Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Identification of SORL1 Binding Partners via Immunoprecipitation-Mass Spectrometry in THP-1 Cells.

ABSTRACT: SORL1 (Sortilin-Related Receptor 1) is a key player in endosomal trafficking and has been implicated in neurodegenerative disorders. To identify SORL1 binding partners, we performed immunoprecipitation (IP) of SORL1, followed by mass spectrometry-based proteomic analysis. THP-1 cell lysates were used as the source material for immunoprecipitation, and IgG controls were included to filter out non-specific interactions. The resulting datasets provide insights into SORL1-associated protein complexes, offering potential targets for further functional studies.

INSTRUMENT(S):

ORGANISM(S): Homo Sapiens (human)

SUBMITTER: Rajesh Soni

LAB HEAD: Falak Sher

PROVIDER: PXD061057 | Pride | 2026-04-13

REPOSITORIES: Pride

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	FS1156.zip	Other
	FS1156_timstofPro_PASEF_Maxqaunt_ProteinGroups.xlsx	Xlsx
	IP_ProteinGroups.xlsx	Xlsx

Items per page:

1 - 3 of 3

Publications

Alzheimer's disease risk protein SorLA regulates ER homeostasis and lipid metabolism in human microglia, with conserved effects in neurons.

Haq Imdadul I Ngo Jason C JC Roy Nainika N Lee Emily E Choudhury Muniyat A MA Soni Rajesh K RK Teich Andrew F AF Mayeux Richard P RP De Jager Philip L PL He Ye Y Wu Xuebing X Bennett David A DA Olah Marta M Sher Falak F

Acta neuropathologica 20260406 1

Microglial dysfunction is a hallmark of Alzheimer's disease (AD), yet the molecular mechanisms driving these impairments remain poorly defined. Genetic studies implicate several AD-associated genes in regulating microglial activity, including SORL1, which encodes the sorting receptor SorLA. Although SorLA is highly expressed in microglia, its functional role in cellular homeostasis has remained unclear. Here, we investigated SorLA function using human brain tissue, primary microglia from rapid a ...[more]

PMID: 41942750

Similar Datasets

Genome-wide maps of H3K4me1 in Mycobacterium tuberculosis H37Rv-infected macrophages

Project description:Host macrophage transcriptional responses to intracellular pathogens remain poorly characterized. We screened transcriptional enhancers engaged in response to M. tuberculosis (Mtb) infection by ChIPseq analysis of histone H3 lysine 4 monomethylation (H3K4me1). De novo monomethylation during infection was associated with genes implicated in host defense and apoptosis. These regions were enriched for binding sites for ETS transcription factor family members and response elements for nuclear receptors, including liver X receptors (LXRs) and peroxisomal proliferator activated receptors (PPARs), many of which were encompassed by transposable elements. LXRa expression was strongly induced by infection, whereas that of PPARs was unaffected. LXR DNA binding and NCoR corepressor recruitment increased proportionately in infected cells but coactivator association was unchanged, consistent with a lack of induction of endogenous agonists. However, treatment of infected cells with LXR agonist T0901317 strongly increased coactivator recruitment and induced a gene expression program characterized by enhanced innate immune signaling and lipid metabolism. Remarkably, T0901317 treatment selectively induced apoptosis in infected macrophages, and was accompanied by Mtb death, reducing mycobacterial burden 18-fold relative to vehicle 5d after infection. These studies define macrophage transcriptional responses to Mtb infection, and suggest that tissue-specific LXRa agonists may be efficacious in clinical management of tuberculosis.

2015-10-15 | E-MTAB-3192 | biostudies-arrayexpress

Differential gene expression in human THP-1 monocytes expressing the RdRPâ??cat mutant transgene compared to THP-1 empty vector control cells

