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Protein interactions with HA-tagged cytoplasmic dynein-2 DATASET2

ABSTRACT: To identify those proteins interacting with the cytoplasmic dynein-2 using mammalian cell lines stably expressing HA-tagged intermediate chain subunits, WDR34 (DYNC2I2) or WDR60 (DYNC2I1).

INSTRUMENT(S): LTQ Orbitrap Velos

ORGANISM(S): Homo Sapiens (human)

TISSUE(S): Epithelial Cell

SUBMITTER: David Stephens

LAB HEAD: DAvid Stephens

PROVIDER: PXD031152 | Pride | 2023-01-24

REPOSITORIES: Pride

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			Action	DRS
	BlankPreRun.msf	Msf
	BlankPreRun.raw	Raw
	Fraction_1.raw	Raw
	Fraction_2.raw	Raw
	Fraction_3.raw	Raw

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1 - 5 of 21

Publications

Multiple interactions of the dynein-2 complex with the IFT-B complex are required for effective intraflagellar transport.

Hiyamizu Shunya S Qiu Hantian H Vuolo Laura L Stevenson Nicola L NL Shak Caroline C Heesom Kate J KJ Hamada Yuki Y Tsurumi Yuta Y Chiba Shuhei S Katoh Yohei Y Stephens David J DJ Nakayama Kazuhisa K

Journal of cell science 20230207 5

The dynein-2 complex must be transported anterogradely within cilia to then drive retrograde trafficking of the intraflagellar transport (IFT) machinery containing IFT-A and IFT-B complexes. Here, we screened for potential interactions between the dynein-2 and IFT-B complexes and found multiple interactions among the dynein-2 and IFT-B subunits. In particular, WDR60 (also known as DYNC2I1) and the DYNC2H1-DYNC2LI1 dimer from dynein-2, and IFT54 (also known as TRAF3IP1) and IFT57 from IFT-B contr ...[more]

PMID: 36632779

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An integrated multi-omics analysis of identiﬁes distinct molecular characteristics in pulmonary infections of Pseudomonas aeruginosa

Project description:Pseudomonas aeruginosa (P. aeruginosa) can cause severe acute infections, including pneumonia and sepsis, and also cause chronic infections commonly in patients with structural respiratory diseases. However, the molecular and pathophysiological mechanisms of P. aeruginosa respiratory infection are largely unknown. Here, we profiled performed to assay for transposase-accessible chromatin using sequencing (ATAC-seq), transcriptomics, and quantitative mass spectrometry-based proteomics and ubiquitin-proteomics in P. aeruginosa-infected lung tissues for multi-omics analysis, while ATAC-seq and transcriptomics were also examined in P. aeruginosa-infected mouse macrophages. To find the pivotal transcription factors that are likely involved in host immune defense, we integrally investigated systematic changes in chromatin accessibility and gene expression in P. aeruginosa-infected lung tissues combined with proteomics and ubiquitin-proteomics studies. We discovered that Stat1 and Stat3 were altered in various omics and found similar results in mouse alveolar macrophages. Taken together, these findings indicate that these crucial transcription factors and their downstream signaling molecules play a critical role in the mobilization of host immune response against P. aeruginosa infection and may serve as potential targets for bacterial infections and inflammatory diseases, as well as provide clear insights and resources for using integrative histological analyses.

2023-07-27 | PXD042381 | Pride

Pharmacological Targeting of Casein Kinase 1δ Suppresses Oncogenic NRAS-Driven Melanoma

Project description:Activating mutations in NRAS account for 15-20% of melanoma, yet effective anti-NRAS therapies are still lacking. In this study, we unveil the casein kinase 1δ (CK1δ) as an uncharacterized regulator of oncogenic NRAS mutations, specifically Q61R and Q61K, which are the most prevalent NRAS mutations in melanoma. The genetic ablation or pharmacological inhibition of CK1δ markedly destabilizes NRAS mutants and suppresses their oncogenic functions. Moreover, we identify USP46 as a bona fide deubiquitinase of NRAS mutants. Mechanistically, CK1δ directly phosphorylates USP46 and activates its deubiquitinase activity towards NRAS mutants, thus promoting oncogenic NRAS-driven melanocyte malignant transformation and melanoma progression in vitro and in vivo. Our findings underscore the significance of the CK1δ-USP46 axis in stabilizing oncogenic NRAS mutants and provide preclinical evidence that targeting this axis holds promise as a therapeutic strategy for human melanoma harboring NRAS mutations.

