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Galectin Therapeutics galectin 3 positive puncta
Galectin 3 Positive Puncta, supplied by Galectin Therapeutics, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/galectin-3+puncta/10__1097_slash_hep__0000000000001718-178-12-12
Average 86 stars, based on 1 article reviews
galectin 3 positive puncta - by Bioz Stars, 2026-09
86/100 stars

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Related Articles

Staining:

Article Title: Staphylococcal toxin PVL ruptures model membranes under acidic conditions through interactions with cardiolipin and phosphatidic acid.
Article Snippet: Cells containing Galectin-3 puncta (% Gal3 puncta) were quantified from >50 individual cells per experiments.

Article Title: Intraneuronal Aβ accumulation causes tau hyperphosphorylation via endolysosomal leakage
Article Snippet: Galectin-3 puncta was present in neurons with abnormal Tau phosphorylation (AT8).

Article Title: The TECPR1:ATG5-ATG12 complex conjugates LC3/ATG8 to damaged lysosomes that expose luminal glycans in response to osmotic imbalance.
Article Snippet: The TECPR1-∆LIR mutant was not recruited to galectin-3 puncta (Figure 11B iv-vi).

Article Title: Proteostasis and lysosomal repair deficits in transdifferentiated neurons of Alzheimer's disease.
Article Snippet: Nature Cell Biology Extended Data Fig. 7 | Abnormal lysosomal damage response links to defective organelle and calcium homeostasis in aged/sAD and fAD-PSEN1 tNeurons. (a) Quantification of numbers of ESCRT-III CHMP2B and Galectin-3 puncta in the cell body of young, aged/sAD and fAD-PSEN1 tNeurons in the absence of lysosomal damage insults. tNeurons: CHMP2B: n = 117 (young), 97 (aged/sAD) and 104 (fAD-PSEN1) cells; Galectin-3: n = 111 (young), 95 (aged/sAD) and 104 (fAD-PSEN1) cells. (b) Quantification of numbers of ESCRT-0 HGS puncta in the cell body of young, aged/sAD and fAD-PSEN1 tNeurons during lysosomal damage insults mediated by LLOME treatment, and recovery from lysosomal damage after LLOME washout for up to 8 hr.

Article Title: Proteostasis and lysosomal repair deficits in transdifferentiated neurons of Alzheimer’s disease
Article Snippet: Extended Data Fig. 7 Abnormal lysosomal damage response links to defective organelle and calcium homeostasis in aged/sAD and fAD-PSEN1 tNeurons. ( a ) Quantification of numbers of ESCRT-III CHMP2B and Galectin-3 puncta in the cell body of young, aged/sAD and fAD-PSEN1 tNeurons in the absence of lysosomal damage insults. tNeurons: CHMP2B: n = 117 (young), 97 (aged/sAD) and 104 (fAD-PSEN1) cells; Galectin-3: n = 111 (young), 95 (aged/sAD) and 104 (fAD-PSEN1) cells. ( b ) Quantification of numbers of ESCRT-0 HGS puncta in the cell body of young, aged/sAD and fAD-PSEN1 tNeurons during lysosomal damage insults mediated by LLOME treatment, and recovery from lysosomal damage after LLOME washout for up to 8 hr.

Article Title: Proteostasis and lysosomal repair deficits in transdifferentiated neurons of Alzheimer's disease.
Article Snippet: Numbers of CHMP2B and galectin-3 puncta (immunofluorescence quantification) in the cell body of tNeurons (right).

Article Title: Glucosylated cholesterol accumulates in atherosclerotic lesions and impacts macrophage immune response.
Article Snippet: In agreement with these results, we also did not find any signs of damage to the lysosomal membrane (Galectin-3 puncta) at the time point studied (data not shown).


Marker:

Article Title: Staphylococcal toxin PVL ruptures model membranes under acidic conditions through interactions with cardiolipin and phosphatidic acid.
Article Snippet: Cells containing Galectin-3 puncta (% Gal3 puncta) were quantified from >50 individual cells per experiments.

