anti galectin3 gal3 goat polyclonal  (R&D Systems)

Journal: Acta Neuropathologica

Article Title: Galectin-3, a novel endogenous TREM2 ligand, detrimentally regulates inflammatory response in Alzheimer’s disease

doi: 10.1007/s00401-019-02013-z

Figure Lengend Snippet: Galectin-3 is increased in human and mouse AD brains and marks a microglial phenotype associated with Aβ plaques. a Western blot analyses of cortex from human AD cases ( n = 6) and age-matched healthy controls ( n = 5). b Galectin-3 (gal3) staining mainly coincided with Iba1 + microglia found around Aβ plaques in human AD brains. c Immunohistochemistry showed high levels of gal3 in microglia in AD brains, as compared to Iba1-staining (low levels of gal3 was detected in association to blood vessels). d Gal3 protein was significantly upregulated in the cortex of 5xFAD mice in a time-dependent fashion (WT, 6 months old). e Gal3 expression was found in Iba1 + cells around Αβ plaques. Statistical significance was calculated by one-way ANOVA with Tukey’s correction ( d ) or Student’s t test ( a ). *p < 0.05; **p < 0.01. Data are shown as mean ± SD. The human AD cases are described in suppl. Tables S1 and S2 (online resources 8 and 9)

Article Snippet: For single immunolabeling, sections were immunoreacted with one of the following primary antibodies: anti-Aβ42 rabbit polyclonal (1:5000 dilution, Abcam), anti-amyloid precursor protein (APP) rabbit polyclonal (1:20,000 dilution, Sigma), anti-CD45 rat monoclonal (clone IBL-3/16, 1:500 dilution, AbD Serotec), anti-galectin3 (gal3) goat polyclonal (1:3000 dilution, R&D) over 24 or 48 h at room temperature.

Techniques: Western Blot, Staining, Immunohistochemistry, Expressing

Journal: Acta Neuropathologica

Article Title: Galectin-3, a novel endogenous TREM2 ligand, detrimentally regulates inflammatory response in Alzheimer’s disease

doi: 10.1007/s00401-019-02013-z

Figure Lengend Snippet: Galectin-3 deficiency/inhibition reduces the microglial inflammatory response in vitro. a Reduced cytokine levels in culture medium from Gal3KO primary microglial cultures compared to WT after fΑβ treatment for 12 h. b WT primary microglial cultures increase the release of gal3 upon stimulation with fAβ. In vitro experiments represent a minimum of three independent experiments. Statistical significance was calculated by Student’s t-test ( b ), or one-way ANOVA with Tukey’s correction ( a ) *p < 0.05; **p < 0.01; ***p < 0.001. Data are shown as mean ± SD

Article Snippet: For single immunolabeling, sections were immunoreacted with one of the following primary antibodies: anti-Aβ42 rabbit polyclonal (1:5000 dilution, Abcam), anti-amyloid precursor protein (APP) rabbit polyclonal (1:20,000 dilution, Sigma), anti-CD45 rat monoclonal (clone IBL-3/16, 1:500 dilution, AbD Serotec), anti-galectin3 (gal3) goat polyclonal (1:3000 dilution, R&D) over 24 or 48 h at room temperature.

Techniques: Inhibition, In Vitro

Journal: Acta Neuropathologica

Article Title: Galectin-3, a novel endogenous TREM2 ligand, detrimentally regulates inflammatory response in Alzheimer’s disease

doi: 10.1007/s00401-019-02013-z

Figure Lengend Snippet: Galectin-3 colocalizes with TREM2. a , b Iba1 + cells expressing galectin-3 (gal3) around Aβ plaque in 5xFAD mice. c Reduced number of Iba1 + microglial cells around Αβ plaques in 5xFAD/Gal3KO mice compared to 5xFAD mice (% of Αβ area). d Number of Iba1 + cells expressing gal3 in 5xFAD (% of Αβ area). e , f Gal3 and TREM2 in plaque-associated microglia in the brain of 5xFAD mice reveals colocalization of gal3 and TREM2. g Gal3 and TREM2 colocalization in 5xFAD mouse brain using STORM microscopy. Statistical significance was calculated by Student’s t test. *p < 0.05. Data are shown as mean ± SEM. All images were taken in 5xFAD mice at 18 months

