Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

LC-MS/MS of extracellular vesicles from murine osteosarcoma cell line K7 and K7M2

ABSTRACT: Extracellular vesicles have been shown to be highly enriched in proteins with various functions, including organotropic metastasis. To identify possible protein cargos involved in regulating mestastatic potential of osteosarcoma cell line, we performed quantitative mass spectrometry analysis of EVs from highly metastatic K7M2 cells and poorly metastatic parental K7 cells.

INSTRUMENT(S): Q Exactive

ORGANISM(S): Mus Musculus (mouse)

TISSUE(S): B Cell, Osteosarcoma Cell

DISEASE(S): Osteosarcoma

SUBMITTER: Chuangzhong Deng

LAB HEAD: Chuangzhong Deng

PROVIDER: PXD035216 | Pride | 2024-01-15

REPOSITORIES: Pride

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	20210103-DCZ123-1.mgf	Mgf
	20210103-DCZ123-1.raw	Raw
	20210103-DCZ123-2.mgf	Mgf
	20210103-DCZ123-2.raw	Raw
	20210103-DCZ123-3.mgf	Mgf

Items per page:

1 - 5 of 14

Similar Datasets

EP300 promotes ferroptosis via HSPA5 acetylation in pancreatic cancer

Project description:Ferroptosis is a form of regulated cell death characterized by oxidative injury-induced lipid peroxidation. However, the detailed protein post-translational modification regulatory mechanism of ferroptosis remains largely unknown. Here, we report that E1A binding protein P300 (EP300) acetyltransferase promotes ferroptosis in human pancreatic ductal adenocarcinoma (PDAC) cells via the acetylation of heat shock protein family A (Hsp70) member 5 (HSPA5, also known as GRP78 or BIP) on the site of K353. Acetylated HSPA5 loses its ability to inhibit lipid peroxidation and subsequent ferroptotic cell death. Genetic or pharmacological inhibition of EP300-mediated HSPA5 acetylation on K353 increases PDAC cell resistance to ferroptosis. Moreover, histone deacetylase 6 (HDAC6) limits HSPA5 acetylation and subsequent ferroptosis.

2023-10-24 | PXD039998 | Pride

Ribosome profiling upon glucose starvation in S. cerevisiae

Project description:A universal feature of the response to stress and nutrient limitation is transcriptional upregulation of genes encoding proteins important for survival. Interestingly, under many of these conditions overall protein synthesis levels are reduced, thereby dampening the stress response at the level of protein expression. For example, during glucose starvation in yeast, translation is rapidly and reversibly repressed, yet transcription of many stress- and glucose-repressed genes is increased. Using ribosome profiling and microscopy, we found that this transcriptionally upregulated gene set consists of two classes: (1) one producing mRNAs that are preferentially translated during glucose limitation and are diffusely localized in the cytoplasm – this class includes many heat shock protein mRNAs; and (2) another producing mRNAs that are poorly translated during glucose limitation, have high rates of translation initiation, and are concentrated in foci that co-localize with P bodies and stress granules – this class is enriched for glucose metabolism mRNAs. Remarkably, the information specifying differential localization and translation of these two classes of mRNAs is encoded in the promoter sequence – promoter responsiveness to heat shock factor (Hsf1) specifies diffuse cytoplasmic localization and preferential translation upon glucose starvation, whereas different promoter elements upstream of genes encoding poorly translated glucose metabolism mRNAs direct these mRNAs to RNA granules under glucose starvation. Thus, promoter sequences and transcription factor binding can influence not only mRNA levels, but also subcellular localization of mRNAs and the efficiency with which they are translated, enabling cells to tailor protein production to environmental conditions. Examination of mRNA translation in S. cerevisiae upon glucose starvation.

2014-07-28 | E-GEOD-56622 | biostudies-arrayexpress

Proteins bound to BTBD7_hsa_circ_0000563 in coronary artery disease

Project description:We aimed to clarify the possible functional role of hsa_circ_0000563 in coronary artery disease. Therefore, the ChIRP-MS was conducted to explore the interaction between BTBD7_hsa_circ_0000563 and proteins on a genomic scale in human peripheral blood mononuclear cell (PBMC). This project is the raw files of the proteins bound to hsa_circ_0000563 found by ChIRP-MS in PBMC.

