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ATCC n2a mouse neuroblastoma cells

Endogenous Grx1 is upregulated in <t>N2a-hTDP-43</t> cells. (a) Validation of TDP-43 overexpression in N2a-hTDP-43 cells; 48 h post-transfection as indicated, TDP-43 was visualized with a TDP-43–specific antibody. Yellow arrows indicate cytoplasmic TDP-43 aggregates. (b, c) Intracellular ROS levels are increased in N2a-hTDP-43 cells. Intracellular ROS levels were measured using CellROX Deep Red and normalized to corresponding cell numbers ( n = 3, unpaired t test). (d, e) Validation of Grx1 antibody specificity. N2a cells were transfected with 20 nM Grx1-specific siRNA (siGrx1) or control siRNA (siCon). Endogenous Grx1 levels were normalized to corresponding cell numbers ( n = 3, unpaired t test). (f, g) Endogenous Grx1 levels are increased in N2a-hTDP-43 cells. Each level was normalized to the corresponding cell number and presented as a relative fold change to control ( n = 3, unpaired t test). Nuclei were stained with DAPI (blue). Scale bars, 25 µm. Grx1, glutaredoxin-1; <t>N2a-hTDP-43,</t> <t>neuro-2a</t> cells expressing human wild-type TDP-43; ROS, reactive oxygen species; TDP-43, transactive response DNA-binding protein 43.

N2a Mouse Neuroblastoma Cells, supplied by ATCC, used in various techniques. Bioz Stars score: 99/100, based on 4114 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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1) Product Images from "Glutaredoxin-1 attenuates transactive response DNA-binding protein 43–induced neurotoxicity by suppressing oxidative stress and transactive response DNA-binding protein 43 aggregation"

Article Title: Glutaredoxin-1 attenuates transactive response DNA-binding protein 43–induced neurotoxicity by suppressing oxidative stress and transactive response DNA-binding protein 43 aggregation

Journal: Neuroreport

doi: 10.1097/WNR.0000000000002266

Endogenous Grx1 is upregulated in N2a-hTDP-43 cells. (a) Validation of TDP-43 overexpression in N2a-hTDP-43 cells; 48 h post-transfection as indicated, TDP-43 was visualized with a TDP-43–specific antibody. Yellow arrows indicate cytoplasmic TDP-43 aggregates. (b, c) Intracellular ROS levels are increased in N2a-hTDP-43 cells. Intracellular ROS levels were measured using CellROX Deep Red and normalized to corresponding cell numbers ( n = 3, unpaired t test). (d, e) Validation of Grx1 antibody specificity. N2a cells were transfected with 20 nM Grx1-specific siRNA (siGrx1) or control siRNA (siCon). Endogenous Grx1 levels were normalized to corresponding cell numbers ( n = 3, unpaired t test). (f, g) Endogenous Grx1 levels are increased in N2a-hTDP-43 cells. Each level was normalized to the corresponding cell number and presented as a relative fold change to control ( n = 3, unpaired t test). Nuclei were stained with DAPI (blue). Scale bars, 25 µm. Grx1, glutaredoxin-1; N2a-hTDP-43, neuro-2a cells expressing human wild-type TDP-43; ROS, reactive oxygen species; TDP-43, transactive response DNA-binding protein 43.

Figure Legend Snippet: Endogenous Grx1 is upregulated in N2a-hTDP-43 cells. (a) Validation of TDP-43 overexpression in N2a-hTDP-43 cells; 48 h post-transfection as indicated, TDP-43 was visualized with a TDP-43–specific antibody. Yellow arrows indicate cytoplasmic TDP-43 aggregates. (b, c) Intracellular ROS levels are increased in N2a-hTDP-43 cells. Intracellular ROS levels were measured using CellROX Deep Red and normalized to corresponding cell numbers ( n = 3, unpaired t test). (d, e) Validation of Grx1 antibody specificity. N2a cells were transfected with 20 nM Grx1-specific siRNA (siGrx1) or control siRNA (siCon). Endogenous Grx1 levels were normalized to corresponding cell numbers ( n = 3, unpaired t test). (f, g) Endogenous Grx1 levels are increased in N2a-hTDP-43 cells. Each level was normalized to the corresponding cell number and presented as a relative fold change to control ( n = 3, unpaired t test). Nuclei were stained with DAPI (blue). Scale bars, 25 µm. Grx1, glutaredoxin-1; N2a-hTDP-43, neuro-2a cells expressing human wild-type TDP-43; ROS, reactive oxygen species; TDP-43, transactive response DNA-binding protein 43.

