Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Macrophages transfer functional target-cell proteins to their surface during live cell uptake

ABSTRACT: A cell’s proteome is assumed to reflect its transcriptional and translational activity. Macrophages regularly acquire xenobiotic material from neighboring cells, which is thought to result in degradation of the material. However, increasing lines of evidence suggest that not all uptaken material is degraded and that other transfer-like processes also occur. Field standard technologies are unable to rigorously report on precisely how and by whom the macrophage protein repertoire is altered during these interactions, leaving unresolved the extent to which non-degradative processes contribute to altered phenotypes. Here, we leveraged chemical tools and proteomics to show that intact target cancer cell surface proteins are transferred to the macrophage cell surface at functionally impactful levels in a manner associated with live cell uptake. Widespread acquisition of proteins during cell uptake reengineers the macrophage cell surface proteome and is a transcriptionally silent, cell non-autonomous process with the potential to alter metabolic uptake.

ORGANISM(S): Homo sapiens

PROVIDER: GSE329293 | GEO | 2026/06/10

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Macrophage-augmenting targeted chimaeras for extracellular protein degradation

Project description:Extracellular targeted protein degradation (eTPD) systems typically function through passive endocytic trafficking mechanisms that direct extracellular proteins toward lysosomal degradation without actively modulating the functional state of the target cell. Here we report macrophage-augmenting targeted chimaeras (MATACs), a dual-effector eTPD platform inspired by macrophage-mediated efferocytosis. MATACs are constructed by conjugating target-binding antibodies with synthetic polyphosphoserine (PPS) polymers that mimic the polyvalent phosphatidylserine "eat-me" signals displayed on apoptotic cells. We show that PPS functions as a programmable macrophage-targeting ligand that induces macrophage-specific uptake, lysosomal activation, and M2-like immune repolarization. By leveraging this biology, MATACs simultaneously direct extracellular and membrane-associated proteins toward macrophage lysosomes for degradation while actively reprogramming the engulfing macrophages into enhanced degradative and anti-inflammatory states. We show that MATACs efficiently degrade multiple inflammatory targets, including tumor necrosis factor-alpha (TNF-alpha), granulocyte-macrophage colony-stimulating factor (GM-CSF), matrix metalloproteinase-9 (MMP-9), CD86, and CD40. Mechanistically, PPS engagement promotes feed-forward enhancement of macrophage phagocytic and lysosomal functions, establishing a self-amplifying degradation cascade distinct from existing eTPD systems. In murine models of rheumatoid arthritis and ulcerative colitis, TNF-alpha-targeted MATACs exhibit potent therapeutic efficacy, superior suppression of inflammatory signaling, and restoration of immune homeostasis relative to the conventional neutralizing antibody. Collectively, these findings establish MATACs as the first dual-effector extracellular degrader platform in which the effector ligand itself actively reprograms the degradative immune cell during target elimination.

2026-06-22 | GSE336034 | GEO

Phenotypic screens for SIRPA expression reveal RAB21 as a general regulator of macrophage surface identity

Project description:Factors influencing the macrophage surfaceome define macrophage identity and behaviour. Here, we use genome-wide phenotypic screens to identify genes affecting the accessibility and surface expression of macrophage SIRPA. Our data are consistent with previous evidence but also implicate QPCTL in cis CD47-SIRPA interactions. We also identify endolysosomal factors encoded by RAB21 and members of the CCC and WASH complexes as modulators of SIRPA expression. Surface immunophenotyping and surfaceome profiling show that inactivation of either Sirpa or Rab21 remodels cell surface protein expression. In contrast to Sirpa, Rab21 appears to be a general regulator of established macrophage cell surface markers. Perturbation of RAB21/Rab21 reduced Fc gamma receptor expression, leading to decreased uptake of antibody-nanoparticle conjugates and impaired phagocytosis of opsonized cells. To summarize, our study describes circuitry controlling SIRPA expression on macrophages and reveals a conserved RAB21-dependent trafficking pathway that has a role in modelling the cell surface of macrophages.

2025-06-03 | GSE297202 | GEO

Quality assurance of hematopoietic stem cells by macrophages determines stem cell clonality

Project description:There are no described quality assurance mechanisms for newly formed stem cells. We observed intimate interactions between macrophages and blood stem cells in zebrafish embryos. Stressed stem cells were marked by surface Calreticulin, which stimulates macrophage interaction as an eat me signal. Macrophage-stem cell interactions either lead to removal of cytoplasmic material and stem cell proliferation or resulted in complete stem cell engulfment. Calreticulin knock down or embryonic macrophage depletion reduced the number of stem cell clones into adulthood. Our work supports a model in which embryonic macrophages determine hematopoietic clonality by monitoring stem cell quality.