2024-09-19 | PXD051431 | Pride

Identification of potential interactors of NKS1 and QUA1

Project description:Adjacent plant cells are connected by specialized cell wall regions, called middle lamellae, which influence critical agricultural characteristics, including fruit ripening and organ abscission. Middle lamellae are enriched in pectin polysaccharides, specifically homogalacturonan (HG). Pectins are made in the Golgi apparatus by the coordinated action of transporters and enzymes. Here, in this project, we identify a plant-specific Arabidopsis DUF1068 protein, called NKS1/ELMO4, that is required for middle lamellae integrity and cell adhesion. We did an immunoprecipitation-mass spectrometry (IP-MS) analysis to identify potential interactors of NKS1. And we also performed an IP-MS analysis of QUA1, which is one of the interactors of NKS1.

2024-03-20 | PXD047727 | Pride

Comparison of gene expression from surviving and dying Pacific oysters reveals a motality signature

Project description:This experiment was designed to enable the identification of field mortality sensitive Pacific oysters while also permitting the repetitive, non-lethal sampling of tissue from identifiable individual oysters. These samples have been difficult to obtain because pre-mortality phenotypes are obscured by the presence of an outer shell which occludes all views of body tissues. Additionally, mortality triggers have not been identified and there is need to better characterize the pathophysiology preceding mortality. 300 three year old oysters were sampled on 6 dates from May to October, 2008 from their grow out site at Totten Inlet, WA, USA. 100-200ul of hemolymph was withdrawn from the adductor muscle and preserved for possible mRNA analysis by microarray. At the end of the summer, mortality phenotypes were assigned to individuals (alive vs. dead/mortality). Gene expression profiles from screened mortality individuals showed up-regulation of a set of 124/11904 ESTs within one month of death that were not usually found in the alive individuals. This indicates that the path to death in oysters occurs over several days and maybe weeks, and is a molecularly coordinated response in which the hemolymph is involved. Gene expression predictors of survival fate could be developed from this data set.

2011-03-16 | E-MTAB-548 | 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

Proteome and phosphoproteome of hippocampus after focal cerebral ischemia 2 h in mice

Project description:We obtained the profiles of neuronal phosphoproteome after cerebral ischemia onset by isolating mice hippocampus. Hippocampus combined from either ten sham or ten focal cerebral ischemia 2 h mice were lysed, digested, labeled with different TMT tags, then pooled and analyzed by LC/LC-MS/MS. Five percent of the pool was used for whole proteome analysis, and the remaining 95% was subjected to phosphoproteome profiling. In total, we quantified 5,174 proteins and 9,062 phosphopeptides. Interesting, 21 proteins were upregulated and 7 proteins were downregulated in hippocampus lysates of cerebral ischemia 2 h relative to sham base on fold change. S100a9, Alpha-2-HS-glycoprotein (Ahsg), Fibrinogen beta chain (Fga) and Complement Component C3(c3) are the top significantly changed, which were highly consistent with previous reports in cerebral ischemia injury. Using wolfpsort software to analysis the Subcellular Location, 57% of detected proteins were location to extracellular, 15% were cytoplasmic protein, another 11% were transport to nucleus, and the others were location to plasma membranes (10%), mitochondria (4%) and endoplasmic reticulum (3%). Moreover,184 phosphorylation sites of 135 proteins were upregulated and 689 phosphorylation sites of 420 proteins were downregulated in hippocampus during cerebral ischemia 2 h compare with sham operation. Employing wolfpsort software analysis the subcellular location, 50% of phosphorylated proteins were location to nucleus, 26% were cytoplasmic protein, another 16% were transport to plasma membranes, and the others were location to mitochondria (4%), extracellular (3%) and cytoskeleton (1%). Motif analysis showed that 85% were belongs to serine-type phosphorylation, about 14 were threonine-type phosphorylation and 1% were tyrosine-type phosphorylation.

