Browse
Submit Data
Databases
API
Help

Dataset Information

496 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Proteomic profile of deleted in breast cancer 1 protein-protein interactions

ABSTRACT: Deleted in breast cancer 1 (DBC1) has emerged as an important regulator of multiple cellular processes, ranging from gene expression to cell cycle progression. DBC1 has been linked to tumorigenesis both as an inhibitor of histone deacetylases (HDAC), HDAC3 and sirtuin 1 (SIRT1), and as a transcriptional cofactor for nuclear hormone receptors. However, despite mounting interest in DBC1, relatively little is known about the range of its interacting partners and the scope of its functions. DBC1 protien interactions were studied in two cell types, T cells and HEK293 kidney cells

INSTRUMENT(S): LTQ Orbitrap Velos

ORGANISM(S): Homo Sapiens (human)

TISSUE(S): T Cell, Cell Culture, Kidney Cell

SUBMITTER: Todd Greco

LAB HEAD: Ileana M Cristea

PROVIDER: PXD002733 | Pride | 2015-12-17

REPOSITORIES: Pride

ACCESS DATA

Json Xml

Publications

The Proteomic Profile of Deleted in Breast Cancer 1 (DBC1) Interactions Points to a Multifaceted Regulation of Gene Expression.

Giguère Sophie S B SS Guise Amanda J AJ Jean Beltran Pierre M PM Joshi Preeti M PM Greco Todd M TM Quach Olivia L OL Kong Jeffery J Cristea Ileana M IM

Molecular & cellular proteomics : MCP 20151209 3

Deleted in breast cancer 1 (DBC1) has emerged as an important regulator of multiple cellular processes, ranging from gene expression to cell cycle progression. DBC1 has been linked to tumorigenesis both as an inhibitor of histone deacetylases, HDAC3 and sirtuin 1, and as a transcriptional cofactor for nuclear hormone receptors. However, despite mounting interest in DBC1, relatively little is known about the range of its interacting partners and the scope of its functions. Here, we carried out a ...[more]

PMID: 26657080

Similar Datasets

Interactome analysis of PYHIN immune regulators

Project description:The human PYHIN proteins, AIM2, IFI16, IFIX, and MNDA, are regulators of immune response, transcription, apoptosis, and cell cycle. However, their protein interactions and underlying mechanisms remain largely uncharacterized. Here, we provide the interaction network for all PYHIN proteins. By designing a cell-based inducible system and integrating microscopy, immunoaffinity capture, quantitative mass spectrometry, and bioinformatics, we identified over 300 PYHIN interactions reflective of diverse functions.

2015-03-12 | PXD001572 | Pride

SIRT3 interactions and mitochondrial proteome during HCMV infection

Project description:SIRT3 has been shown to inhibit HCMV infection, but the mechanism under the antiviral effect is not clear. To identify the mediator of SIRT3 antiviral function, we aim to identify and quantify SIRT3 interactions during HCMV infection. A set of large-scale IPs were performed to determine the specific interactions with SIRT3 during infection, while small-scale IPs were conducted to determine the temporal interactions over the life cycle of infection. The mitochondrial proteome was used to characterize the changes of protein abundances after infection, and it was used for the normalization of acetylation.

2021-04-01 | PXD018995 | Pride

Multiple Arkadia/RNF111 structures coordinate its Polycomb body association and transcriptional control

Project description:The RING domain protein Arkadia/RNF111 is a ubiquitin ligase in the transforming growth factor beta (TGFβ) pathway. We previously identified Arkadia as a small ubiquitin-like modifier (SUMO)-binding protein with clustered SUMO-interacting motifs (SIMs) that together form a SUMO-binding domain (SBD). However, precisely how SUMO interaction contributes to the function of Arkadia was not resolved. Through analytical molecular and cell biology, we found that the SIMs share redundant function with Arkadia's M domain, a region distinguishing Arkadia from its paralogs ARKL1/ARKL2 and the prototypical SUMO-targeted ubiquitin ligase (STUbL) RNF4. The SIMs and M domain together promote both Arkadia's colocalization with CBX4/Pc2, a component of Polycomb bodies, and the activation of a TGFbeta pathway transcription reporter. Transcriptome profiling through RNA sequencing showed that Arkadia can both promote and inhibit gene expression, indicating that Arkadia's activity in transcriptional control may depend on the epigenetic context, defined by Polycomb repressive complexes and DNA methylation [Sun, Liu, and Hunter (2014) Mol Cell Biol 34(16):2981-2995]. To determine the role of Arkadia in TGFβ signaling at the transcriptome level, the profiles of TGFβ-stimulated gene expression were examined in Ark+/+ (Ark_WT), Ark-/- (Ark_null), and Arkadia (WT and sim mutant)-reconstituted Ark-/- MEFs. RNA sequencing was carried out using poly(A)-enriched RNA samples from unstimulated cells and cells treated with TGFβ for 1h, 4h, or 16h as indicated. Two batches of sequencing data for a total of 16 independent samples were submitted.