Article Title: Intraneuronal Aβ accumulation causes tau hyperphosphorylation via endolysosomal leakage
Article Snippet: Galectin-3 puncta was present in neurons with abnormal Tau phosphorylation (AT8).

Article Title: The TECPR1:ATG5-ATG12 complex conjugates LC3/ATG8 to damaged lysosomes that expose luminal glycans in response to osmotic imbalance.
Article Snippet: The TECPR1-∆LIR mutant was not recruited to galectin-3 puncta (Figure 11B iv-vi).

Article Title: Proteostasis and lysosomal repair deficits in transdifferentiated neurons of Alzheimer's disease.
Article Snippet: Nature Cell Biology Extended Data Fig. 7 | Abnormal lysosomal damage response links to defective organelle and calcium homeostasis in aged/sAD and fAD-PSEN1 tNeurons. (a) Quantification of numbers of ESCRT-III CHMP2B and Galectin-3 puncta in the cell body of young, aged/sAD and fAD-PSEN1 tNeurons in the absence of lysosomal damage insults. tNeurons: CHMP2B: n = 117 (young), 97 (aged/sAD) and 104 (fAD-PSEN1) cells; Galectin-3: n = 111 (young), 95 (aged/sAD) and 104 (fAD-PSEN1) cells. (b) Quantification of numbers of ESCRT-0 HGS puncta in the cell body of young, aged/sAD and fAD-PSEN1 tNeurons during lysosomal damage insults mediated by LLOME treatment, and recovery from lysosomal damage after LLOME washout for up to 8 hr.

Article Title: Proteostasis and lysosomal repair deficits in transdifferentiated neurons of Alzheimer’s disease
Article Snippet: Extended Data Fig. 7 Abnormal lysosomal damage response links to defective organelle and calcium homeostasis in aged/sAD and fAD-PSEN1 tNeurons. ( a ) Quantification of numbers of ESCRT-III CHMP2B and Galectin-3 puncta in the cell body of young, aged/sAD and fAD-PSEN1 tNeurons in the absence of lysosomal damage insults. tNeurons: CHMP2B: n = 117 (young), 97 (aged/sAD) and 104 (fAD-PSEN1) cells; Galectin-3: n = 111 (young), 95 (aged/sAD) and 104 (fAD-PSEN1) cells. ( b ) Quantification of numbers of ESCRT-0 HGS puncta in the cell body of young, aged/sAD and fAD-PSEN1 tNeurons during lysosomal damage insults mediated by LLOME treatment, and recovery from lysosomal damage after LLOME washout for up to 8 hr.

Article Title: Proteostasis and lysosomal repair deficits in transdifferentiated neurons of Alzheimer's disease.
Article Snippet: Numbers of CHMP2B and galectin-3 puncta (immunofluorescence quantification) in the cell body of tNeurons (right).

Article Title: Glucosylated cholesterol accumulates in atherosclerotic lesions and impacts macrophage immune response.
Article Snippet: In agreement with these results, we also did not find any signs of damage to the lysosomal membrane (Galectin-3 puncta) at the time point studied (data not shown).


Microscopy:

Article Title: Staphylococcal toxin PVL ruptures model membranes under acidic conditions through interactions with cardiolipin and phosphatidic acid.
Article Snippet: Cells containing Galectin-3 puncta (% Gal3 puncta) were quantified from >50 individual cells per experiments.

Article Title: Intraneuronal Aβ accumulation causes tau hyperphosphorylation via endolysosomal leakage
Article Snippet: Galectin-3 puncta was present in neurons with abnormal Tau phosphorylation (AT8).

Article Title: The TECPR1:ATG5-ATG12 complex conjugates LC3/ATG8 to damaged lysosomes that expose luminal glycans in response to osmotic imbalance.
Article Snippet: The TECPR1-∆LIR mutant was not recruited to galectin-3 puncta (Figure 11B iv-vi).

