Identification of proteins able to interact with the WD40 domain of ATG16L1
Ontology highlight
ABSTRACT:
INSTRUMENT(S):
ORGANISM(S): Homo Sapiens (human)
TISSUE(S): Monocyte
SUBMITTER: 
Nieves Ibarrola
LAB HEAD: Felipe X. Pimentel-Muiños
PROVIDER: PXD013180 | Pride | 2019-03-21
REPOSITORIES: Pride
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| 0060_01.mgf | Mgf | |||
| 0060_01.pride.mgf.gz | Mgf | |||
| 0060_02.mgf | Mgf | |||
| 0060_02.pride.mgf.gz | Mgf | |||
| 0060_03.mgf | Mgf |
Items per page: 5 1 - 5 of 264 |
Similar Datasets
Project description:Macrophages are sentinels of the immune system and THP1 monocytic cells are one of the widely used models to study immune responses in macrophages. Several monocyte-to-macrophage differentiation protocols exist with phorbol 12-myristate-13-acetate (PMA) being widely used and accepted. However, the concentrations and durations of PMA treatment to induce differentiation varies widely in published literature. In this study, we determined the proteome expression dynamics of THP1 macrophages differentiated from monocytes by three commonly used PMA-based differentiation protocols using dimethyl labeling-based quantitative proteomics analysis. Our analysis shows that variations in PMA concentration and varying periods of rest post-stimulation result in downstream differences in proteome expression and cellular processes. We demonstrate that these differences result in altered expression of cytokines upon stimulation with different TLR ligands. Together, these findings provide a valuable resource that significantly expands the knowledge of protein expression dynamics in in vitro models of macrophages which in turn has profound impact on the immune responses being studied.
2021-09-08 | PXD015872 | Pride
Project description:Transcriptome analysis of the human monocytic cell line THP1 (ATCC TIB-202) treated or not with phorbol myristate acetate (PMA) +/- lipopolysaccharides-lipopolysaccharides binding protein (LPS-LBP)
2018-07-17 | GSE117162 | GEO
Project description:Microvesicles (MV) are small membrane-bound particles comprised of exosomes and various sized extracellular vesicles. These are released by a number of cell types. Microvesicles have a variety of cellular functions from communication to mediating growth and differentiation. Microvesicles contain proteins and nucleic acids. Previously, we showed that plasma microvesicles contain microRNAs (miRNAs). Based on our previous report, the majority of peripheral blood microvesicles are derived from platelets while mononuclear phagocytes, including macrophages, are the second most abundant population. Here, we characterized macrophage-derived microvesicles and whether they influenced the differentiation of naM-CM-/ve monocytes. We also identified the miRNA content of the macrophage-derived microvesicles. We found that RNA molecules contained in the macrophage-derived microvesicles were transported to target cells, including monocytes, endothelial cells, epithelial cells and fibroblasts. Furthermore, we found that miR-223 was transported to target cells and was functionally active. Based on our observations, we hypothesize that microvesicles bind to and activate target cells. Furthermore, we find that microvesicles induce the differentiation of macrophages. Thus, defining key components of this response may identify novel targets to regulate host defense and inflammation. We used GeneChip microarrays to examine changes in gene expression induced by MV in primary monocyte-derived macrophages (MDM) and in THP1 cells, and compare this to cells treated with GM-CSF and PMA, respectively. All experiments were done in triplicates. Primary monocytes were collected from buffy coats (BC). The freshly isolated monocytes from three donors (Mono1-3) were either treated with GM-CSF or subjected to RNA isolation. Following treatment, MVs were isolated from the GM-CSF-treated macrophage cultures. RNA was isolated from the remaining cells for profiling (GM1-3). The isolated MVs were then used to treat new BC monocytes for 24 h (BC-GMCSF-MV24). A fraction of the new BC monocytes was subjected to RNA extraction for profiling (BC1-3). For THP1 cells, they were treated with either DMSO or PMA to produce MVs. The MVs were collected and the remaining cells lyzed for RNA extraction and profiling (DMSO1-3 and PMA1-3). The collected MVs from the DMSO or PMA-treated THP1 cells were incubated with new THP1 for 24 h and designated DMSO-MV24 or PMA-MV24. We had a total of 24 samples.
