magnetically controlled reactor simulation model Search Results


5 site magnet scanner channels  (Philips Healthcare)
90
Philips Healthcare 5 site magnet scanner channels
5 Site Magnet Scanner Channels, supplied by Philips Healthcare, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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simulated magnetic gradient field  (COMSOL Inc)
90
COMSOL Inc simulated magnetic gradient field
Simulated Magnetic Gradient Field, supplied by COMSOL Inc, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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temperature-controlled time domain 1h nmr  (Molecular Dynamics Inc)
90
Molecular Dynamics Inc temperature-controlled time domain 1h nmr
Temperature Controlled Time Domain 1h Nmr, supplied by Molecular Dynamics Inc, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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cdc biofilm reactors  (BioSurface Technologies Corporation)
90
BioSurface Technologies Corporation cdc biofilm reactors
Cdc Biofilm Reactors, supplied by BioSurface Technologies Corporation, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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simon wilkinson climp63 ckap4 proteintech  (Proteintech)
94
Proteintech simon wilkinson climp63 ckap4 proteintech
Fig. 5 | FAM134B-mediated ER-phagy requires ARL6IP1 in mice and humans. a, Rational of the mCherry–GFP–FAM134B reporter. b,c, ARL6IP1 loss-of-function compromises ER-phagy. Arl6ip1 WT and KO MEFs (b) or fibroblasts from the patient and the healthy individual (control) (c) were transfected with mCherry– GFP–FAM134B and stained for LC3B. Quantifications of LC3B+mCherry+GFP+ puncta and LC3B+mCherry+GFP– puncta per cell area suggest that the formation of autophagosomes (3 experiments with 10 cells per genotype each; two-sided Mann–Whitney U-test; MEFs, P = 0.0479; human cells, P = 0.0005) and autolysosomes (3 experiments with 10 cells per genotype each; two-sided Mann–Whitney U-test; MEFs, P = 0.0307; human cells, P = 0.0096) is impaired. d,e, ARL6IP1 loss-of-function enlarges ER sheets. Arl6ip1 WT and KO MEFs (d) or fibroblasts from the patient and healthy individual (e) were stained for the ER sheet protein <t>CLIMP63</t> and the relative CLIMP63+ area per cell calculated (3 experiments with 15 cells per genotype; two-sided Mann–Whitney U-test; MEFs, P = 0.0001; human cells, P = 0.0001). f,g, TEM images showed increased numbers of small highly curved ER protrusions emanating from ER sheets in
Simon Wilkinson Climp63 Ckap4 Proteintech, supplied by Proteintech, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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peristaltic pumps (120s  (Watson-Marlow)
90
Watson-Marlow peristaltic pumps (120s
Fig. 5 | FAM134B-mediated ER-phagy requires ARL6IP1 in mice and humans. a, Rational of the mCherry–GFP–FAM134B reporter. b,c, ARL6IP1 loss-of-function compromises ER-phagy. Arl6ip1 WT and KO MEFs (b) or fibroblasts from the patient and the healthy individual (control) (c) were transfected with mCherry– GFP–FAM134B and stained for LC3B. Quantifications of LC3B+mCherry+GFP+ puncta and LC3B+mCherry+GFP– puncta per cell area suggest that the formation of autophagosomes (3 experiments with 10 cells per genotype each; two-sided Mann–Whitney U-test; MEFs, P = 0.0479; human cells, P = 0.0005) and autolysosomes (3 experiments with 10 cells per genotype each; two-sided Mann–Whitney U-test; MEFs, P = 0.0307; human cells, P = 0.0096) is impaired. d,e, ARL6IP1 loss-of-function enlarges ER sheets. Arl6ip1 WT and KO MEFs (d) or fibroblasts from the patient and healthy individual (e) were stained for the ER sheet protein <t>CLIMP63</t> and the relative CLIMP63+ area per cell calculated (3 experiments with 15 cells per genotype; two-sided Mann–Whitney U-test; MEFs, P = 0.0001; human cells, P = 0.0001). f,g, TEM images showed increased numbers of small highly curved ER protrusions emanating from ER sheets in
Peristaltic Pumps (120s, supplied by Watson-Marlow, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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single-phase magnetically controlled reactor simulation model  (MathWorks Inc)
90
MathWorks Inc single-phase magnetically controlled reactor simulation model
Fig. 5 | FAM134B-mediated ER-phagy requires ARL6IP1 in mice and humans. a, Rational of the mCherry–GFP–FAM134B reporter. b,c, ARL6IP1 loss-of-function compromises ER-phagy. Arl6ip1 WT and KO MEFs (b) or fibroblasts from the patient and the healthy individual (control) (c) were transfected with mCherry– GFP–FAM134B and stained for LC3B. Quantifications of LC3B+mCherry+GFP+ puncta and LC3B+mCherry+GFP– puncta per cell area suggest that the formation of autophagosomes (3 experiments with 10 cells per genotype each; two-sided Mann–Whitney U-test; MEFs, P = 0.0479; human cells, P = 0.0005) and autolysosomes (3 experiments with 10 cells per genotype each; two-sided Mann–Whitney U-test; MEFs, P = 0.0307; human cells, P = 0.0096) is impaired. d,e, ARL6IP1 loss-of-function enlarges ER sheets. Arl6ip1 WT and KO MEFs (d) or fibroblasts from the patient and healthy individual (e) were stained for the ER sheet protein <t>CLIMP63</t> and the relative CLIMP63+ area per cell calculated (3 experiments with 15 cells per genotype; two-sided Mann–Whitney U-test; MEFs, P = 0.0001; human cells, P = 0.0001). f,g, TEM images showed increased numbers of small highly curved ER protrusions emanating from ER sheets in
Single Phase Magnetically Controlled Reactor Simulation Model, supplied by MathWorks Inc, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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simuli k simulation platform  (MathWorks Inc)
90
MathWorks Inc simuli k simulation platform
Fig. 5 | FAM134B-mediated ER-phagy requires ARL6IP1 in mice and humans. a, Rational of the mCherry–GFP–FAM134B reporter. b,c, ARL6IP1 loss-of-function compromises ER-phagy. Arl6ip1 WT and KO MEFs (b) or fibroblasts from the patient and the healthy individual (control) (c) were transfected with mCherry– GFP–FAM134B and stained for LC3B. Quantifications of LC3B+mCherry+GFP+ puncta and LC3B+mCherry+GFP– puncta per cell area suggest that the formation of autophagosomes (3 experiments with 10 cells per genotype each; two-sided Mann–Whitney U-test; MEFs, P = 0.0479; human cells, P = 0.0005) and autolysosomes (3 experiments with 10 cells per genotype each; two-sided Mann–Whitney U-test; MEFs, P = 0.0307; human cells, P = 0.0096) is impaired. d,e, ARL6IP1 loss-of-function enlarges ER sheets. Arl6ip1 WT and KO MEFs (d) or fibroblasts from the patient and healthy individual (e) were stained for the ER sheet protein <t>CLIMP63</t> and the relative CLIMP63+ area per cell calculated (3 experiments with 15 cells per genotype; two-sided Mann–Whitney U-test; MEFs, P = 0.0001; human cells, P = 0.0001). f,g, TEM images showed increased numbers of small highly curved ER protrusions emanating from ER sheets in