Article Snippet: For single immunolabeling, sections were immunoreacted with one of the following primary antibodies: anti-Aβ42 rabbit polyclonal (1:5000 dilution, Abcam), anti-amyloid precursor protein (APP) rabbit polyclonal (1:20,000 dilution, Sigma), anti-CD45 rat monoclonal (clone IBL-3/16, 1:500 dilution, AbD Serotec), anti-galectin3 (gal3) goat polyclonal (1:3000 dilution, R&D) over 24 or 48 h at room temperature.

Techniques: Expressing, Microscopy

Journal: Acta Neuropathologica

Article Title: Galectin-3, a novel endogenous TREM2 ligand, detrimentally regulates inflammatory response in Alzheimer’s disease

doi: 10.1007/s00401-019-02013-z

Figure Lengend Snippet: Galectin-3 interacts with TREM2 through its carbohydrate-binding domain. a Fluorescent anisotropy assay for galectin-3 (gal3)/TREM2 interaction. Data are presented as % of TREM2–gal3 binding (gal3, WT and mutant gal3 with deficient carbohydrate-binding domain, R186S) and fluorescent probe interaction, by increasing concentrations of TREM2, together with the calculated K d values for the gal3/TREM2 interaction ( n = 2). b Control and DAP12 reporter cell lines were stimulated with increasing concentrations of gal3 (250 nM–2.5 µM), ionomycin and phosphatidylserine (PS). Statistical significance was calculated by Student’s t test or one-way ANOVA with Bonferroni’s post hoc test. *p < 0.05; **p < 0.01. Data are shown as mean ± SD

Article Snippet: For single immunolabeling, sections were immunoreacted with one of the following primary antibodies: anti-Aβ42 rabbit polyclonal (1:5000 dilution, Abcam), anti-amyloid precursor protein (APP) rabbit polyclonal (1:20,000 dilution, Sigma), anti-CD45 rat monoclonal (clone IBL-3/16, 1:500 dilution, AbD Serotec), anti-galectin3 (gal3) goat polyclonal (1:3000 dilution, R&D) over 24 or 48 h at room temperature.

Techniques: Binding Assay, Mutagenesis

Journal: Acta Neuropathologica

Article Title: Galectin-3, a novel endogenous TREM2 ligand, detrimentally regulates inflammatory response in Alzheimer’s disease

doi: 10.1007/s00401-019-02013-z

Figure Lengend Snippet: Galectin-3 induces the formation of insoluble Αβ aggregates following injections of Αβ monomers in the hippocampi of WT mice. Αβ monomers were injected with galectin-3 (Gal3) (Aβ + Gal3) or without (Aβ) after 1 h Aβ monomers incubation w/o gal3 into the right or left hippocampi of WT mice, respectively. a Staining for Αβ and gal3 in the left hippocampus (only Aβ monomers injected). b , c Staining for Αβ and gal3 in the right hippocampus (Aβ + gal3 injected). Dashed frames in b are magnified and shown in c . d Thioflavin-S and Αβ staining of the left hippocampus (only Aβ injected). e Thioflavin-S and Αβ staining of the right hippocampus (Aβ + gal3 injected). White arrows point to gal3 and thioflavin-S + aggregates. f , g Iba1 and GFAP immunoreactivity in the right hippocampus (Αβ + gal3 were injected)

Article Snippet: For single immunolabeling, sections were immunoreacted with one of the following primary antibodies: anti-Aβ42 rabbit polyclonal (1:5000 dilution, Abcam), anti-amyloid precursor protein (APP) rabbit polyclonal (1:20,000 dilution, Sigma), anti-CD45 rat monoclonal (clone IBL-3/16, 1:500 dilution, AbD Serotec), anti-galectin3 (gal3) goat polyclonal (1:3000 dilution, R&D) over 24 or 48 h at room temperature.

Techniques: Injection, Incubation, Staining