Techniques Used: Biomarker Discovery, Over Expression, Transfection, Control, Staining, Expressing, Binding Assay

Increasing Grx1 decreases oxidative stress in N2a-hTDP-43 cells. (a, b) Validation of Grx1 overexpression in N2a-hTDP-43 cells; 48 h post-transfection as indicated, cells were simultaneously stained for TDP-43 (red) and Myc-tagged Grx1 (green) ( n = 3, one-way ANOVA). (c, d) Grx1 overexpression suppresses decreases ROS levels in N2a-hTDP-43 cells. Scale bars correspond to 25 µm. Each level was normalized to the corresponding cell number and presented as a relative fold change to control ( n = 3, one-way ANOVA). ANOVA, analysis of variance; Grx1, glutaredoxin-1; N2a-hTDP-43, neuro-2a cells expressing human wild-type TDP-43; ROS, reactive oxygen species; TDP-43, transactive response DNA-binding protein 43.

Figure Legend Snippet: Increasing Grx1 decreases oxidative stress in N2a-hTDP-43 cells. (a, b) Validation of Grx1 overexpression in N2a-hTDP-43 cells; 48 h post-transfection as indicated, cells were simultaneously stained for TDP-43 (red) and Myc-tagged Grx1 (green) ( n = 3, one-way ANOVA). (c, d) Grx1 overexpression suppresses decreases ROS levels in N2a-hTDP-43 cells. Scale bars correspond to 25 µm. Each level was normalized to the corresponding cell number and presented as a relative fold change to control ( n = 3, one-way ANOVA). ANOVA, analysis of variance; Grx1, glutaredoxin-1; N2a-hTDP-43, neuro-2a cells expressing human wild-type TDP-43; ROS, reactive oxygen species; TDP-43, transactive response DNA-binding protein 43.

Techniques Used: Biomarker Discovery, Over Expression, Transfection, Staining, Control, Expressing, Binding Assay

$Increasing Grx1 prevents TDP-43 aggregation in N2a-hTDP-43 cells. (a, b) Overexpressing Grx1 significantly reduces cytoplasmic TDP-43 aggregates in N2a-hTDP-43 cells. N2a cells were stained for TDP-43 (red) and DAPI (blue). Cells with cytoplasmic TDP-43 aggregates (yellow arrows) were presented as a percentage of cells ( n = 3, one-way ANOVA). Scale bars correspond to 25 µm. (c, d) Overexpressing Grx1 decreases total TDP-43 levels in N2a-hTDP-43 cells; 48 h post-transfection as indicated, total proteins were extracted using SDS-containing RIPA lysis buffer. TDP-43 protein levels were normalized to corresponding GAPDH levels ( n = 3, one-way ANOVA). (e–g) Overexpressing Grx1 decreases both soluble and insoluble TDP-43 levels in N2a-hTDP-43 cells. TDP-43 protein levels were assessed by western blot in Triton X-100 soluble (f) and insoluble fractions (g) and normalized to corresponding GAPDH and Ponceau S levels, respectively ( n = 3, one-way ANOVA). ANOVA, analysis of variance; Grx1, glutaredoxin-1; N2a-hTDP-43, neuro-2a cells expressing human wild-type TDP-43; TDP-43, transactive response DNA-binding protein 43.$
Figure Legend Snippet: Increasing Grx1 prevents TDP-43 aggregation in N2a-hTDP-43 cells. (a, b) Overexpressing Grx1 significantly reduces cytoplasmic TDP-43 aggregates in N2a-hTDP-43 cells. N2a cells were stained for TDP-43 (red) and DAPI (blue). Cells with cytoplasmic TDP-43 aggregates (yellow arrows) were presented as a percentage of cells ( n = 3, one-way ANOVA). Scale bars correspond to 25 µm. (c, d) Overexpressing Grx1 decreases total TDP-43 levels in N2a-hTDP-43 cells; 48 h post-transfection as indicated, total proteins were extracted using SDS-containing RIPA lysis buffer. TDP-43 protein levels were normalized to corresponding GAPDH levels ( n = 3, one-way ANOVA). (e–g) Overexpressing Grx1 decreases both soluble and insoluble TDP-43 levels in N2a-hTDP-43 cells. TDP-43 protein levels were assessed by western blot in Triton X-100 soluble (f) and insoluble fractions (g) and normalized to corresponding GAPDH and Ponceau S levels, respectively ( n = 3, one-way ANOVA). ANOVA, analysis of variance; Grx1, glutaredoxin-1; N2a-hTDP-43, neuro-2a cells expressing human wild-type TDP-43; TDP-43, transactive response DNA-binding protein 43.