2022-02-04 | MSV000088780 | MassIVE

Project description:Indoor material surface genome

| PRJNA719799 | ENA

Comparative single-cell transcriptional and proteomic atlas of clinical-grade injectable mesenchymal source tissues

Project description:Bone marrow aspirate concentrate (BMAC) and adipose-derived stromal vascular fraction (ADSVF) are the most marketed stem cell therapies to treat a variety of conditions in the general population and elite athletes. Both tissues have been used interchangeably clinically even though their detailed composition, heterogeneity, and mechanisms of action have neither been rigorously inventoried nor compared. This lack of information has prevented investigations into ideal dosages and has facilitated anecdata and misinformation. Here, we analyzed single-cell transcriptomes, proteomes, and flow cytometry profiles from paired clinical-grade BMAC and ADSVF. This comparative transcriptional atlas challenges the prevalent notion that there is one therapeutic cell type present in both tissues. We also provide data of surface markers that may enable isolation and investigation of cell (sub)populations. Furthermore, the proteome atlas highlights intertissue and interpatient heterogeneity of injected proteins with potentially regenerative or immunomodulatory capacities.

2024-07-22 | GSE217244 | GEO

Quality assurance of hematopoietic stem cells by macrophages determines stem cell clonality [HSCP]

Project description:Tissue-specific stem cells persist for a lifetime and can differentiate to maintain homeostasis or transform to initiate cancer. Despite their importance, there are no described quality assurance mechanisms for newly formed stem cells. We observed intimate and specific interactions between macrophages and blood stem cells in zebrafish embryos. Stressed stem cells were marked by surface Calreticulin, which stimulates macrophage interaction as an “eat me” signal. Macrophage-stem cell interactions either lead to removal of cytoplasmic material and stem cell proliferation or resulted in complete stem cell engulfment. Using cellular barcoding, we found that calreticulin knock-down or embryonic macrophage depletion substantially reduced the number of stem cell clones into adulthood. Our work supports a model in which embryonic macrophages determine hematopoietic clonality by monitoring stem cell quality.

2022-10-19 | GSE196552 | GEO

Quality assurance of hematopoietic stem cells by macrophages determines stem cell clonality [macrophages]

2022-10-19 | GSE196551 | GEO

Pathways for macrophage uptake of cell-free circular RNAs

Project description:Pathways for macrophage uptake of cell-free circular RNAs

| PRJNA1101075 | ENA

Human p11-mediated re-direction of phagosomes to the recycling endosome-expulsion pathway by a fungal pathogen

Project description:The decision whether endosomes in mammalian cells enter the degradative or non-degradative pathway is of fundamental importance for killing of ingested pathogens and an essential basic mechanism whose malfunctioning has pathological consequences. We discovered that the human p11 protein is a decisive factor for directing phagosomes either to the degradative or secretory pathway. The HscA protein present on the spore surface of the human-pathogenic fungus Aspergillus fumigatus anchors p11 on the phagosome and thereby inhibits phagosome maturation that would result in for expulsion of spores. The clinical relevance of our findings is supported by the identification of an SNP in the non-coding region of the human p11 gene that affects its mRNA level and is associated with protection against invasive pulmonary aspergillosis.

2023-03-08 | GSE217895 | GEO

Cell surface mapping and monitoring of cell surface dynamics

Project description:Here, we present a simple and robust N-linked glycoproteome enrichment protocol optimized for deep coverage of the plasma membrane proteome. The procedure was applied to characterize the cell surface proteome of 15 standard laboratory human cell lines and three primary cell types. We observed significant differences in receptor diversity and transporter abundances between primary cells and corresponding cell lines. Relative quantification using isobaric mass tagging enabled quantitative monitoring of dynamic processes on the cell surface in multiplexed experiments. We for the first time report a comprehensive analysis of the profound remodeling of the plasma membrane proteome during monocyte to macrophage differentiation of THP-1 cells. Treatment of these cells with the kinase inhibitor dasatinib (Sprycel) during differentiation severely compromised macrophage differentiation due to an off-target activity resulting in substantial morphological and functional changes and the loss of many macrophage-associated proteins.

2017-03-27 | PXD005846 | Pride

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