Simuli K Simulation Platform, supplied by MathWorks Inc, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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simulx  (Simulations Plus Inc)
90
Simulations Plus Inc simulx
Fig. 5 | FAM134B-mediated ER-phagy requires ARL6IP1 in mice and humans. a, Rational of the mCherry–GFP–FAM134B reporter. b,c, ARL6IP1 loss-of-function compromises ER-phagy. Arl6ip1 WT and KO MEFs (b) or fibroblasts from the patient and the healthy individual (control) (c) were transfected with mCherry– GFP–FAM134B and stained for LC3B. Quantifications of LC3B+mCherry+GFP+ puncta and LC3B+mCherry+GFP– puncta per cell area suggest that the formation of autophagosomes (3 experiments with 10 cells per genotype each; two-sided Mann–Whitney U-test; MEFs, P = 0.0479; human cells, P = 0.0005) and autolysosomes (3 experiments with 10 cells per genotype each; two-sided Mann–Whitney U-test; MEFs, P = 0.0307; human cells, P = 0.0096) is impaired. d,e, ARL6IP1 loss-of-function enlarges ER sheets. Arl6ip1 WT and KO MEFs (d) or fibroblasts from the patient and healthy individual (e) were stained for the ER sheet protein <t>CLIMP63</t> and the relative CLIMP63+ area per cell calculated (3 experiments with 15 cells per genotype; two-sided Mann–Whitney U-test; MEFs, P = 0.0001; human cells, P = 0.0001). f,g, TEM images showed increased numbers of small highly curved ER protrusions emanating from ER sheets in
Simulx, supplied by Simulations Plus Inc, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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ab-initio molecular dynamics simulation  (Molecular Dynamics Inc)
90
Molecular Dynamics Inc ab-initio molecular dynamics simulation
Fig. 5 | FAM134B-mediated ER-phagy requires ARL6IP1 in mice and humans. a, Rational of the mCherry–GFP–FAM134B reporter. b,c, ARL6IP1 loss-of-function compromises ER-phagy. Arl6ip1 WT and KO MEFs (b) or fibroblasts from the patient and the healthy individual (control) (c) were transfected with mCherry– GFP–FAM134B and stained for LC3B. Quantifications of LC3B+mCherry+GFP+ puncta and LC3B+mCherry+GFP– puncta per cell area suggest that the formation of autophagosomes (3 experiments with 10 cells per genotype each; two-sided Mann–Whitney U-test; MEFs, P = 0.0479; human cells, P = 0.0005) and autolysosomes (3 experiments with 10 cells per genotype each; two-sided Mann–Whitney U-test; MEFs, P = 0.0307; human cells, P = 0.0096) is impaired. d,e, ARL6IP1 loss-of-function enlarges ER sheets. Arl6ip1 WT and KO MEFs (d) or fibroblasts from the patient and healthy individual (e) were stained for the ER sheet protein <t>CLIMP63</t> and the relative CLIMP63+ area per cell calculated (3 experiments with 15 cells per genotype; two-sided Mann–Whitney U-test; MEFs, P = 0.0001; human cells, P = 0.0001). f,g, TEM images showed increased numbers of small highly curved ER protrusions emanating from ER sheets in
Ab Initio Molecular Dynamics Simulation, supplied by Molecular Dynamics Inc, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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simulx 2021r1  (SAS institute)
90
SAS institute simulx 2021r1
Fig. 5 | FAM134B-mediated ER-phagy requires ARL6IP1 in mice and humans. a, Rational of the mCherry–GFP–FAM134B reporter. b,c, ARL6IP1 loss-of-function compromises ER-phagy. Arl6ip1 WT and KO MEFs (b) or fibroblasts from the patient and the healthy individual (control) (c) were transfected with mCherry– GFP–FAM134B and stained for LC3B. Quantifications of LC3B+mCherry+GFP+ puncta and LC3B+mCherry+GFP– puncta per cell area suggest that the formation of autophagosomes (3 experiments with 10 cells per genotype each; two-sided Mann–Whitney U-test; MEFs, P = 0.0479; human cells, P = 0.0005) and autolysosomes (3 experiments with 10 cells per genotype each; two-sided Mann–Whitney U-test; MEFs, P = 0.0307; human cells, P = 0.0096) is impaired. d,e, ARL6IP1 loss-of-function enlarges ER sheets. Arl6ip1 WT and KO MEFs (d) or fibroblasts from the patient and healthy individual (e) were stained for the ER sheet protein <t>CLIMP63</t> and the relative CLIMP63+ area per cell calculated (3 experiments with 15 cells per genotype; two-sided Mann–Whitney U-test; MEFs, P = 0.0001; human cells, P = 0.0001). f,g, TEM images showed increased numbers of small highly curved ER protrusions emanating from ER sheets in
Simulx 2021r1, supplied by SAS institute, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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simulx 2021r1 - by Bioz Stars, 2026-03
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discovery studio v21.1.0.20298  (Accelrys)
90
Accelrys discovery studio v21.1.0.20298
Fig. 5 | FAM134B-mediated ER-phagy requires ARL6IP1 in mice and humans. a, Rational of the mCherry–GFP–FAM134B reporter. b,c, ARL6IP1 loss-of-function compromises ER-phagy. Arl6ip1 WT and KO MEFs (b) or fibroblasts from the patient and the healthy individual (control) (c) were transfected with mCherry– GFP–FAM134B and stained for LC3B. Quantifications of LC3B+mCherry+GFP+ puncta and LC3B+mCherry+GFP– puncta per cell area suggest that the formation of autophagosomes (3 experiments with 10 cells per genotype each; two-sided Mann–Whitney U-test; MEFs, P = 0.0479; human cells, P = 0.0005) and autolysosomes (3 experiments with 10 cells per genotype each; two-sided Mann–Whitney U-test; MEFs, P = 0.0307; human cells, P = 0.0096) is impaired. d,e, ARL6IP1 loss-of-function enlarges ER sheets. Arl6ip1 WT and KO MEFs (d) or fibroblasts from the patient and healthy individual (e) were stained for the ER sheet protein <t>CLIMP63</t> and the relative CLIMP63+ area per cell calculated (3 experiments with 15 cells per genotype; two-sided Mann–Whitney U-test; MEFs, P = 0.0001; human cells, P = 0.0001). f,g, TEM images showed increased numbers of small highly curved ER protrusions emanating from ER sheets in
Discovery Studio V21.1.0.20298, supplied by Accelrys, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Image Search Results