Article Title: Proteostasis and lysosomal repair deficits in transdifferentiated neurons of Alzheimer's disease.
Article Snippet: Nature Cell Biology Extended Data Fig. 7 | Abnormal lysosomal damage response links to defective organelle and calcium homeostasis in aged/sAD and fAD-PSEN1 tNeurons. (a) Quantification of numbers of ESCRT-III CHMP2B and Galectin-3 puncta in the cell body of young, aged/sAD and fAD-PSEN1 tNeurons in the absence of lysosomal damage insults. tNeurons: CHMP2B: n = 117 (young), 97 (aged/sAD) and 104 (fAD-PSEN1) cells; Galectin-3: n = 111 (young), 95 (aged/sAD) and 104 (fAD-PSEN1) cells. (b) Quantification of numbers of ESCRT-0 HGS puncta in the cell body of young, aged/sAD and fAD-PSEN1 tNeurons during lysosomal damage insults mediated by LLOME treatment, and recovery from lysosomal damage after LLOME washout for up to 8 hr.

Article Title: Proteostasis and lysosomal repair deficits in transdifferentiated neurons of Alzheimer’s disease
Article Snippet: Extended Data Fig. 7 Abnormal lysosomal damage response links to defective organelle and calcium homeostasis in aged/sAD and fAD-PSEN1 tNeurons. ( a ) Quantification of numbers of ESCRT-III CHMP2B and Galectin-3 puncta in the cell body of young, aged/sAD and fAD-PSEN1 tNeurons in the absence of lysosomal damage insults. tNeurons: CHMP2B: n = 117 (young), 97 (aged/sAD) and 104 (fAD-PSEN1) cells; Galectin-3: n = 111 (young), 95 (aged/sAD) and 104 (fAD-PSEN1) cells. ( b ) Quantification of numbers of ESCRT-0 HGS puncta in the cell body of young, aged/sAD and fAD-PSEN1 tNeurons during lysosomal damage insults mediated by LLOME treatment, and recovery from lysosomal damage after LLOME washout for up to 8 hr.

Article Title: Proteostasis and lysosomal repair deficits in transdifferentiated neurons of Alzheimer's disease.
Article Snippet: Numbers of CHMP2B and galectin-3 puncta (immunofluorescence quantification) in the cell body of tNeurons (right).

Article Title: Glucosylated cholesterol accumulates in atherosclerotic lesions and impacts macrophage immune response.
Article Snippet: In agreement with these results, we also did not find any signs of damage to the lysosomal membrane (Galectin-3 puncta) at the time point studied (data not shown).


Clone Assay:

Article Title: Staphylococcal toxin PVL ruptures model membranes under acidic conditions through interactions with cardiolipin and phosphatidic acid.
Article Snippet: Cells containing Galectin-3 puncta (% Gal3 puncta) were quantified from >50 individual cells per experiments.

Article Title: Intraneuronal Aβ accumulation causes tau hyperphosphorylation via endolysosomal leakage
Article Snippet: Galectin-3 puncta was present in neurons with abnormal Tau phosphorylation (AT8).

Article Title: The TECPR1:ATG5-ATG12 complex conjugates LC3/ATG8 to damaged lysosomes that expose luminal glycans in response to osmotic imbalance.
Article Snippet: The TECPR1-∆LIR mutant was not recruited to galectin-3 puncta (Figure 11B iv-vi).

Article Title: Proteostasis and lysosomal repair deficits in transdifferentiated neurons of Alzheimer's disease.
Article Snippet: Nature Cell Biology Extended Data Fig. 7 | Abnormal lysosomal damage response links to defective organelle and calcium homeostasis in aged/sAD and fAD-PSEN1 tNeurons. (a) Quantification of numbers of ESCRT-III CHMP2B and Galectin-3 puncta in the cell body of young, aged/sAD and fAD-PSEN1 tNeurons in the absence of lysosomal damage insults. tNeurons: CHMP2B: n = 117 (young), 97 (aged/sAD) and 104 (fAD-PSEN1) cells; Galectin-3: n = 111 (young), 95 (aged/sAD) and 104 (fAD-PSEN1) cells. (b) Quantification of numbers of ESCRT-0 HGS puncta in the cell body of young, aged/sAD and fAD-PSEN1 tNeurons during lysosomal damage insults mediated by LLOME treatment, and recovery from lysosomal damage after LLOME washout for up to 8 hr.