Techniques Used: Staining, Transfection, Lysis, Western Blot, Expressing, Binding Assay

Increasing Grx1 attenuates neurotoxicity in N2a cells overexpressing hTDP-43; 48 h post-transfection as indicated, N2a cells were stained with cleaved caspase-3–specific antibody and DAPI (blue) (a). Scale bars correspond to 25 µm. Each level was normalized to the corresponding cell number and presented as a percentage of cells with cleaved caspase-3 signal (b) ( n = 3, one-way ANOVA). ANOVA, analysis of variance; Grx1, glutaredoxin-1; N2a, neuro-2a; TDP-43, transactive response DNA-binding protein 43

Figure Legend Snippet: Increasing Grx1 attenuates neurotoxicity in N2a cells overexpressing hTDP-43; 48 h post-transfection as indicated, N2a cells were stained with cleaved caspase-3–specific antibody and DAPI (blue) (a). Scale bars correspond to 25 µm. Each level was normalized to the corresponding cell number and presented as a percentage of cells with cleaved caspase-3 signal (b) ( n = 3, one-way ANOVA). ANOVA, analysis of variance; Grx1, glutaredoxin-1; N2a, neuro-2a; TDP-43, transactive response DNA-binding protein 43

Techniques Used: Transfection, Staining, Binding Assay

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Journal: Neuroreport

doi: 10.1097/WNR.0000000000002266

Figure Lengend Snippet: Endogenous Grx1 is upregulated in N2a-hTDP-43 cells. (a) Validation of TDP-43 overexpression in N2a-hTDP-43 cells; 48 h post-transfection as indicated, TDP-43 was visualized with a TDP-43–specific antibody. Yellow arrows indicate cytoplasmic TDP-43 aggregates. (b, c) Intracellular ROS levels are increased in N2a-hTDP-43 cells. Intracellular ROS levels were measured using CellROX Deep Red and normalized to corresponding cell numbers ( n = 3, unpaired t test). (d, e) Validation of Grx1 antibody specificity. N2a cells were transfected with 20 nM Grx1-specific siRNA (siGrx1) or control siRNA (siCon). Endogenous Grx1 levels were normalized to corresponding cell numbers ( n = 3, unpaired t test). (f, g) Endogenous Grx1 levels are increased in N2a-hTDP-43 cells. Each level was normalized to the corresponding cell number and presented as a relative fold change to control ( n = 3, unpaired t test). Nuclei were stained with DAPI (blue). Scale bars, 25 µm. Grx1, glutaredoxin-1; N2a-hTDP-43, neuro-2a cells expressing human wild-type TDP-43; ROS, reactive oxygen species; TDP-43, transactive response DNA-binding protein 43.

Article Snippet: N2a mouse neuroblastoma cells (CCL-131, ATCC, Manassas, Virginia, USA) were plated at a density of 2 × 10 5 cells/ml and grown in DMEM with 10% FBS and 1% penicillin/streptomycin (P/S) at 37 °C, in a humidified 5% CO 2 incubator.

Techniques: Biomarker Discovery, Over Expression, Transfection, Control, Staining, Expressing, Binding Assay

Journal: Neuroreport

doi: 10.1097/WNR.0000000000002266

Figure Lengend Snippet: Increasing Grx1 decreases oxidative stress in N2a-hTDP-43 cells. (a, b) Validation of Grx1 overexpression in N2a-hTDP-43 cells; 48 h post-transfection as indicated, cells were simultaneously stained for TDP-43 (red) and Myc-tagged Grx1 (green) ( n = 3, one-way ANOVA). (c, d) Grx1 overexpression suppresses decreases ROS levels in N2a-hTDP-43 cells. Scale bars correspond to 25 µm. Each level was normalized to the corresponding cell number and presented as a relative fold change to control ( n = 3, one-way ANOVA). ANOVA, analysis of variance; Grx1, glutaredoxin-1; N2a-hTDP-43, neuro-2a cells expressing human wild-type TDP-43; ROS, reactive oxygen species; TDP-43, transactive response DNA-binding protein 43.