Fig. 5 | FAM134B-mediated ER-phagy requires ARL6IP1 in mice and humans. a, Rational of the mCherry–GFP–FAM134B reporter. b,c, ARL6IP1 loss-of-function compromises ER-phagy. Arl6ip1 WT and KO MEFs (b) or fibroblasts from the patient and the healthy individual (control) (c) were transfected with mCherry– GFP–FAM134B and stained for LC3B. Quantifications of LC3B+mCherry+GFP+ puncta and LC3B+mCherry+GFP– puncta per cell area suggest that the formation of autophagosomes (3 experiments with 10 cells per genotype each; two-sided Mann–Whitney U-test; MEFs, P = 0.0479; human cells, P = 0.0005) and autolysosomes (3 experiments with 10 cells per genotype each; two-sided Mann–Whitney U-test; MEFs, P = 0.0307; human cells, P = 0.0096) is impaired. d,e, ARL6IP1 loss-of-function enlarges ER sheets. Arl6ip1 WT and KO MEFs (d) or fibroblasts from the patient and healthy individual (e) were stained for the ER sheet protein CLIMP63 and the relative CLIMP63+ area per cell calculated (3 experiments with 15 cells per genotype; two-sided Mann–Whitney U-test; MEFs, P = 0.0001; human cells, P = 0.0001). f,g, TEM images showed increased numbers of small highly curved ER protrusions emanating from ER sheets in

