Journal: Journal of Korean Neurosurgical Society

Article Title: S100ß, Matrix Metalloproteinase-9, D-dimer, and Heat Shock Protein 70 Are Serologic Biomarkers of Acute Cerebral Infarction in a Mouse Model of Transient MCA Occlusion

doi: 10.3340/jkns.2017.0200

Figure Lengend Snippet: Plasma S100β concentration in all groups. The concentration of S100β increases with occlusion time (p=0.001; A) and correlates significantly with infarct volume (r=0.867, p <0.001; b) and neurological deficit (r=0.802, p <0.001; c). * p <0.05.

Article Snippet: The plasma concentrations of S100β, MMP-9, D-dimer, and HSP70 were calculated using mouse protein S100β (CSB-EL-0206643MO; CUSABIO, Wuhan, China), mouse total MMP-9 (MMPT90; R&D Systems, Minneapolis, MN, USA), mouse D-dimer (E03D0224; BlueGene, Shanghai, China), and mouse HSP70 (CSB-E08311m; CUSABIO) ELISA kits.

Techniques: Clinical Proteomics, Concentration Assay

Journal: Journal of Korean Neurosurgical Society

Article Title: S100ß, Matrix Metalloproteinase-9, D-dimer, and Heat Shock Protein 70 Are Serologic Biomarkers of Acute Cerebral Infarction in a Mouse Model of Transient MCA Occlusion

doi: 10.3340/jkns.2017.0200

Figure Lengend Snippet: Sensitivity and specificity of the biomarkers. MMP-9 and HSP70 both have an AUc of 1. S100β has an AUc of 0.98. The AUc for D-dimer is 0.58. MMP-9 : matrix metalloproteinase-9, HSP70 : heat shock protein 70, AUc : the area under the receiver operating characteristic curve.

Article Snippet: The plasma concentrations of S100β, MMP-9, D-dimer, and HSP70 were calculated using mouse protein S100β (CSB-EL-0206643MO; CUSABIO, Wuhan, China), mouse total MMP-9 (MMPT90; R&D Systems, Minneapolis, MN, USA), mouse D-dimer (E03D0224; BlueGene, Shanghai, China), and mouse HSP70 (CSB-E08311m; CUSABIO) ELISA kits.

Techniques:

Journal: Cell reports

Article Title: Neuronal and astrocytic contributions to Huntington’s disease dissected with zinc finger protein transcriptional repressors

doi: 10.1016/j.celrep.2022.111953

Figure Lengend Snippet: KEY RESOURCES TABLE

Article Snippet: chicken anti-S100β , Synaptic Systems , Cat# 287006; RRID:AB_2713986.

Techniques: Virus, Recombinant, Saline, Mutagenesis, Software

Journal: bioRxiv

Article Title: Aβ-induced distress of astrocytes triggers Alzheimer disease pathology through non-canonical δ secretase activity