Techniques: Biomarker Discovery, Over Expression, Transfection, Staining, Control, Expressing, Binding Assay

Journal: Neuroreport

doi: 10.1097/WNR.0000000000002266

Figure Lengend Snippet: Increasing Grx1 prevents TDP-43 aggregation in N2a-hTDP-43 cells. (a, b) Overexpressing Grx1 significantly reduces cytoplasmic TDP-43 aggregates in N2a-hTDP-43 cells. N2a cells were stained for TDP-43 (red) and DAPI (blue). Cells with cytoplasmic TDP-43 aggregates (yellow arrows) were presented as a percentage of cells ( n = 3, one-way ANOVA). Scale bars correspond to 25 µm. (c, d) Overexpressing Grx1 decreases total TDP-43 levels in N2a-hTDP-43 cells; 48 h post-transfection as indicated, total proteins were extracted using SDS-containing RIPA lysis buffer. TDP-43 protein levels were normalized to corresponding GAPDH levels ( n = 3, one-way ANOVA). (e–g) Overexpressing Grx1 decreases both soluble and insoluble TDP-43 levels in N2a-hTDP-43 cells. TDP-43 protein levels were assessed by western blot in Triton X-100 soluble (f) and insoluble fractions (g) and normalized to corresponding GAPDH and Ponceau S levels, respectively ( n = 3, one-way ANOVA). ANOVA, analysis of variance; Grx1, glutaredoxin-1; N2a-hTDP-43, neuro-2a cells expressing human wild-type TDP-43; TDP-43, transactive response DNA-binding protein 43.

Techniques: Staining, Transfection, Lysis, Western Blot, Expressing, Binding Assay

Journal: Neuroreport

doi: 10.1097/WNR.0000000000002266

Figure Lengend Snippet: Increasing Grx1 attenuates neurotoxicity in N2a cells overexpressing hTDP-43; 48 h post-transfection as indicated, N2a cells were stained with cleaved caspase-3–specific antibody and DAPI (blue) (a). Scale bars correspond to 25 µm. Each level was normalized to the corresponding cell number and presented as a percentage of cells with cleaved caspase-3 signal (b) ( n = 3, one-way ANOVA). ANOVA, analysis of variance; Grx1, glutaredoxin-1; N2a, neuro-2a; TDP-43, transactive response DNA-binding protein 43

Techniques: Transfection, Staining, Binding Assay

(a) Schematic of targeted histone deacetylation at the Cdk5 promoter using CRISPR/dCas9-HDAC3. (b) CUT&Tag bigwig-normalized signal and called peak for H3K9/14ac in mouse hippocampus (top), and positions of designed sgRNAs targeting 62–1107 bp upstream of the Cdk5 TSS (bottom). (c) Cdk5 mRNA expression in N2a cells treated with dCas9-HDAC3 paired with each designed sgRNA, or dCas9-AM tag with Cdk5 -sgRNA ( n = 3). One-way ANOVA: main effect of sgRNA, F(6, 14) = 13.35, p < 0.0001; post-hoc NT vs. Cdk5 -sgRNA, p = 0.0049; dCas9-AM tag vs. NT, p = 0.0907 (ns). (d) Intra-NAc injection of the neuronal hSyn-dCas9-HDAC3 with NT (left hemisphere) or Cdk5 -sgRNA (right hemisphere) reduces Cdk5 mRNA at days 5 and 6 post-injection ( n = 9-10). Two-way ANOVA: main effect of sgRNA, F (1, 84) = 12.91, p = 0.0005; post-hoc NT vs. Cdk5 -sgRNA at day 5, p = 0.0276; day 6, p = 0.0034. (e) Intra-dHPC injection of hSyn-dCas9-HDAC3 with NT (left hemisphere) or Cdk5 -sgRNA (right hemisphere) reduces Cdk5 mRNA at day 6 post-injection in males (left; paired t-test, p = 0.0395, n = 3) and females (right; paired t-test, p = 0.0425; n = 4). (f) hSyn-dCas9-HDAC3 with Cdk5 -sgRNA reduces Cdk5 protein levels at day 6 PI in the dorsal hippocampus of a mixed-sex cohort (paired Wilcoxon test, p = 0.0312; n = 5). (g) hSyn-dCas9-HDAC3 with Cdk5 -sgRNA reduces phosphorylation of Tau at Serine 396 in the dorsal hippocampus of a mixed-sex cohort (paired Wilcoxon test, p = 0.0292; n = 4). All data are presented as mean ± SEM.