Journal: Nature

Article Title: Heteromeric clusters of ubiquitinated ER-shaping proteins drive ER-phagy.

doi: 10.1038/s41586-023-06090-9

Figure Lengend Snippet: Fig. 5 | FAM134B-mediated ER-phagy requires ARL6IP1 in mice and humans. a, Rational of the mCherry–GFP–FAM134B reporter. b,c, ARL6IP1 loss-of-function compromises ER-phagy. Arl6ip1 WT and KO MEFs (b) or fibroblasts from the patient and the healthy individual (control) (c) were transfected with mCherry– GFP–FAM134B and stained for LC3B. Quantifications of LC3B+mCherry+GFP+ puncta and LC3B+mCherry+GFP– puncta per cell area suggest that the formation of autophagosomes (3 experiments with 10 cells per genotype each; two-sided Mann–Whitney U-test; MEFs, P = 0.0479; human cells, P = 0.0005) and autolysosomes (3 experiments with 10 cells per genotype each; two-sided Mann–Whitney U-test; MEFs, P = 0.0307; human cells, P = 0.0096) is impaired. d,e, ARL6IP1 loss-of-function enlarges ER sheets. Arl6ip1 WT and KO MEFs (d) or fibroblasts from the patient and healthy individual (e) were stained for the ER sheet protein CLIMP63 and the relative CLIMP63+ area per cell calculated (3 experiments with 15 cells per genotype; two-sided Mann–Whitney U-test; MEFs, P = 0.0001; human cells, P = 0.0001). f,g, TEM images showed increased numbers of small highly curved ER protrusions emanating from ER sheets in

Article Snippet: 4 nature portfolio | reporting sum m ary M arch 2021 Materials & experimental systems n/a Involved in the study Antibodies Eukaryotic cell lines Palaeontology and archaeology Animals and other organisms Human research participants Clinical data Dual use research of concern Methods n/a Involved in the study ChIP-seq Flow cytometry MRI-based neuroimaging Antibodies Antibodies used Primary: Actin Sigma (A-5441, Lot 064M4789V) AMFR Proteintech (16675-AP, Lot: 00046373) ARL6IP1 Sigma (PRS3305, Lot 33050404) ARL6IP1 Atlas Antibodies (HPA045307, Lot B118670) ATL2 Proteintech (16688-1-AP, Lot 00053330 ATL3 Proteintech (16921-1-AP, Lot 00008332) CCPG1 polyclonal rabbit, affinity purified with N-term peptide, gift from Simon Wilkinson CLIMP63 (CKAP4) Proteintech (16686-1-AP, Lot 00045668) CLIMP63 (CKAP4) R&D Systems (AF7355, Lot CGDG0118071) FAM134B Proteintech (21537-I-AP, Lot 00014408) FAM134B Genscript.

Techniques: Control, Transfection, Staining, MANN-WHITNEY