doi: 10.1101/2025.01.30.635618

Figure Lengend Snippet: SORCS2-deficient primary astrocytes exhibit enhanced cell stress in response to Aβ ( A ) Levels of Sorcs2 transcripts as determined by qRT-PCR in primary astrocytes from wildtype (WT) mice treated with control (−) or Aβ-conditioned media (+) for 24h or 48h. Aβ-conditioned medium had been generated from SY5Y cells stably overexpressing human APP . Data are expressed as relative expression levels (set to 1 for –Aβ) and given as mean ± SEM from n=6-11 independent cell preparations per group (unpaired Mann-Whitney U test). (B) Primary WT or SORCS2-deficient (KO) astrocytes were treated with control (−) or Aβ-conditioned medium (+) and residual levels of Aβ were measured after 24h using ELISA. Media from KO astrocytes showed lower levels of Aβ 40 and Aβ 42 , indicating increased cellular Aβ uptake. Data are given as mean ± SEM from n=15-17 biological replicates (unpaired Mann-Whitney U-test). (C, D) Primary WT and KO astrocytes were treated with 1 µM HiLyte-Aβ 40 for 6h. Aβ uptake was visualized by fluorescence microscopy for HiLyte-Aβ 40 (C, green) and quantified by ELISA in cell lysates (D). In D, intracellular Aβ levels are higher in KO as compared to WT cells. No Aβ is detected in WT cells treated with control medium (Ctr). Data are given as mean ± SEM from n=8 animals per group (two-sided unpaired Student’s t -test). Scale bar: 50 μm (inset: 200 μm) . (E) Western blot analysis of glial fibrillary acidic protein (GFAP) levels in WT and KO astrocytes after 48h of treatment with control (−) or Aβ-conditioned (+) medium (upper panel) and quantification thereof (lower panel). Data are expressed as levels relative to WT –Aβ (set to 100%) and given as mean ± SEM from n=3-4 independent cell preparations per genotype and condition (ordinary two-way ANOVA with Tukeýs multiple comparisons test to test significance for genotype). (F) Primary WT or KO astrocytes were cultured for 24h in the presence or absence of Aβ-conditioned medium followed by live staining with LysoTracker Red dye (lysotracker). Lysotracker fluorescence signals (upper panel) were used to quantify lysosome numbers as well as cumulative signal intensity per cell (lower panel; in arbitrary units, a.u.). In KO, and to a lesser extent in WT cells, Aβ treatment decreases lysotracker intensities without impacting lysosome numbers, suggesting impaired lysosomal acidification. Data are given as mean ± SEM from n=13 independent cell preparations per genotype (two-sided unpaired Student’s t -test). Scale bar: 50 μm. (G) Cell viability was measured using presto blue in primary astrocytes treated with control or Aβ-containing medium for 24h and 48h. Data are given as mean ± SEM of fluorescent signal ratio (+Aβ)/(−Aβ) from n=19-21 independent cell preparations per genotype and condition (two-sided unpaired Student’s t -test). Aβ treatment decreased viability in KO to a higher extent than in WT cells. (H-I) Western blot analyses of cleaved poly (ADP-Ribose) polymerase 1 (cl. PARP) and cleaved caspase 3 (cl. casp3) levels in WT and KO astrocytes after 24h (cl. PARP) or 48h (cl. casp3) of treatment with control (−Aβ) or Aβ medium (+Aβ). Exemplary blots from 3 independent experiments per condition (H) as well as quantification from densitometric scanning of replicate blots (I) are given. Levels are expressed as relative to WT –Aβ (set to 1), and are given as mean ± SEM from n=9-12 independent cell preparations per genotype and condition (ordinary Two-way ANOVA with Holm-Sidak’s multiple comparisons test). *, p<0.05; **, P < 0.01; ***, P < 0.001

Article Snippet: Antibodies used for sorting were directed against markers of microglia and macrophages (CD45-BV421; 1:200, BD Biosciences #563890), endothelia (CD49a-FITC; 1:200, Miltenyi Biotec #130-107-636), oligodendrocytes (O4-PE; 1:200, Miltenyi Biotec #130-117-357) and astrocytes (ACSA2-APC, 1:100, Miltenyi Biotec #130-116-245; S100β-PE, 1:100, Novus Bio #NBP2-45267; GFAP-BV421, 1:100, Biolegend #644710; Aldh1l1-FITC, 1:100, Novus Bio #NBP2-50045F).

Techniques: Quantitative RT-PCR, Control, Generated, Stable Transfection, Expressing, MANN-WHITNEY, Enzyme-linked Immunosorbent Assay, Fluorescence, Microscopy, Western Blot, Cell Culture, Staining

Journal: bioRxiv

Article Title: Aβ-induced distress of astrocytes triggers Alzheimer disease pathology through non-canonical δ secretase activity