2015-02-11 | E-GEOD-65796 | biostudies-arrayexpress

Gene expression in mouse liver depleted of HDAC3

Project description:Liver-specific depletion of HDAC3 leads to liver steatosis (fatty liver), suggesting disregulation of lipid metabolism. This is correlated with changes in lipid metabolic gene expression. Livers depleted of HDAC3 were removed from 12 week old male HDAC3 fl/fl mice (loxP sites flanking exon 4 to 7 of the HDAC3 gene encoding the catalytic domain of HDAC3) one week after the injection of AAV2/8-Tbg-Cre virus. Livers from the HDAC3 fl/fl mice injected with AAV2/8-Tbg-GFP were used as normal controls. mRNA was extracted from 100mg mouse liver samples and hybridized to Affymetrix microarrays. For each group (HDAC3 depleted liver and normal liver), we have 5 samples from different mice.

2011-03-11 | E-GEOD-25937 | biostudies-arrayexpress

Expression data of Sox9+ and Ngn3+ mouse pancreas cells at different stages of development

Project description:Genes specific to Sox9+ pancreatic progenitors were identified by comparing the gene expression in embryonic and adult Sox9+ cells. We used microarray analysis to detail the global changes in gene expression as Sox9 positive embryonic pancreatic progenitors differentiatiate into adult ductal cells or the endocrine lineage. GFP positive cells from Sox9-EGFP mouse pancreas were isolated by FACS at different stages of development (e10.5, e15.5, and p23) for RNA extraction and hybridization to Affymetrix microarrays. To obtain populations highly enriched in Sox9 expression, we collected only GFP Hi populations for analysis. To identify gene expression changes specific to the differentiation of progenitors to ductal cells or endocrine cells, we also isolated and analyzed the gene expression profile of GFP negative cells isolated at p23, as well as GFP positive cells isolated from Ngn3-EGFP mouse pancreas at e15.5. These two populations allow the identification of genes whose expression is associated with the newly differentiated endocrine progeny in the embryo (Ngn3-GFP positive) and adult acinar and endocrine cells at p23.

2012-08-01 | E-GEOD-34060 | biostudies-arrayexpress

Decoding the signalling profile of hematopoietic progenitor kinase 1 (HPK1) in innate immunity: a proteomic approach

Project description:The fine-tuned spatiotemporal response of leukocytes to external stimuli is a hallmark of the immune system. Sensing of stimuli occurs through cell surface receptors, which transmit signals into the cell. Signaling via β2 integrins, B cell, and T cell receptors involve similar pathways. However, the activation of the same signaling molecule can result in opposing cell effector functions. One such example is the hematopoietic progenitor kinase 1 (HPK1), which negatively regulates activation of B and T cells but in contrast enforces neutrophil activation upon β2 integrin receptor engagement. Whether this difference is determined by specific interacting proteins might be disclosed by decoding the binding partners of HPK1. In the adaptive immune system, the interactome of HPK1 has already been described, whereas it is unknown in innate immune cells. Therefore, we set out to identify interacting proteins of HPK1 in the myeloid system. Neutrophil-like differentiated HL-60 cells were exposed to immobilized fibrinogen and either stimulated with Mn2+ to allow β2 integrin-mediated adhesion or left unstimulated for control. Co-immunoprecipitation experiments followed by mass spectrometry led to the identification of 116 proteins interacting with HPK1 in total. Here, 58 proteins were found only in unstimulated cells and 39 proteins only in Mn2+-stimulated adherent cells. From these results we constructed the interacting network of HPK1 with signaling, cytoskeleton-associated, transmembrane, adapter, and other proteins. Taken together, our study provides comprehensive insights into the HPK1 interactome in innate immune cells paving the way to a deeper understanding of the complex signaling profile of HPK1 in leukocytes.