Project description:Previously, we reported that mice made transgenic for a picornaviral RdRP â?? the 3Dpol protein of Theilerâ??s murine encephalomyelitis virus (TMEV) â?? suppress infection by diverse viruses. Using mouse genetic studies, we determined that uninfected RdRP transgenic mice inherently induce an arsenel of prominent antiviral effectors and that this phenotype is MDA5-, MAVS- and IFNÎ±Î²R-dependent. To determine the mechanism underlying MDA5 activation and induction of constitutive antiviral signaling by the picornaviral RdRP, we constructed mutant RdRP transgenes. First, we introduced pervasive, coding-neutral point mutations into the RdRP cDNA to maximally disrupt primary and secondary RNA structure (RdRPâ??rna). Another mutant, RdRPâ??cat, lacks catalytic activity due to alanine substitution of the key catalytic center triad aspartate residues (D233, D328, and D329), but is otherwise intact at the nucleotide and amino acid levels. The WT, RdRPâ??rna, and RdRPâ??cat versions of the RdRP transgenes were transduced with lentiviral vectors into human THP-1 monocytes, with RdRP mRNA transcription controlled by the Spleen Focus Forming Virus (SFFV) promoter. In parallel a control cell line transduced with a vector lacking any RdRP transgene (null THP-1) was generated. RdRP cDNAs and a GFP-puromycin fusion protein selection marker were cloned into transfer constructs containing HIV LTRs, a small portion of gag, an RRE, and a cPPT. Transfer constructs were transfected into HEK 293T cells along with packaging construct Râ??8.9 and envelope pseudotyping construct expressing VSV-G. RT-normalized amounts of vector were used to transduce THP-1 cells. After selection in puromycin, whole-genome expression profiling was performed on total RNA extracted from the different THP-1 lines.

2015-11-08 | E-GEOD-62754 | biostudies-arrayexpress

Differential gene expression in human THP-1 monocytes expressing the RdRP transgene (WT version) compared to THP-1 empty vector control cells

Project description:Previously, we reported that mice made transgenic for a picornaviral RdRP â the 3Dpol protein of Theilerâs murine encephalomyelitis virus (TMEV) â suppress infection by diverse viruses. Using mouse genetic studies, we determined that uninfected RdRP transgenic mice inherently induce an arsenel of prominent antiviral effectors and that this phenotype is MDA5-, MAVS- and IFNÎ±Î²R-dependent. To determine the mechanism underlying MDA5 activation and induction of constitutive antiviral signaling by the picornaviral RdRP, we constructed mutant RdRP transgenes. First, we introduced pervasive, coding-neutral point mutations into the RdRP cDNA to maximally disrupt primary and secondary RNA structure (RdRPârna). Another mutant, RdRPâcat, lacks catalytic activity due to alanine substitution of the key catalytic center triad aspartate residues (D233, D328, and D329), but is otherwise intact at the nucleotide and amino acid levels. The WT, RdRPârna, and RdRPâcat versions of the RdRP transgenes were transduced with lentiviral vectors into human THP-1 monocytes, with RdRP mRNA transcription controlled by the Spleen Focus Forming Virus (SFFV) promoter. In parallel a control cell line transduced with a vector lacking any RdRP transgene (null THP-1) was generated. RdRP cDNAs and a GFP-puromycin fusion protein selection marker were cloned into transfer constructs containing HIV LTRs, a small portion of gag, an RRE, and a cPPT. Transfer constructs were transfected into HEK 293T cells along with packaging construct Râ8.9 and envelope pseudotyping construct expressing VSV-G. RT-normalized amounts of vector were used to transduce THP-1 cells. After selection in puromycin, whole-genome expression profiling was performed on total RNA extracted from the different THP-1 lines.

2015-11-08 | E-GEOD-62753 | biostudies-arrayexpress

Differential gene expression in human THP-1 monocytes expressing the RdRPârna mutant transgene compared to THP-1 empty vector control cells

2015-11-08 | E-GEOD-62755 | biostudies-arrayexpress

RNA-seq of LPS- and palmitate-stimulated THP-1 macrophages

Project description:In this study we performed an RNA-seq analysis of lipopolysaccharide (LPS) and palmitate (PAL) stimulated THP-1 macrophages to study the gene regulatory mechanisms underlying classical innnate immune response and chronical inflammatory response caused by metabolic stress. This analysis was done to complement single-cell transcriptome analyses of the same cell models.

2019-05-15 | E-MTAB-6064 | biostudies-arrayexpress

Single-cell RNA-seq analysis of LPS- and palmitate-stimulated THP-1 macrophages

Project description:In this study we performed single-cell transcriptome analysis of THP-1 macrophages, stimulated with high levels of free fatty acids (palmitate, PAL) typical for obese adipose tissue microenvironment or lipopolysaccharide (LPS), representing a classical stimulus activating innate immune response. Analysing full transcriptomes of individual cells, we were able to distinguish 3 macrophage transcriptional states and decipher gene regulatory pathways underlying macrophage state identity in both stimulations.

