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- Studies (6)
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Organisms: Mus musculus, Rattus norvegicus, Homo sapiens, Macaca mulatta, Sus scrofa
Submitter: Rainer Malik
Studies: A genome-wide in vivo CRISPR screen identifies essential regulators of T..., Correlation spatial transcriptomics/EM, Direct neuronal reprogramming of NDUFS4 patient cells identifies the unf..., Early adaptive immune activation detected in monozygotic twins with prod..., Histone Deacetylase 9 Activates IKK to Regulate Atherosclerotic Plaque V..., Innate immune memory after brain injury drives inflammatory cardiac dysf..., Microglia in white matter aging, Myelin degeneration in leucodystrophies, Oligodendrocytes in AD models, Oligodendrocytes in white matter aging, Phagocyte-mediated synapse removal in cortical neuroinflammation is prom..., Skin and gut imprinted helper T cell subsets exhibit distinct functional..., T cells modulate the microglial response to brain ischemia
Assays: Bulk RNA-seq, Expression profiling by high throughput sequencing, Expression profiling by high throughput sequencing, Expression profiling by high throughput sequencing, Expression profiling by high throughput sequencing, Expression profiling by high throughput sequencing, Expression profiling by high throughput sequencing, Expression profiling by high throughput sequencing, Expression profiling by high throughput sequencing, Expression profiling by high throughput sequencing, Expression profiling by high throughput sequencing, Single cell RNA sequencing experiment, scRNA-seq 5 day, scRNA-seq day 20
Snapshots: No snapshots
Remyelination can occur naturally in demyelinating lesions, but often fails in human demyelinating diseases such as multiple sclerosis (MS). The function of the innate immune system is essential for the regenerative response, but how exactly microglia and macrophages clear myelin debris after injury and tailor a specific regenerative response is unclear. Here, we asked whether pro-inflammatory microglial/macrophage activation is required for this process. We established a novel toxin-based spinal ...
Snapshots: No snapshots
To understand how cells communicate with each other, it is essential to define the cellular secretome, a collection of proteins including soluble secreted, unconventionally secreted and proteolytically-shed proteins. Quantitative methodologies to decipher the secretome are challenging, due to the requirement of large cell numbers and abundant serum proteins that interfere with the detection of low-abundant cellular secretome proteins. Here, we miniaturized secretome analysis by developing the ...
Snapshots: No snapshots
Niemann-Pick type C (NPC) disease is a rare neurodegenerative disorder mainly caused by autosomal recessive mutations in Npc1 which result in abnormal late endosomal/lysosomal lipid storage. Although microgliosis is one of the prominent pathological features, consequences of NPC1 loss on microglial function and disease outcome remain largely unknown. Here, we provide an in-depth characterization of microglial proteomic signatures and phenotypes in an NPC1-deficient (Npc1-/-) murine model. We ...
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Description
Proteolytic ectodomain shedding of membrane proteins is a fundamental mechanism to control the communication between cells and their environment. A key protease for membrane protein shedding is ADAM17, which requires a non-proteolytic subunit, either inactive Rhomboid 1 (iRhom1) or iRhom2 for its activity. While iRhom1 and iRhom2 are coexpressed in most tissues and appear to have largely redundant functions, the brain is an organ with predominant expression of iRhom1. Yet, little is ...
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After demyelinating injury of the central nervous system, resolution of the mounting acute innate inflammation is crucial for the initiation of a regenerative response. To identify factors in lesion recovery after demyelination injury, we used a toxin-induced model, in which a single dose of lysolecithin is injected into the corpus callosum to induce a focal demyelinating lesion. Afterwards, we investigated the proteome of demyelinating lesions at different time points post injection (dpi) in a ...
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Corpus callosum dissections were lysed in 300 µL STET lysis buffer (1% (v/v) Triton X-100, 150 mM NaCl, 2 mM EDTA, 50 mM TrisHCl pH 7.5) with a Precellys Evolution homogenizer (Bertin, Germany) using 0.5 mL soft tissue homogenization kit CK14 applying two cycles of 30 s with a speed of 6500rpm. After 15 min incubation on ice, samples were centrifuged at 16,000×g for 15 min to remove undissolved material and cell debris. The supernatant was transferred to a fresh protein lobind tube (Eppendorf, ...
Submitter: Rainer Malik
Assay type: Experimental Assay Type
Technology type: Technology Type
Investigation: Proteomics
Organisms: Mus musculus
SOPs: No SOPs
Data files: Proteomic and lipidomic profiling of demyelinat...