Article Title: Proteostasis and lysosomal repair deficits in transdifferentiated neurons of Alzheimer’s disease
Article Snippet: Extended Data Fig. 7 Abnormal lysosomal damage response links to defective organelle and calcium homeostasis in aged/sAD and fAD-PSEN1 tNeurons. ( a ) Quantification of numbers of ESCRT-III CHMP2B and Galectin-3 puncta in the cell body of young, aged/sAD and fAD-PSEN1 tNeurons in the absence of lysosomal damage insults. tNeurons: CHMP2B: n = 117 (young), 97 (aged/sAD) and 104 (fAD-PSEN1) cells; Galectin-3: n = 111 (young), 95 (aged/sAD) and 104 (fAD-PSEN1) cells. ( b ) Quantification of numbers of ESCRT-0 HGS puncta in the cell body of young, aged/sAD and fAD-PSEN1 tNeurons during lysosomal damage insults mediated by LLOME treatment, and recovery from lysosomal damage after LLOME washout for up to 8 hr.

Article Title: Proteostasis and lysosomal repair deficits in transdifferentiated neurons of Alzheimer's disease.
Article Snippet: Numbers of CHMP2B and galectin-3 puncta (immunofluorescence quantification) in the cell body of tNeurons (right).

Article Title: Glucosylated cholesterol accumulates in atherosclerotic lesions and impacts macrophage immune response.
Article Snippet: In agreement with these results, we also did not find any signs of damage to the lysosomal membrane (Galectin-3 puncta) at the time point studied (data not shown).


Immunofluorescence:

Article Title: Staphylococcal toxin PVL ruptures model membranes under acidic conditions through interactions with cardiolipin and phosphatidic acid.
Article Snippet: Cells containing Galectin-3 puncta (% Gal3 puncta) were quantified from >50 individual cells per experiments.

Article Title: Intraneuronal Aβ accumulation causes tau hyperphosphorylation via endolysosomal leakage
Article Snippet: Galectin-3 puncta was present in neurons with abnormal Tau phosphorylation (AT8).

Article Title: The TECPR1:ATG5-ATG12 complex conjugates LC3/ATG8 to damaged lysosomes that expose luminal glycans in response to osmotic imbalance.
Article Snippet: The TECPR1-∆LIR mutant was not recruited to galectin-3 puncta (Figure 11B iv-vi).

Article Title: Proteostasis and lysosomal repair deficits in transdifferentiated neurons of Alzheimer's disease.
Article Snippet: Nature Cell Biology Extended Data Fig. 7 | Abnormal lysosomal damage response links to defective organelle and calcium homeostasis in aged/sAD and fAD-PSEN1 tNeurons. (a) Quantification of numbers of ESCRT-III CHMP2B and Galectin-3 puncta in the cell body of young, aged/sAD and fAD-PSEN1 tNeurons in the absence of lysosomal damage insults. tNeurons: CHMP2B: n = 117 (young), 97 (aged/sAD) and 104 (fAD-PSEN1) cells; Galectin-3: n = 111 (young), 95 (aged/sAD) and 104 (fAD-PSEN1) cells. (b) Quantification of numbers of ESCRT-0 HGS puncta in the cell body of young, aged/sAD and fAD-PSEN1 tNeurons during lysosomal damage insults mediated by LLOME treatment, and recovery from lysosomal damage after LLOME washout for up to 8 hr.

Article Title: Proteostasis and lysosomal repair deficits in transdifferentiated neurons of Alzheimer’s disease
Article Snippet: Extended Data Fig. 7 Abnormal lysosomal damage response links to defective organelle and calcium homeostasis in aged/sAD and fAD-PSEN1 tNeurons. ( a ) Quantification of numbers of ESCRT-III CHMP2B and Galectin-3 puncta in the cell body of young, aged/sAD and fAD-PSEN1 tNeurons in the absence of lysosomal damage insults. tNeurons: CHMP2B: n = 117 (young), 97 (aged/sAD) and 104 (fAD-PSEN1) cells; Galectin-3: n = 111 (young), 95 (aged/sAD) and 104 (fAD-PSEN1) cells. ( b ) Quantification of numbers of ESCRT-0 HGS puncta in the cell body of young, aged/sAD and fAD-PSEN1 tNeurons during lysosomal damage insults mediated by LLOME treatment, and recovery from lysosomal damage after LLOME washout for up to 8 hr.