2019-05-15 | E-MTAB-6075 | biostudies-arrayexpress

Arabidopsis thaliana NusG IP-LCMS

Project description:We performed immunoprecipitation analysis with leaves from 35S::NusG:MYC transgenic lines throung the MYCantibody, and the product was subjected to LC-MS analysis.

2022-06-24 | PXD028377 | Pride

RNA-seq analysis of the effect of BSA and NaOH added to standard culturing medium on THP-1 macrophages

Project description:The data is supplementary to the RNA-seq analysis of LPS and palmitate stimulation of THP-1 macrophages (E-MTAB-6064), where palmitate for the cell treatment was dissolved in sodium hydroxide and coupled with BSA at a molar ratio 7.5:1. Here we stimulated THP-1 macrophages with the corresponding concentration of BSA (4%) and NaOH (0.4 mM) in the presence of 10 nM phorbol 12-myristate 13-acetate (PMA) for 24 hours added to the standard RPMI 1640 medium with 10% fetal bovine serum (FBS) to estimate the effects and compared them with unstimulated THP-1 macrophages cultured in RPMI 1640 medium with 10% FBS and 10nM PMA.

2019-05-17 | E-MTAB-6439 | biostudies-arrayexpress

Functional and cellular constraints that shaped the PPARg binding landscape in human and mouse macrophages: human expression

Project description:Genome-wide comparisons of transcription factor binding sites in different species allow for a direct evaluation of the evolutionary constraints that shape transcription factor binding landscapes. To gain insights into the evolution of the PPARg-dependent transcriptional network we obtained binding data for PPARg, RXR and PU.1 in human macrophages and compared the profiles to matching data from mouse macrophages. We found that PPARg binding was highly divergent and only 5% of the PPARg bound regions were occupied in both species. Despite the low conservation of PPARg binding sites, conserved PPARg target genes contribute more than 30% to the functional target genes identified in human macrophages. In addition conserved target genes are strongly enriched for lipid metabolic functions. We detected the lineage-specification factor PU.1 at the majority of human PPARg binding sites. This confirmed the juxtaposed binding configuration found in mouse macrophages and demonstrated the preservation of tissue-specific adjacent PPARg-Pu.1 binding in the absence of individual binding site conservation. Finally, based on this of PPARg and PU.1 binding between human and mouse we suggest a mechanism by which PU.1 facilitates PPARg binding site turnover in macrophages. Comparison of RNAs level in Rosiglitazone (RSG) and vehicle (DMSO) treated PMA differentiated THP-1 cells over a timecourse from 0.5h to 12h

2011-12-01 | E-GEOD-25137 | biostudies-arrayexpress

Overexpression of miR-155 enhances B-cell lymphoma growth by targeting TBRG1

Project description:MYC regulates the expression of multiple microRNA (miRNA) genes and defines the Burkitt lymphoma (BL) miRNA signature. Here, we investigate the role of the MYC-regulated miRNAs by gain- and loss-of-function analysis. Overexpression of 5 miRNAs that were significantly downregulated by MYC resulted in strong (miR-150, miR-26a, miR-26b) and mild (miR-29a, let-7a) impaired cell growth. Overexpression of miR-155 increased proliferation of BL cells. By RNA immunoprecipitation of Argonaute 2 in BL cells with and without miR-155 we identified 54 miR-155 target genes. Using an shRNA approach we identified TBRG1 (NIAM1) as a miR-155 target gene that copied the miR-155-induced phenotype upon its inhibition. Analysis of TBRG1 protein expression and miR-155 levels in primary cases of B-cell lymphoma revealed that miR-155 levels are significantly lower in TBRG1 positive cases suggesting that TBRG1 is also regulated by miR-155 in primary B-cell lymphoma. Our data demonstrate that overexpression of individual MYC-repressed miRNAs has a strong suppressive effect on BL cell growth, whereas overexpression of miR-155 enhances B-cell lymphoma growth by targeting the tumor suppressor gene TBRG1. Gene expression profile was performed in ST486 Burkitt lymphoma cell line in 4 samples: ST486 EV (empty MXW-PGK-IRES-GFP vector) total cell lysate, ST486 EV Ago2-IP, ST486 miR-155 (ST486 with ectopic miR-155) total cell lysate, ST486 miR-155 Ago2-IP.

2015-02-20 | E-GEOD-64484 | biostudies-arrayexpress