doi: 10.1101/2025.01.30.635618

Figure Lengend Snippet: Aβ induces astrogliosis and loss of astrocytes in SORCS2-deficient mice ( A ) Nucleosome fragmentation assay documents increased cell death in cortical (cx, left panel) and hippocampal (hip, right panel) brain extracts of 40 weeks old PDAPP/WT and PDAPP/KO females when compared to WT and KO controls lacking PDAPP. However, PDAPP-induced cell death was significantly higher in PDAPP/KO than PDAPP/WT. Data are given as mean ± SEM from n=18-24 (PDAPP) and n=7-9 (non-PDAPP) animals per genotype group (ordinary two-way ANOVA with Tukeýs multiple comparisons test). ( B ) Transcript levels for Sorcs2 in the indicated cell types isolated by FACS from cx (left panel) and hip (right panel) of PDAPP/WT females. Data are given as mean ± SEM from n=6 animals per genotype. (C) Cell type distribution in cx (upper panel) and hip (lower panel) of 40 weeks old PDAPP/WT and PDAPP/KO females as determined by FACS. PDAPP/KO animals show a significant reduction in relative numbers of astrocytes and endothelial cells, and a concomitant increase in microglia and macrophages. Data are given as mean ± SEM from n=11-12 animals per genotype (two-sided unpaired t -test). (D) Cell type distribution in cx of 20 weeks old PDAPP/WT and PDAPP/KO females based on FACS. Relative abundance of astrocytes is unchanged, while numbers of microglia and macrophages increase in young PDAPP/KO mice. Data are given as mean ± SEM from n=9-11 animals per genotype (unpaired Mann-Whitney U-test). (E-F) FACS documenting relative distribution of various cell types to be unchanged comparing cx (E) and hip (F) of 40 weeks old WT and KO females lacking PDAPP. Data are given as mean ± SEM from n=6 animals per genotype (unpaired Mann-Whitney U-test). (G) Immunostaining of hip regions of 40 weeks old PDAPP/WT and PDAPP/KO females for astrocyte markers ACSA2 and S100β (green). Nuclei were counterstained with DAPI (blue). Scale bar, 400 μm. (H) Representative FACS histogram of GFAP levels in sorted astrocytes documenting higher levels in aged PDAPP/KO as compared to PDAPP/WT female brains. ( I ) Representative Western blot for GFAP in brain extracts (upper panel), and quantification from densitometric scanning of replicate blots (lower panel), show increased levels in cx and hip of 40 weeks PDAPP/KO females compared to matched PDAPP/WT controls. Data are expressed as relative to WT (set to 100%) and given as mean ± SEM from n=13-14 animals per genotype (two-sided unpaired Student’s t -test). (J) Representative images of GFAP immunostaining (red) in brain regions of 40 weeks old PDAPP/KO as compared to PDAPP/WT female mice. A schematic depicting analyzed cortical (cx1, cx2) and dentate gyrus (DG) regions is shown. Nuclei were counterstained with DAPI (blue). Scale bar: 200 μm. ( K ) GFAP signal intensities (arbitrary units, au) quantified from replicate immunostainings exemplified in J, show significant increase in GFAP levels in indicated brain regions in PDAPPP/KO females compared to PDAPP/WT controls. Data are given as mean ± SEM from n=3 animals per genotype (two-sided unpaired Student’s t -test).*, P < 0.05; **, P < 0.01; ***, P < 0.001

Article Snippet: Antibodies used for sorting were directed against markers of microglia and macrophages (CD45-BV421; 1:200, BD Biosciences #563890), endothelia (CD49a-FITC; 1:200, Miltenyi Biotec #130-107-636), oligodendrocytes (O4-PE; 1:200, Miltenyi Biotec #130-117-357) and astrocytes (ACSA2-APC, 1:100, Miltenyi Biotec #130-116-245; S100β-PE, 1:100, Novus Bio #NBP2-45267; GFAP-BV421, 1:100, Biolegend #644710; Aldh1l1-FITC, 1:100, Novus Bio #NBP2-50045F).

Techniques: Isolation, MANN-WHITNEY, Immunostaining, Western Blot

Journal: bioRxiv

Article Title: Aβ-induced distress of astrocytes triggers Alzheimer disease pathology through non-canonical δ secretase activity