Journal: bioRxiv

Article Title: Neuron-specific epigenetic repression of Cdk5 impairs hippocampal-dependent memory in male and female mice

doi: 10.64898/2026.04.08.716689

Figure Lengend Snippet: (a) Schematic of targeted histone deacetylation at the Cdk5 promoter using CRISPR/dCas9-HDAC3. (b) CUT&Tag bigwig-normalized signal and called peak for H3K9/14ac in mouse hippocampus (top), and positions of designed sgRNAs targeting 62–1107 bp upstream of the Cdk5 TSS (bottom). (c) Cdk5 mRNA expression in N2a cells treated with dCas9-HDAC3 paired with each designed sgRNA, or dCas9-AM tag with Cdk5 -sgRNA ( n = 3). One-way ANOVA: main effect of sgRNA, F(6, 14) = 13.35, p < 0.0001; post-hoc NT vs. Cdk5 -sgRNA, p = 0.0049; dCas9-AM tag vs. NT, p = 0.0907 (ns). (d) Intra-NAc injection of the neuronal hSyn-dCas9-HDAC3 with NT (left hemisphere) or Cdk5 -sgRNA (right hemisphere) reduces Cdk5 mRNA at days 5 and 6 post-injection ( n = 9-10). Two-way ANOVA: main effect of sgRNA, F (1, 84) = 12.91, p = 0.0005; post-hoc NT vs. Cdk5 -sgRNA at day 5, p = 0.0276; day 6, p = 0.0034. (e) Intra-dHPC injection of hSyn-dCas9-HDAC3 with NT (left hemisphere) or Cdk5 -sgRNA (right hemisphere) reduces Cdk5 mRNA at day 6 post-injection in males (left; paired t-test, p = 0.0395, n = 3) and females (right; paired t-test, p = 0.0425; n = 4). (f) hSyn-dCas9-HDAC3 with Cdk5 -sgRNA reduces Cdk5 protein levels at day 6 PI in the dorsal hippocampus of a mixed-sex cohort (paired Wilcoxon test, p = 0.0312; n = 5). (g) hSyn-dCas9-HDAC3 with Cdk5 -sgRNA reduces phosphorylation of Tau at Serine 396 in the dorsal hippocampus of a mixed-sex cohort (paired Wilcoxon test, p = 0.0292; n = 4). All data are presented as mean ± SEM.

Article Snippet: Murine Neuro-2a (N2a) cells (ATCC, #CCL-131) were maintained in EMEM (ATCC, #30-2003) supplemented with 10% fetal bovine serum (FBS; ATCC #30-2020).

Techniques: CRISPR, Expressing, Injection, Phospho-proteomics

( A ) Schematic illustration of TBI/sham mouse brain-derived EV isolation, incubation of N2a cells with EVs, and downstream functional analyses (transcriptomics and protein assays). ( B ) Heat map of transcriptomic changes in N2a cells incubated without EVs (control, n = 9), with sham EVs ( n = 9), or with TBI EVs ( n = 9). ( C ) STRING analysis of transcripts with p < 0.04 selected for cluster analysis of oxidative phosphorylation, mitochondrial translation, and sphingolipid metabolism. ( D ) Immunoblot of VDAC1 and p53 in mouse brain cortex (upper panel) and in N2a cells treated with sham or TBI EVs (lower panel) normalized to loading control β-actin. ( E ) Quantification expressed in fold-change for the blots shown above. Mean ± SD, unpaired t-test, n = 4 for brain cortex and n =3 for N2a cells, * p < 0.05, ** p < 0.01, *** p < 0.001, and **** for p < 0.0001. ( F ) LDH release assay showing fold change in N2a cell death after incubation with brain-derived EVs from TBI and sham mice. n = 8 for sham and n =9 for TBI. Mean ± SD, unpaired t-test, * p < 0.05, ** p < 0.01, *** p < 0.001, and **** for p < 0.0001.