Snapshots: No snapshots
Secretome analysis of primary neuronal cultures was performed using the high-performance secretome protein enrichment with click sugars" (hiSPECS) method, described in detail previously (Tüshaus et al, 2020). In brief, neurons were cultured for 48 h (DIV 5-7) in the presence of 50 µM ManNAz (#88904, ThermoFisher), cultivation media was filtered through 0.45 µm spin columns (Sigma-Aldrich, CLS8163). Glycoproteins were enriched using ConA agarose beads (Sigma, C7555) and clicked to magnetic DBCO ...
Submitter: Rainer Malik
Assay type: Experimental Assay Type
Technology type: Technology Type
Investigation: Proteomics
Organisms: Mus musculus
SOPs: No SOPs
Data files: The pseudoprotease iRhom1 controls ectodomain s...
Snapshots: No snapshots
Blood samples (20 ml) from clinically affected homozygous Npc1 mutation carriers and healthy donors were collected. Negative selection of peripheral blood monocyte-derived macrophages was performed by incubating full blood for 20 min at RT with RosetteSep Human Monocyte Enrichment Cocktail (StemCell Technologies). An equal volume of washing buffer (D-PBS/2% FBS/1 mM EDTA) was added to each sample and layer of macrophages was separated from red blood cells and plasma by centrifugation on a Ficoll ...
Submitter: Rainer Malik
Assay type: Experimental Assay Type
Technology type: Technology Type
Investigation: Proteomics
Organisms: Homo sapiens, Mus musculus
SOPs: No SOPs
Data files: Proteomic analysis of monocyte derived macropha..., Proteomic signature of NPC1 KO microglia, Proteomic signature of NPC1 KO microglia from c...
Snapshots: No snapshots
After washing the primary cells with 1x PBS, cell-type specific growth media containing serum supplements with 50 µM of ManNAz (Thermo) was added for 48h. Afterwards, conditioned media was collected and filtered through Spin-X 0.45 µM cellulose acetate centrifuge tube filter (#8163, Costar) and stored at -20°C in protein Lobind tubes until further usage. Glycoprotein enrichment was performed using 60 µL Concanavalin A (ConA) bead slurry per sample (Sigma). ConA beads were washed twice with 1 mL ...
Submitter: Rainer Malik
Assay type: Experimental Assay Type
Technology type: Technology Type
Investigation: Proteomics
Organisms: Mus musculus
SOPs: No SOPs
Data files: Quantitative secretome analysis using improved ..., Secretome Analysis of hippocampal and cortical ...
Snapshots: No snapshots
Microglia isolated by MACS from WT and Myd88-/- mouse pups were seeded at a density of 1×106 cells per 60-mm dish in DMEM/FCS/L929 medium. After 2 DIV, microglia were washed with warm DMEM/pyruvate medium and treated with 20 µg/mL myelin debris (or HEPES control) in 2 mL of TIC medium for 4 h. After treatment, the cells were washed with DMEM/pyruvate medium, and incubated with 4 mL of DMEM containing 0.2% BSA for 16 h. The cells in each dish were washed with 2 mL of cold PBS on ice, and lysed ...
Submitter: Rainer Malik
Assay type: Experimental Assay Type
Technology type: Technology Type
Investigation: Proteomics
Organisms: Mus musculus
SOPs: No SOPs
Data files: Pro-inflammatory activity following demyelinati...
Snapshots: No snapshots
Remyelination can occur naturally in demyelinating lesions, but often fails in human demyelinating diseases such as multiple sclerosis (MS). The function of the innate immune system is essential for the regenerative response, but how exactly microglia and macrophages clear myelin debris after injury and tailor a specific regenerative response is unclear. Here, we asked whether pro-inflammatory microglial/macrophage activation is required for this process. We established a novel toxin-based spinal ...
Creators: Rainer Malik, Stephan Müller, Stefan Lichtenthaler, Martina Fetting, Mikael Simons
Submitter: Rainer Malik
Investigations: Proteomics
Studies: Pro-inflammatory activation following demyelina...
Assays: Shotgun proteomics
To understand how cells communicate with each other, it is essential to define the cellular secretome, a collection of proteins including soluble secreted, unconventionally secreted and proteolytically-shed proteins. Quantitative methodologies to decipher the secretome are challenging, due to the requirement of large cell numbers and abundant serum proteins that interfere with the detection of low-abundant cellular secretome proteins. Here, we have use the highe perfomance ...
Creators: Rainer Malik, Stephan Müller, Mikael Simons, Stefan Lichtenthaler
Submitter: Rainer Malik
Investigations: Proteomics
Studies: An optimized quantitative proteomics method est...