2023-03-11 | PXD033196 | Pride

Potential proteins interacted with S100A11

Project description:To explore the mechanism by which the S100A11 protein activate macrophage, we screened potential proteins that interacted with S100A11 using immunoprecipitation-mass spectrometry (IP-MS) analysis. IP was performed in 293T cells overexpressing FLAG-tagged Vector or S100A11

2024-01-16 | PXD048589 | Pride

LC-MS/MS of human MFN2 interaction proteins

Project description:LC-MS/MS of human MFN2 interaction proteins from 293T cells or 786-O cells

2023-10-24 | PXD033112 | Pride

PsAF5 functions as an essential adapter for PsPHB2-mediated mitophagy under ROS stress in Phytophthora sojae

Project description:Host-derived reactive oxygen species (ROS) is an important defense means to protect against pathogens. Although mitochondria are the main intracellular targets of ROS, how pathogens regulate mitochondrial physiology in response to oxidative stress remains elusive. Prohibitin 2 (PHB2) is an inner mitochondrial membrane (IMM) protein, recognized as a mitophagy receptor in animals and fungi. Here, we found that an ANK and FYVE domain-containing protein PsAF5, as an adapter of PsPHB2, interacting with PsATG8 under ROS stress. Unlike PHB2 can recruit ATG8 directly to mitochondria in animals, PsPHB2 cannot recruit PsATG8 to stressed mitochondria without PsAF5. PsAF5 deletion in P. sojae impairs mitophagy under ROS stress and increases its sensitivity to H2O2, resulting the attenuation of P. sojae pathogenicity. The first discovery of PsPHB2-PsAF5-PsATG8 axis in plant pathogenic oomycetes revealed that the IMM protein as a receptor to mediate mitophagy is conserved in eukaryotes, but with differences in the detail of ATG8 recruitment.

2024-05-21 | PXD044242 | Pride

LC-MS/MS of Rab21 pull-down or control sample

Project description:LC-MS/MS of Rab21 pull-down or control sample from 786-O cells

2023-10-24 | PXD033104 | Pride

LC-MSMS of mitochondria of human 786-O cells

Project description:Mass spectrum analysis of mitochondria isolated from 786-O cells

2023-10-24 | PXD033099 | Pride

Mouse macrophage derived mirasome iTRAQ

Project description:To explore the mechanisms of migrasome-induced BBB damage, Aβ40 induced migrasome and PBS induced migrasome were subjected to isobaric tags for relative and absolute quantification (ITRAQ)

2023-06-09 | PXD039329 | Pride

gene expression profiling of brain metastatic melanoma cell lines

Project description:Cerebral metastases occur in a majority of metastatic melanoma patients and are a major cause of mortality. Despite this, there is a poor understanding of the molecules/pathways that lead to the brain-metastatic phenotype. Studies designed to address this deficiency and test novel therapeutic approaches have until recently been slowed by an absence of preclinical models of spontaneous CNS metastatic melanoma disease. To address this, we isolated two variants of the human melanoma cell line WM239 (named 131/4-5B1 and 131/4-5B2) which can metastasize spontaneously to brain parenchyma from an orthotopic primary transplant. We have performed gene expression profiling on both brain metastatic cell lines (131/4-5B1 and 131/4-5B2) and compared to the poorly metastatic parental cell line WM239A and a derived highly metastatic variant 113/6-4L in order to examine the mechanisms that influence the progression of malignant melanoma to a brain-metastatic phenotype. Two-condition experiment, brain metastatic cell lines (131/4-5B1 and 131/4-5B2) and compared to the poorly metastatic parental cell line WM239A and a derived highly metastatic variant 113/6-4L. Biological replicates: 4 independently grown and harvested cell line passages. Two technical replicate per condition (including dye swap).

2012-11-21 | E-GEOD-23601 | 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