified, for the first time, the phosphorylation of serine 687 (S687), which islocated in the highly conserved nuclear localization signal (NLS) region of human pol and is mediated by cyclin-dependent kinase 2 (CDK2). We also showed that this phosphorylation is stimulated in human cells upon UV light exposure and results in diminished interaction of pol with proliferating cell nuclear antigen (PCNA). Furthermore, we demonstrated that the phosphorylation of S687 in polconfers cellular protection fromUV irradiation and increases the efficiency in replication across a site-specifically incorporated cyclobutane pyrimidine dimer in human cells. Based on these results, we proposed a mechanistic model where S687 phosphorylation functions in the reverse polymerase switching step of translesion synthesis: The phosphorylation brings negative charges to the NLS of pol, which facilitates its departure from PCNA, thereby resetting the replication fork for highly accurate and processive DNA replication. Thus, our study, together with previous findings, supported that the post-translational modifications of NLS of pol played a dual role in polymerase switching, where K682 deubiquitination promotes the recruitment of pol to PCNA immediately prior to lesion bypass and S687 phosphorylation stimulates its departure from the replication fork immediately after lesion bypass.

2016-07-19 | PXD002946 | Pride

NSMF promotes the replication stress-induced DNA damage response for genome maintenance

Project description:Proper activation of DNA repair pathways in response to DNA replication stress is critical for maintaining genomic integrity. Due to the complex nature of the replication fork (RF), problems at the RF require multiple proteins, which remain unidentified, for resolution. In this study, we identified the NMDA receptor synaptonuclear signaling and neuronal migration factor (NSMF) as a key replication stress response factor that is important for ataxia telangiectasia and Rad3-related protein (ATR) activation. NSMF localizes rapidly to stalled RFs and acts as a scaffold to modulate replication protein A (RPA) complex formation with cell division cycle 5-like (CDC5L) and ATR/ATR-interacting protein (ATRIP). Depletion of NSMF compromised phosphorylation and ubiquitination of RPA2 and the ATR signaling cascade, resulting in genomic instability at RFs under DNA replication stress. Consistently, NSMF knockout (KO) mice exhibited increased genomic instability and hypersensitivity to genotoxic stress. NSMF deficiency in human and mouse cells also caused increased chromosomal instability. Collectively, these findings demonstrate that NSMF regulates the ATR pathway and the replication stress response network for genome maintenance and cell survival.

2021-09-09 | PXD021942 | Pride

AP-MS of different isoforms of Axin

Project description:This project aims to identify and differentiate the interaction partners of Axin1 isoforms including 1 wild type and 3 different mutants (L106R, L106R_F119R, deltaRGS).

2016-02-26 | PXD003116 | Pride

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

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