doi: 10.1101/2025.01.30.635618

Figure Lengend Snippet: Astrocyte-specific inactivation of Sorcs2 increases Aβ levels and induces cell stress in the AD mouse brain ( A ) Levels of soluble Aβ 40 and Aβ 42 in hippocampus (hip) and cortex (cx) of 32 weeks old PDAPP animals (20 weeks post tamoxifen injection) homozygous for Sorcs2 lox/lox (PDAPP/loxWT) or carrying an astrocyte-specific Sorcs2 gene defect (PDAPP/asKO). Data are given as mean ± SEM from n=9 animals per genotype (two-sided unpaired Student’s t -test). (B) Data as in A, but from hip and cx extracts of 38 weeks old PDAPP/loxWT and PDAPP/asKO animals. Data are given as mean ± SEM for n=9-12 animals per genotype (two-sided unpaired Student’s t -test). (C) Levels of soluble Aβ 40 and Aβ 42 in cx and hip of 38 weeks old male or female PDAPP mice, either PDAPP/loxWT or carrying a neuron-specific Sorcs2 gene defect (PDAPP/nsKO). Data are given as mean ± SEM for n=16-20 animals per genotype (unpaired Mann-Whitney U-test). (D-E) Representative Western blot for GFAP and IBA1 in hip (D, upper panel) or cx brain extracts (D, lower panel), and quantification from densitometric scanning of replicate blots thereof (E), are shown. Hip GFAP levels increase in 38 weeks PDAPP/asKO females compared to matched PDAPP/loxWT controls. Data are expressed as relative to WT (set to 100%) and given as mean ± SEM from n=6 animals per genotype (unpaired Mann-Whitney U-test). (F) Nucleosome fragmentation assay documents increased cell death in hip extracts of 38 weeks old PDAPP/asKO females compared to matched PDAPP/WT. Data are given as mean ± SEM from n=9-12 animals per genotype (unpaired Mann-Whitney U-test). (G) Levels of IL33 in hip and cx extracts of PDAPP/WT or PDAPP/KO female mice at 38 weeks of age. Young females are separated into two groups based on low versus high brain Aβ levels (cut off: 300 pg/ml Aβ 40 and 800 pg/ml Aβ 42 for hip; 35 pg/ml Aβ 40 and 60 pg/ml Aβ 42 for cx). Data are given as mean ± SEM from n=8-14 animals per genotype (two-sided unpaired Student’s t -test) *, P < 0.05; **, P < 0.01; ***, P < 0.001

Article Snippet: Antibodies used for sorting were directed against markers of microglia and macrophages (CD45-BV421; 1:200, BD Biosciences #563890), endothelia (CD49a-FITC; 1:200, Miltenyi Biotec #130-107-636), oligodendrocytes (O4-PE; 1:200, Miltenyi Biotec #130-117-357) and astrocytes (ACSA2-APC, 1:100, Miltenyi Biotec #130-116-245; S100β-PE, 1:100, Novus Bio #NBP2-45267; GFAP-BV421, 1:100, Biolegend #644710; Aldh1l1-FITC, 1:100, Novus Bio #NBP2-50045F).

Techniques: Injection, MANN-WHITNEY, Western Blot

Journal: bioRxiv

Article Title: Aβ-induced distress of astrocytes triggers Alzheimer disease pathology through non-canonical δ secretase activity

doi: 10.1101/2025.01.30.635618

Figure Lengend Snippet: Amyloid peptide overproduction in SORCS2-deficient mice is caused by enhanced δ secretase activity ( A ) Schematic presentation of APP processing pathways and the resulting cleavage products. non-amyloidogenic processing initiated by α secretase, amyloidogenic processing by β and γ secretases, alternative amyloidogenic processing by sequential cleavage from δ, β, and γ secretases. CTFδ and sAPPδ are cleavage products unique to δ secretase action. ( B ) Levels of soluble (s)APPα and sAPPβ in cortex (cx) and hippocampus (hip) of 40 weeks old female PDAPP/WT and PDAPP/KO animals as determined by ELISA. Levels of sAPPα are reduced, while levels of sAPPβ are undetectable in PDAPP/KO. Data are given as mean ± SEM from n=11-36 animals per genotype (unpaired Mann-Whitney U test for cx, two-sided unpaired Student’s t -test for hip). (C, D) Representative Western blot (C), and densitometric scanning of replicate blots (D), quantifying levels of APP, CTFβ, sAPP species, as well as full-length and cleaved forms of δ secretase in the cx lysates of 40 weeks old PDAPP/WT and PDAPP/KO females. Immunoreactive bands representing mature and immature forms of APP as well as APPα/b and sAPPδ are marked. Data are expressed as relative to WT (set to 100%) and given as mean ± SEM from n=6-7 (for APP, CTFβ, and sAPPs) and n=14 (for δ secretase) animals per genotype (unpaired Mann-Whitney U test for APP, CTFβ, and sAPP; two-sided unpaired Student’s t -test for δ secretase). (E, F) Experiment as in C and D, but testing hip extracts of 40 weeks old PDAPP females. (G) Activity of δ secretase is increased in cx and hip lysates of 40 weeks old PDAPP/KO compared to PDAPP/WT females, as documented by activity assays using a fluorogenic substrate (see methods for details). Data are given as mean ± SEM from n=6-7 animals per genotype (repeated measures two-way ANOVA to test significance for genotypes). (H) Experiment as in G, but using cx and hip extracts from 12 weeks old PDAPP/WT and PDAPP/KO females, showing comparable levels of δ secretase activity. Data are given as mean ± SEM from n=3 animals per genotype (repeated measures two-way ANOVA). rfu, relative fluorescence units. *, P < 0.05; **, P < 0.01; ***, P < 0.001. ( I ) Model of pathological cascade induced by Aβ stress imposed on astrocytes (see discussion section for details).