2013-03-08 | E-GEOD-41889 | biostudies-arrayexpress
Project description:Macrophages are key cell types of the innate immune system regulating host defense, inflammation, tissue homeostasis and cancer. Within this functional spectrum diverse and often opposing phenotypes are displayed which are dictated by environmental clues and depend on highly plastic transcriptional programs. Among these the ‘classical’ (M1) and ‘alternative’ (M2) macrophage polarization phenotypes are the best characterized. Understanding macrophage polarization in humans may reveal novel therapeutic intervention possibilities for chronic inflammation, wound healing and cancer. Systematic loss of function screening in human primary macrophages is limited due to lack of robust gene delivery methods and limited sample availability. To overcome these hurdles we developed cell-autonomous assays using the THP-1 cell line allowing genetic screens for human macrophage phenotypes. To confirm the relevance of the THP1-based system we performed microarray studies on THP1 cells and primary human cells subjected to various conditions. THP1 cells were treated with PMA (phorbol 12-myristate 13-acetate) to derive macrophages which were then cultured 1, 3 or 6 days with different stimuli.
2017-08-25 | E-MTAB-5917 | biostudies-arrayexpress
Project description:ISOLATION OF AGAROSE DIGESTERS FROM AGAROSE ENRICHED EARTHWORM GUT
| PRJEB27741 | ENA
Project description:ra16-04_3wd40 - stem transcriptome in a triple wd40 mutant. - Are cell wall genes affected in a triple WD40 mutant (LWD1xLWD2xTTG1)? - Not specified
2018-09-17 | GSE119889 | GEO
Project description:The NPL encodes an enzyme that regulates cellular concentrations of sialic acid (N-acetyl-neuraminic acid) by mediating the reversible conversion of sialic acid into N-acetylmannosamine and pyruvate. As functions of NPL gene in obesity and gluco-metabolic phenotypes is not studied, we knocked down NPL in THP1 cells to understand its roles in modulating the human monocyte-macrophage expression network. Transduction of THP1 cells by NPL-specific lentiviral shRNA stably knocked down its expression at baseline monocytes and in the PMA-induced macrophage state. Global transcriptomic analysis by RNA-seq validated the downregulation of NPL, and comparison of NPL knockdown cells with control-shRNA treated cells further identified 1,183 differentially expressed genes (DEGs). Genes downregulated by the NPL knockdown were significantly enriched for cytokine production, while upregulated genes were enriched for extracellular structure organization. We further compared the effect of macrophage conditioned media (MCM) derived from NPL-shRNA and control-shRNA-expressing THP1 macrophages on SGBS adipocytes. Compared to unconditioned media, MCM derived from either of the THP1 cells differentially regulated key genes involved in adipocyte function and IR. The expression of ADIPOQ, peroxisome proliferator activated receptor gamma (PPARG), and glucose transporter-4 (SLC2A4/GLUT4) was downregulated, while expression of LEP was upregulated in SGBS cells treated with MCM starting from day 4 of the in vitro differentiation. However, PPARG was less repressed and LEP was less activated when SGBS adipocytes were treated on day 4 differentiation with MCM from NPL-shRNA-THP1 cells, suggesting knockdown of NPL partially ameliorated macrophage-induced inflammation of adipocytes.
2022-02-21 | GSE196888 | GEO
Project description:We had evidence that TRIM5 regulates signal transduction, specifically NFkB and MAPK pathways. To test the role of endogenous TRIM5 we used the myelomonocytic leukemia cell line THP1. These cells were transduced with a lentiviral vector that delivers a miRNA engineered to knockdown TRIM5. The vector also encoded a puromycin-resistance cassette and transduced cells were selected in poold with puromycin. As a control, cells were transduced with a vector targeting luciferase instead of TRIM5. After selection in puromycin, the TRIM5 KD and Luciferase KD cells were differentiated into macrophages by treatment with PMA. 3 days later, RNA was harvested for analysis.