Article Title: Proteostasis and lysosomal repair deficits in transdifferentiated neurons of Alzheimer's disease.
Article Snippet: Numbers of CHMP2B and galectin-3 puncta (immunofluorescence quantification) in the cell body of tNeurons (right).

Article Title: Glucosylated cholesterol accumulates in atherosclerotic lesions and impacts macrophage immune response.
Article Snippet: In agreement with these results, we also did not find any signs of damage to the lysosomal membrane (Galectin-3 puncta) at the time point studied (data not shown).


Activation Assay:

Article Title: Staphylococcal toxin PVL ruptures model membranes under acidic conditions through interactions with cardiolipin and phosphatidic acid.
Article Snippet: Cells containing Galectin-3 puncta (% Gal3 puncta) were quantified from >50 individual cells per experiments.

Article Title: Intraneuronal Aβ accumulation causes tau hyperphosphorylation via endolysosomal leakage
Article Snippet: Galectin-3 puncta was present in neurons with abnormal Tau phosphorylation (AT8).

Article Title: The TECPR1:ATG5-ATG12 complex conjugates LC3/ATG8 to damaged lysosomes that expose luminal glycans in response to osmotic imbalance.
Article Snippet: The TECPR1-∆LIR mutant was not recruited to galectin-3 puncta (Figure 11B iv-vi).

Article Title: Proteostasis and lysosomal repair deficits in transdifferentiated neurons of Alzheimer's disease.
Article Snippet: Nature Cell Biology Extended Data Fig. 7 | Abnormal lysosomal damage response links to defective organelle and calcium homeostasis in aged/sAD and fAD-PSEN1 tNeurons. (a) Quantification of numbers of ESCRT-III CHMP2B and Galectin-3 puncta in the cell body of young, aged/sAD and fAD-PSEN1 tNeurons in the absence of lysosomal damage insults. tNeurons: CHMP2B: n = 117 (young), 97 (aged/sAD) and 104 (fAD-PSEN1) cells; Galectin-3: n = 111 (young), 95 (aged/sAD) and 104 (fAD-PSEN1) cells. (b) Quantification of numbers of ESCRT-0 HGS puncta in the cell body of young, aged/sAD and fAD-PSEN1 tNeurons during lysosomal damage insults mediated by LLOME treatment, and recovery from lysosomal damage after LLOME washout for up to 8 hr.

Article Title: Proteostasis and lysosomal repair deficits in transdifferentiated neurons of Alzheimer’s disease
Article Snippet: Extended Data Fig. 7 Abnormal lysosomal damage response links to defective organelle and calcium homeostasis in aged/sAD and fAD-PSEN1 tNeurons. ( a ) Quantification of numbers of ESCRT-III CHMP2B and Galectin-3 puncta in the cell body of young, aged/sAD and fAD-PSEN1 tNeurons in the absence of lysosomal damage insults. tNeurons: CHMP2B: n = 117 (young), 97 (aged/sAD) and 104 (fAD-PSEN1) cells; Galectin-3: n = 111 (young), 95 (aged/sAD) and 104 (fAD-PSEN1) cells. ( b ) Quantification of numbers of ESCRT-0 HGS puncta in the cell body of young, aged/sAD and fAD-PSEN1 tNeurons during lysosomal damage insults mediated by LLOME treatment, and recovery from lysosomal damage after LLOME washout for up to 8 hr.

Article Title: Proteostasis and lysosomal repair deficits in transdifferentiated neurons of Alzheimer's disease.
Article Snippet: Numbers of CHMP2B and galectin-3 puncta (immunofluorescence quantification) in the cell body of tNeurons (right).

Article Title: Glucosylated cholesterol accumulates in atherosclerotic lesions and impacts macrophage immune response.
Article Snippet: In agreement with these results, we also did not find any signs of damage to the lysosomal membrane (Galectin-3 puncta) at the time point studied (data not shown).




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