Article Snippet: Antibodies used for sorting were directed against markers of microglia and macrophages (CD45-BV421; 1:200, BD Biosciences #563890), endothelia (CD49a-FITC; 1:200, Miltenyi Biotec #130-107-636), oligodendrocytes (O4-PE; 1:200, Miltenyi Biotec #130-117-357) and astrocytes (ACSA2-APC, 1:100, Miltenyi Biotec #130-116-245; S100β-PE, 1:100, Novus Bio #NBP2-45267; GFAP-BV421, 1:100, Biolegend #644710; Aldh1l1-FITC, 1:100, Novus Bio #NBP2-50045F).

Techniques: Activity Assay, Enzyme-linked Immunosorbent Assay, MANN-WHITNEY, Western Blot, Fluorescence

Journal: Molecular biomedicine

Article Title: Enteric glial cells aggravate the intestinal epithelial barrier damage by secreting S100β under high-altitude conditions.

doi: 10.1186/s43556-023-00143-1

Figure Lengend Snippet: Fig. 1 The levels of EGC biomarkers are significantly increased by HA conditions. a Serum concentrations of GFAP, S100β, GDNF, and NGF in control and HA group participants. b Relative mRNA expression per β-Actin of GFAP, S100β, GDNF, and NGF-β in the small intestines of control and HA group mice. c Immunohistochemical staining of the small intestine for GFAP and S100β. (n = 6–8 mice/group), Mean ± SD represent the findings. ****p < 0.0001, **p < 0.01, *p < 0.05. MOD—Mean Optical Density, IHC - immunohistochemistry

Article Snippet: To explore the role of S100β, MODE-K cells were treated with 5 μM recombinant mouse S100β (Solarbio, P00208) and subjected to hypoxia for 12 h, and control MODE-K cells were subjected to hypoxia alone.

Techniques: Control, Expressing, Immunohistochemical staining, Staining, Immunohistochemistry

Journal: Molecular biomedicine

Article Title: Enteric glial cells aggravate the intestinal epithelial barrier damage by secreting S100β under high-altitude conditions.

doi: 10.1186/s43556-023-00143-1

Figure Lengend Snippet: Fig. 5 S100β mediates the effect of EGCs to aggravate epithelial cell injury under hypoxic conditions. a Effect of exogenous S100β on MODE-K epithelial cell proliferation under hypoxic conditions. b Representative flow cytometric plots of MODE-K cell apoptosis. Annexin V and PI were used to label the cells before they were analyzed by flow cytometry. The figures show what proportion of the total occur in each quadrant. c Statistical analysis of the frequency percentage in late-phase apoptosis. d Relative mRNA expression per β-Actin of IL-6, -10, -1α, -1β, and TNF-α, claudin-1, occludin, and ZO-1. e Occludin and ZO-1 protein expression. Representation of findings and significance as previously stated

Article Snippet: To explore the role of S100β, MODE-K cells were treated with 5 μM recombinant mouse S100β (Solarbio, P00208) and subjected to hypoxia for 12 h, and control MODE-K cells were subjected to hypoxia alone.

Techniques: Flow Cytometry, Expressing

Journal: Molecular Neurodegeneration Advances

Article Title: Neuroinflammatory stress preferentially impacts synaptic MAPK signaling and mitochondria in excitatory neurons