2022-02-10 | PXD021136 | Pride

Yorkie and Bonus protein interactome-Hippo pathway and Bonus control developmental cell fate decisions in the Drosophila eye

Project description:To identify novel regulators of the Hippo pathway, we performed affinity purification-mass spectrometry (AP-MS) using Drosophila embryos overexpressing Yki-EGFP with a ubiquitous driver da-GAL4, as well as cultured S2 cells expressing Yki-SBP. We identified the core Hippo pathway components, multiple Hippo pathway regulators and functional groups, and several putative Yki interactors including Bonus (Bon). To identify additional cofactors that are recruited by Bon, we performed AP-MS using Bon-SBP expressed in Drosophila S2 cells. Further genetic tests revealed the involvement of Bon interactors, HDAC1, Su(var)2-10, and Hrb27C, in the Drosophila eye specification that is regulated by the Yki-Bon complex.

2023-01-17 | PXD027934 | Pride

Transcription profiling of human T4-2 neoplastic breast epithelial cells that overexpressed N-CoR2 in response to death induction

Project description:The series represent gene expression profiles of T4-2 neoplastic breast epithelial cells that overexpressed N-CoR2 and were treated with the death ligand TRAIL in three-dimensional reconstituted basement membrane culture. Experiment Overall Design: Four replicate cultures were established for each of the 4 experiment groups, including those using T4-2 cells that stably expressed N-CoR2 (T4-2_NCOR2), T4-2 cells expressing the empty vector (T4-2_vector), TRAIL-treated T4-2 N-CoR2 cells (T4-2_NCOR2_TRAIL), and TRAIL-treated T4-2 vector cells (T4-2_vector_TRAIL). Cells were grown on top of reconstituted basement membrane for 6 days and then treated with TRAIL (1 Î¼g/mL) or vehicles for 4 hours before the collection of RNA samples.

2008-10-25 | E-GEOD-8346 | biostudies-arrayexpress

Mouse CDC73 AP-MS in AML - PAF1 complex interactions with SETDB1 mediate promoter H3K9 methylation and transcriptional repression of Hoxa9 and Meis1 in acute myeloid leukemia

Project description:Here we performed AP-MS experiments to find novel binding partners of CDC73 in mouse M1 AML cells. We also utilized a CDC73 mutant that does not support AML cell growth to determine functional consequences of gainin/ losing protein-protein interactions on mutation of this protein.

2018-05-22 | PXD009439 | Pride

Functional Dissection of the Retrograde Shiga Toxin Trafficking Inhibitor Retro-2

Project description:The retrograde transport inhibitor Retro-2 has a protective effect on cells and in mice against Shiga-like toxins and ricin. Retro-2 causes toxin accumulation in early endosomes, and the relocalization of the Golgi SNARE protein syntaxin-5 to the endoplasmic reticulum. The molecular mechanisms by which this is achieved remain unknown. Here, we show that Retro-2 targets the endoplasmic reticulum exit site component Sec16A, affecting anterograde transport of syntaxin-5 from the endoplasmic reticulum to the Golgi. The formation of canonical SNARE complexes involving syntaxin-5 is not affected in Retro-2-treated cells. In contrast, the interaction of syntaxin-5 with a newly discovered binding partner, the retrograde trafficking chaperone GPP130, is abolished, and we show that GPP130 must indeed bind to syntaxin-5 to drive Shiga toxin transport from endosomes to the Golgi. We thereby identify Sec16A as a druggable target, and provide evidence for a non-SNARE function for syntaxin-5 in interaction with the retrograde cycling protein GPP130. a) Clickable Retro-2 pulldown. To identify protein target of Retro-2.1, providing the first steps to explain effects of Retro-2 on inhibition of STxB retrograde trafficking from endosomes to Golgi. b) GFP-STX5 pulldown. To find interactors of STX5, to build a hypothesis to explain the affect of Retro-2-inhibited anterograde trafficking of STX5 to Golgi, which in turn inhibits STxB retrograde transport from endosomes to Golgi. c) GFP-Sec16A pulldown. The aim of this proteomics assay is to show the effects of Retro-2 on the Sec16A interactome. Results show the differential effects of Retro-2 treatment on the Sec16A interactome, giving insight into the mechanism by which Retro-2, via Sec16A, specifically affects the anterograde trafficking of Syntaxin-5.

2020-02-24 | PXD015642 | 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