Assays: Shotgun proteomics
To understand how cells communicate with each other, it is essential to define the cellular secretome, a collection of proteins including soluble secreted, unconventionally secreted and proteolytically-shed proteins. Quantitative methodologies to decipher the secretome are challenging, due to the requirement of large cell numbers and abundant serum proteins that interfere with the detection of low-abundant cellular secretome proteins. Here, we miniaturized secretome analysis by developing the ...
Creators: Rainer Malik, Stephan Müller, Stefan Lichtenthaler, Mikael Simons
Submitter: Rainer Malik
Investigations: Proteomics
Studies: An optimized quantitative proteomics method est...
Assays: Shotgun proteomics
Niemann-Pick type C disease is a rare neurodegenerative disorder mainly caused by mutations in Npc1, resulting in abnormal late endosomal/lysosomal lipid storage. Although microgliosis is a prominent pathological feature, direct consequences of NPC1 loss on microglial function remain uncharacterized. Previously, we have characterized microglial proteome alterations in the NPC1 KO mouse model (PXD019447). In order to investigate similar changes in humans, we have cultured monocyte derived macrophages ...
Creators: Rainer Malik, Stefan Lichtenthaler, Stephan Müller, Mikael Simons, Martina Fetting
Submitter: Rainer Malik
Investigations: Proteomics
Studies: Loss of NPC1 enhances phagocytic uptake and imp...
Assays: Shotgun proteomics
Niemann-Pick type C (NPC) disease is a rare neurodegenerative disorder mainly caused by autosomal recessive mutations in Npc1 which result in abnormal late endosomal/lysosomal lipid storage. Although microgliosis is one of the prominent pathological features, consequences of NPC1 loss on microglial function and disease outcome remain largely unknown. Here, we provide an in-depth characterization of microglial proteomic signatures and phenotypes in an NPC1-deficient (Npc1-/-) murine model. We ...
Creators: Rainer Malik, Stephan Müller, Stefan Lichtenthaler, Martina Fetting, Mikael Simons
Submitter: Rainer Malik
Investigations: Proteomics
Studies: Loss of NPC1 enhances phagocytic uptake and imp...
Assays: Shotgun proteomics
Abstract (Expand)
Authors: J. Groh, T. Abdelwahab, Y. Kattimani, M. Horner, S. Loserth, V. Gudi, R. Adalbert, F. Imdahl, A. E. Saliba, M. Coleman, M. Stangel, M. Simons, R. Martini
Date Published: 30th Oct 2023
Publication Type: Journal
PubMed ID: 37903797
Citation: Nat Commun. 2023 Oct 30;14(1):6911. doi: 10.1038/s41467-023-42570-2.
Abstract (Expand)
Authors: P. Androvic, M. Schifferer, K. Perez Anderson, L. Cantuti-Castelvetri, H. Jiang, H. Ji, L. Liu, G. Gouna, S. A. Berghoff, S. Besson-Girard, J. Knoferle, M. Simons, O. Gokce
Date Published: 11th Jul 2023
Publication Type: Journal
PubMed ID: 37433806
Citation: Nat Commun. 2023 Jul 11;14(1):4115. doi: 10.1038/s41467-023-39447-9.
Abstract (Expand)
Authors: T. Kaya, N. Mattugini, L. Liu, H. Ji, L. Cantuti-Castelvetri, J. Wu, M. Schifferer, J. Groh, R. Martini, S. Besson-Girard, S. Kaji, A. Liesz, O. Gokce, M. Simons
Date Published: 26th Oct 2022
Publication Type: Journal
PubMed ID: 36280798
Citation: Nat Neurosci. 2022 Nov;25(11):1446-1457. doi: 10.1038/s41593-022-01183-6. Epub 2022 Oct 24.
Abstract (Expand)
Authors: H. Penkert, A. Bertrand, V. Tiwari, S. Breimann, S. A. Muller, P. M. Jordan, M. J. Gerl, C. Klose, L. Cantuti-Castelvetri, M. Bosch-Queralt, I. Levental, S. F. Lichtenthaler, O. Werz, M. Simons
Date Published: 26th Oct 2021
Publication Type: Journal
PubMed ID: 34706241
Citation: Cell Rep. 2021 Oct 26;37(4):109898. doi: 10.1016/j.celrep.2021.109898.
Abstract (Expand)
Authors: J. Tushaus, S. A. Muller, J. Shrouder, M. Arends, M. Simons, N. Plesnila, C. P. Blobel, S. F. Lichtenthaler
Date Published: 6th Oct 2021
Publication Type: Journal
PubMed ID: 34613632
Citation: FASEB J. 2021 Nov;35(11):e21962. doi: 10.1096/fj.202100936R.