doi: 10.1186/s44477-026-00024-1

Figure Lengend Snippet: Global effects of systemic LPS. ( A ) LPS-treated mice exhibited a significant reduction in body weight. Two-way repeated measures ANOVA [F(9, 36) = 14.37, p < 0.0001] followed by Tukey’s multiple comparison test (* p < 0.05, ** p < 0.01, *** p < 0.001). ( B ) Representative immunofluorescence images showing the distribution of Iba1 + cells (microglia in cyan), and S100β + cells (astrocytes in red) in the somatosensory cortex and hippocampal CA1 region and from Camk2a-CIBOP mice treated with LPS compared to saline controls. Systemic LPS administration induced microglial activation and astrocyte reactivity. ( C ) LPS-treated mice exhibited similar NF-L plasma levels than saline controls; non-CIBOP + saline vs non-CIBOP + LPS, 102.8 ± 21.7 pg/mL vs 110.7 ± 21.6 pg/mL; Camk2a-CIBOP + saline vs Camk2a-CIBOP + LPS, 172.9 ± 58.4 pg/mL vs 91.4 ± 18.5 pg/mL. Data are expressed as mean ± SEM. One-way ANOVA [F(3, 12) = 1.135, p = 0.3741], ns = no significant. ( D ) Selected chemokine, cytokine, and growth factor levels were measured in bulk brain homogenates using a standard multiplexed Luminex assay. Upregulation of Eotaxin and IP-10 expression were the most relevant protein changes in LPS-treated mice. Data are expressed as mean ± SEM. Unpaired two-tailed t-test [Eotaxin: t = 3.464, df = 6, p = 0.0134; IP-10: t = 2.846, df = 6, p = 0.0293] (* p < 0.05). Volcano plots showing the effects of LPS on ( E ) bulk brain proteomes and on ( F ) P2 synaptosomal fraction proteomes. ( G ) Venn diagram of the unique and shared proteins that were induced by LPS in bulk brain homogenates and P2 fractions. ( H ) Results of GO enrichment analysis of bulk brain homogenates (LPS homogenate-input vs Saline homogenate-input) and P2 fractions (LPS P2-input vs Saline P2-input). Selected GO terms from each of the three GO groups (biological process, cellular component, and molecular function) are shown. Volcano plots of differentially expressed gene transcripts comparing LPS-treated to saline-treated WT mice in ( H ) brain and ( I ) microglia. Also see Additional files 4, 10, and 11 for related analyses and datasets, and Additional file 14 for Supplementary Figs. S3 and S4. Schematic Fig. 3G was created using BioRender.com

Article Snippet: S100β , Synaptic Systems , 287 004 , RRID:AB_2620025 , 1:1,000 , IF.

Techniques: Comparison, Immunofluorescence, Saline, Activation Assay, Clinical Proteomics, Luminex, Expressing, Two Tailed Test

Journal: iScience

Article Title: The regulation of enteric neuron connectivity by semaphorin 5A is affected by the autism-associated S956G missense mutation

doi: 10.1016/j.isci.2024.109638

Figure Lengend Snippet:

Article Snippet: Mouse monoclonal anti-S100β IgG1 , Abnova , Cat: MAB12455.

Techniques: Recombinant, Western Blot, Mutagenesis, Bicinchoninic Acid Protein Assay, Software, Membrane

Journal: Developmental biology

Article Title: Netrin1 is required for neural and glial precursor migrations into the olfactory bulb.

doi: 10.1016/j.ydbio.2011.04.016

Figure Lengend Snippet: Fig. 6. Analysis of glial populations in Ntn1−/−brains at Pn6. Immunohistochemical staining with anti-PDGFRA (A,B,E,F), anti-OLIG2 (I,J), anti-NG2 (M,N) and anti-GFAP (Q,R) on sagittal paraffin sections from Ntn+/−(A,E,I,M,Q) and Ntn1−/−(B,F,J,N,R) mice. Corresponding Hoechst stainings are shown to the right in C,D,G,H,K,L,O,P,S,T. The white boxes in the images show the areas (325 μm×325 μm) used for calculation of cell numbers shown in Table 2. Scale bars in A–D 200 μm and in E–T 50 μm.

Article Snippet: Antibody dilutions: CNP 1:100, calR 1:200, NG2 1:1000, PSA-NCAM 1:500 and GFAP 1:500 (Chemicon), calB 1:500 (Swant), OLIG2 1:800 (Neuromics), S-100β 1:500 (Sigma), PDGFRA 1:100 (Cell Signaling), NeuN 1:150 and TH 1:500 (Millipore), β-gal 1:1000 (MP Biomedicals, Inc), and TUJ1 1:500 (Biosite).

Techniques: Immunohistochemical staining, Staining

Journal: Communications Biology

Article Title: mGluR5-mediated astrocytes hyperactivity in the anterior cingulate cortex contributes to neuropathic pain in male mice

doi: 10.1038/s42003-025-07733-5

Figure Lengend Snippet:

Article Snippet: antibody , mouse monoclonal anti-s100β , Synaptic systems Cat #287111 , RRID:AB_2814886 , 1/1000.

Techniques: Virus, shRNA, Software