2010-11-02 | E-GEOD-25041 | biostudies-arrayexpress
Project description:Susceptibility to Crohn's disease, a complex inflammatory disease involving the small intestine, is controlled by over 30 loci. One Crohn's disease risk allele is in ATG16L1, a gene homologous to the essential yeast autophagy gene ATG16 (ref. 2). It is not known how ATG16L1 or autophagy contributes to intestinal biology or Crohn's disease pathogenesis. To address these questions, we generated and characterized mice that are hypomorphic for ATG16L1 protein expression, and validated conclusions on the basis of studies in these mice by analysing intestinal tissues that we collected from Crohn's disease patients carrying the Crohn's disease risk allele of ATG16L1. Here we show that ATG16L1 is a bona fide autophagy protein. Within the ileal epithelium, both ATG16L1 and a second essential autophagy protein ATG5 are selectively important for the biology of the Paneth cell, a specialized epithelial cell that functions in part by secretion of granule contents containing antimicrobial peptides and other proteins that alter the intestinal environment. ATG16L1- and ATG5-deficient Paneth cells exhibited notable abnormalities in the granule exocytosis pathway. In addition, transcriptional analysis revealed an unexpected gain of function specific to ATG16L1-deficient Paneth cells including increased expression of genes involved in peroxisome proliferator-activated receptor (PPAR) signalling and lipid metabolism, of acute phase reactants and of two adipocytokines, leptin and adiponectin, known to directly influence intestinal injury responses. Importantly, Crohn's disease patients homozygous for the ATG16L1 Crohn's disease risk allele displayed Paneth cell granule abnormalities similar to those observed in autophagy-protein-deficient mice and expressed increased levels of leptin protein. Thus, ATG16L1, and probably the process of autophagy, have a role within the intestinal epithelium of mice and Crohn's disease patients by selective effects on the cell biology and specialized regulatory properties of Paneth cells.
2008-11-08 | GSE13512 | GEO
Project description:Susceptibility to Crohn's disease, a complex inflammatory disease involving the small intestine, is controlled by over 30 loci. One Crohn's disease risk allele is in ATG16L1, a gene homologous to the essential yeast autophagy gene ATG16 (ref. 2). It is not known how ATG16L1 or autophagy contributes to intestinal biology or Crohn's disease pathogenesis. To address these questions, we generated and characterized mice that are hypomorphic for ATG16L1 protein expression, and validated conclusions on the basis of studies in these mice by analysing intestinal tissues that we collected from Crohn's disease patients carrying the Crohn's disease risk allele of ATG16L1. Here we show that ATG16L1 is a bona fide autophagy protein. Within the ileal epithelium, both ATG16L1 and a second essential autophagy protein ATG5 are selectively important for the biology of the Paneth cell, a specialized epithelial cell that functions in part by secretion of granule contents containing antimicrobial peptides and other proteins that alter the intestinal environment. ATG16L1- and ATG5-deficient Paneth cells exhibited notable abnormalities in the granule exocytosis pathway. In addition, transcriptional analysis revealed an unexpected gain of function specific to ATG16L1-deficient Paneth cells including increased expression of genes involved in peroxisome proliferator-activated receptor (PPAR) signalling and lipid metabolism, of acute phase reactants and of two adipocytokines, leptin and adiponectin, known to directly influence intestinal injury responses. Importantly, Crohn's disease patients homozygous for the ATG16L1 Crohn's disease risk allele displayed Paneth cell granule abnormalities similar to those observed in autophagy-protein-deficient mice and expressed increased levels of leptin protein. Thus, ATG16L1, and probably the process of autophagy, have a role within the intestinal epithelium of mice and Crohn's disease patients by selective effects on the cell biology and specialized regulatory properties of Paneth cells. Experiment Overall Design: 4 Samples: 2 replicates of Atg16-hypomorph Paneth cells and 2 replicates of Wildtype Paneth cells.
2008-11-15 | E-GEOD-13512 | biostudies-arrayexpress