2022-03-14 | PXD027145 | Pride

Detection of Dichlorvos Aducts in Hepatocyte Cell Line LC-MS/MS

Project description:Toxicity of dichlorvos (DDVP), an organophosphate (OP) pesticide, classically results from modification of the serine in the active sites of cholinesterases. However, DDVP also forms adducts on unrelated targets such as transferrin and albumin, suggesting that DDVP causes cellular perturbation by modifying non-cholinesterase targets. Here, we identify novel DDVP-modified targets in lysates of a human hepatocyte-like cell line (HepaRG) using a direct LC-MS assay of DDVP exposed lysates or using a competitive pull-down experiments with a biotin-linked organophosphorus compound (10-fluoroethoxyphosphinyl-N-biotinamidopentyldecanamide; FP-biotin), which competes with DDVP for similar binding sites. Using these strategies, we show that DDVP forms adduct to several proteins important to the cellular metabolic pathways and cellular differentiation, including glyceraldehyde-3-phosphate dehydrogenase (GAPDH) and actin. We validated the results using purified proteins and enzymatic assays. The study not only identified novel DDVP-modified targets but also suggested that the modification directly inhibits the enzymes. The current approach provides information for future hypothesis studies to understand the underlying mechanism of toxicity of DDVP in non-neuronal tissues.

2014-07-31 | PXD001107 | Pride

Ub-like SAMP1 and its associated proteins

Project description:Identifying proteins that associate with Ub like SAMP1 using an amino link column.

2023-06-22 | PXD019931 | Pride

RUNX1 contributes to higher-order chromatin organization and gene regulation in breast cancer cells.

Project description:RUNX1 is a transcription factor functioning both as an oncogene and a tumor suppressor in breast cancer. RUNX1 alters chromatin structure in cooperation with chromatin modifier and remodeling enzymes. In this study, we examined the relationship between RUNX1-mediated transcription and genome organization. We characterized genome-wide RUNX1 localization and performed RNA-seq and Hi-C in RUNX1-depleted and control MCF-7 breast cancer cells. RNA-seq analysis showed that RUNX1 depletion led to up-regulation of genes associated with chromatin structure and down-regulation of genes related to extracellular matrix biology, as well as NEAT1 and MALAT1 lncRNAs. Our ChIP-Seq analysis supports a prominent role for RUNX1 in transcriptional activation. About 30% of all RUNX1 binding sites were intergenic, indicating diverse roles in promoter and enhancer regulation and suggesting additional functions for RUNX1. Hi-C analysis of RUNX1-depleted cells demonstrated that overall three-dimensional genome organization is largely intact, but indicated enhanced association of RUNX1 near Topologically Associating Domain (TAD) boundaries and alterations in long-range interactions. These results suggest an architectural role for RUNX1 in fine-tuning local interactions rather than in global organization. Our results provide novel insight into RUNX1-mediated perturbations of higher-order genome organization that are functionally linked with RUNX1-dependent compromised gene expression in breast cancer cells. Hi-C and RNA-seq experiments were conducted in MCF-7 shNS and shRUNX1 cells. RUNX1 ChIP-seq was conducted in wildtype MCF-7 cells.

2016-08-23 | E-GEOD-75070 | biostudies-arrayexpress

Global Lactylation Profiling Reveals Lactate-Driven Regulatory Mechanisms Promoting Tumor Progression in Oral Squamous Cell Carcinoma

Project description:Cancer cells often rely on aerobic glycolysis for metabolism, and lactylation, a newly discovered post-translational modification, significantly impacts molecular processes. This study comprehensively analyzes lactylation's role in oral squamous cell carcinoma (OSCC), providing initial insights into its impact on progression. Six pairs of OSCC tissues underwent lactylation modification sequencing. 2,765 lactylation modification sites on 1,033 proteins were identified in OSCC, indicating its widespread presence. These modifications influenced metabolic activities, molecular synthesis, and transport.

2024-08-23 | PXD047535 | Pride

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