Journal: bioRxiv

Article Title: Ceramide-rich extracellular vesicles as pathogenic biomarkers in traumatic brain injury

doi: 10.64898/2026.04.01.715607

Figure Lengend Snippet: ( A ) Schematic illustration of TBI/sham mouse brain-derived EV isolation, incubation of N2a cells with EVs, and downstream functional analyses (transcriptomics and protein assays). ( B ) Heat map of transcriptomic changes in N2a cells incubated without EVs (control, n = 9), with sham EVs ( n = 9), or with TBI EVs ( n = 9). ( C ) STRING analysis of transcripts with p < 0.04 selected for cluster analysis of oxidative phosphorylation, mitochondrial translation, and sphingolipid metabolism. ( D ) Immunoblot of VDAC1 and p53 in mouse brain cortex (upper panel) and in N2a cells treated with sham or TBI EVs (lower panel) normalized to loading control β-actin. ( E ) Quantification expressed in fold-change for the blots shown above. Mean ± SD, unpaired t-test, n = 4 for brain cortex and n =3 for N2a cells, * p < 0.05, ** p < 0.01, *** p < 0.001, and **** for p < 0.0001. ( F ) LDH release assay showing fold change in N2a cell death after incubation with brain-derived EVs from TBI and sham mice. n = 8 for sham and n =9 for TBI. Mean ± SD, unpaired t-test, * p < 0.05, ** p < 0.01, *** p < 0.001, and **** for p < 0.0001.

Article Snippet: EVs were added to Neuro-2a (N2a) cells (ATCC (CCL-131TM) to quantify the cytotoxicity of EVs as described previously.

Techniques: Derivative Assay, Isolation, Incubation, Functional Assay, Transcriptomics, Control, Phospho-proteomics, Western Blot, Lactate Dehydrogenase Assay

( A ) Schematic of EV isolation from human plasma, incubation of N2a cells without EVs (Control) or with TBI and non-TBI EVs, and Seahorse assay design. ( B–D ) Bioenergetic profiling of N2a cells incubated without EVs (control) or with human plasma-derived EVs from non-TBI or TBI subjects, analyzed using the Seahorse Flux Analyzer (Cell Mito Stress Test). Oxygen consumption rate (OCR) ( B and C ) are shown as lines ( B ) and box-and-whisker plot ( C ), and extracellular acidification rate (ECAR) ( D ) is shown as line. Mean ± SD, One-way ANOVA multiple comparison Tukey test was performed, n = 5 for control and non-TBI EVs and n =6 for TBI EVs, * p < 0.05, ** p < 0.01, *** p < 0.001, and **** for p < 0.0001.

Journal: bioRxiv

Article Title: Ceramide-rich extracellular vesicles as pathogenic biomarkers in traumatic brain injury

doi: 10.64898/2026.04.01.715607

Figure Lengend Snippet: ( A ) Schematic of EV isolation from human plasma, incubation of N2a cells without EVs (Control) or with TBI and non-TBI EVs, and Seahorse assay design. ( B–D ) Bioenergetic profiling of N2a cells incubated without EVs (control) or with human plasma-derived EVs from non-TBI or TBI subjects, analyzed using the Seahorse Flux Analyzer (Cell Mito Stress Test). Oxygen consumption rate (OCR) ( B and C ) are shown as lines ( B ) and box-and-whisker plot ( C ), and extracellular acidification rate (ECAR) ( D ) is shown as line. Mean ± SD, One-way ANOVA multiple comparison Tukey test was performed, n = 5 for control and non-TBI EVs and n =6 for TBI EVs, * p < 0.05, ** p < 0.01, *** p < 0.001, and **** for p < 0.0001.

Article Snippet: EVs were added to Neuro-2a (N2a) cells (ATCC (CCL-131TM) to quantify the cytotoxicity of EVs as described previously.

Techniques: Isolation, Clinical Proteomics, Incubation, Control, Derivative Assay, Whisker Assay, Comparison

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