biotinylated lectins Search Results


biotin mal ii  (Vector Laboratories)
96
Vector Laboratories biotin mal ii
α2,3-sialylation is required for BCG-induced osteoclast differentiation and activity (A) Comparison of differentially expressed genes (DEGs) between BCG-infected osteoclasts (RB) and uninfected controls (R). (n = 3 biological replicates per group, differential expression was defined as |FoldChange| > 2 and padj <0.05). (B) Volcano plot of DEGs highlighting genes related to sialic acid biosynthesis. (C) KEGG pathway enrichment analysis of upregulated DEGs in RB cells. (D,E) Immunofluorescence staining of α2,3-SA in mouse calvarial sections <t>using</t> <t>MAL</t> <t>II</t> lectin, with quantification of α2,3-SA fluorescence intensity (n = 5). Intensity density was normalized to the PBS group mean. (F) In vitro osteoclasts subjected to MAL II lectin staining and TRAP staining, with or without sialidase treatment to enzymatically remove α2,3-SA. (G) Quantification of α2,3-SA fluorescence intensity in cultured osteoclasts (n = 5). Intensity density was measured in cellular ROIs after background subtraction and normalized to the RANKL group mean. (H) Quantification of TRAP + multinucleated cells (≥3 nuclei) per field (randomly selected fields, fixed magnification) in vitro (n = 5). (I) mRNA expression levels of osteoclast differentiation markers ( Fos, Mmp9, Nfatc1, and Ocstamp ) in osteoclasts (n = 3). Data are presented as mean ± SD. Statistical significance was determined by two-tailed unpaired Student’s t-test for two-group comparisons (E) and one-way ANOVA followed by Tukey’s post hoc test for three-group comparisons (G–I) .
Biotin Mal Ii, supplied by Vector Laboratories, used in various techniques. Bioz Stars score: 96/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/biotinylated+lectins/Biotinylated+Maackia+Amurensis+Lectin+II+(MAL+II)/pmc13084157-4-0-3
Average 96 stars, based on 1 article reviews
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biotinylated wisteria floribunda agglutinin  (Vector Laboratories)
96
Vector Laboratories biotinylated wisteria floribunda agglutinin
Neonatal sevoflurane exposure induces PNNs damage in the hippocampus. (A) Schematic of the experimental protocol for hippocampal extracellular matrix (ECM) analyses. (B) Representative scanning electron micrographs (SEM) of hippocampal ECM ultrastructure in Con and Sev ‑treated groups. Scale bars = 5 µm (5K×), 1.2 µm (20K×), and 500 nm (50K×). (C) Quantification of mean gray value (left) and fiber diameter (right) of hippocampal ECM in Con and Sev groups. (D, E) Wisteria <t>floribunda</t> <t>agglutinin</t> (WFA) staining and quantitative analysis of PNN intensity in the CA2 region at 7, 14, 30, and 60 days post‐exposure (dpe). Scale bar = 50 µm. (F, G) Western blotting and quantification of hapln1 and aggrecan protein levels in the hippocampus of Con and Sev groups. (H, I) Immunofluorescence staining and quantitative analysis of aggrecan in the hippocampus of Con and Sev groups at 60 dpe. Green: aggrecan. Blue: DAPI. Scale bar = 50 µm. (J–M) PNNs in the Con group exhibit bright, well‐organized mesh‐like architecture, whereas PNNs in the Sev group display reduced WFA intensity and a disrupted staining pattern. (J) Representative WFA staining. Purple: WFA. Scale bar = 10 µm. (K) Binary images of the regions in (J). (L) Quantification of black/white pixel ratio. (M) Representative surface intensity profiles of WFA‐positive PNNs. (N) Immunoelectron microscopy of PNNs in the Con and Sev groups. High‐magnification images (right panels) display immunogold labeling within WFA (red arrows) in both groups. Scale bars = 1 µm (left), 500 nm (right). Data represent the mean ± SEM. n = 3 mice per group for SEM (B, C, J–N); n = 6 mice per group for all other experiments. Statistical comparisons were conducted using unpaired Student's t‐test. ∗∗ p < 0.01, ∗∗∗ p < 0.001, ∗∗∗∗ P < 0.0001.
Biotinylated Wisteria Floribunda Agglutinin, supplied by Vector Laboratories, used in various techniques. Bioz Stars score: 96/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/biotinylated+lectins/Biotinylated+Wisteria+Floribunda+Lectin+(WFA%2C+WFL)/pmc13624421-299-26-31
Average 96 stars, based on 1 article reviews
biotinylated wisteria floribunda agglutinin - by Bioz Stars, 2026-10
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biotinylated erythrina cristagalli lectin  (Vector Laboratories)
95
Vector Laboratories biotinylated erythrina cristagalli lectin
Neonatal sevoflurane exposure induces PNNs damage in the hippocampus. (A) Schematic of the experimental protocol for hippocampal extracellular matrix (ECM) analyses. (B) Representative scanning electron micrographs (SEM) of hippocampal ECM ultrastructure in Con and Sev ‑treated groups. Scale bars = 5 µm (5K×), 1.2 µm (20K×), and 500 nm (50K×). (C) Quantification of mean gray value (left) and fiber diameter (right) of hippocampal ECM in Con and Sev groups. (D, E) Wisteria <t>floribunda</t> <t>agglutinin</t> (WFA) staining and quantitative analysis of PNN intensity in the CA2 region at 7, 14, 30, and 60 days post‐exposure (dpe). Scale bar = 50 µm. (F, G) Western blotting and quantification of hapln1 and aggrecan protein levels in the hippocampus of Con and Sev groups. (H, I) Immunofluorescence staining and quantitative analysis of aggrecan in the hippocampus of Con and Sev groups at 60 dpe. Green: aggrecan. Blue: DAPI. Scale bar = 50 µm. (J–M) PNNs in the Con group exhibit bright, well‐organized mesh‐like architecture, whereas PNNs in the Sev group display reduced WFA intensity and a disrupted staining pattern. (J) Representative WFA staining. Purple: WFA. Scale bar = 10 µm. (K) Binary images of the regions in (J). (L) Quantification of black/white pixel ratio. (M) Representative surface intensity profiles of WFA‐positive PNNs. (N) Immunoelectron microscopy of PNNs in the Con and Sev groups. High‐magnification images (right panels) display immunogold labeling within WFA (red arrows) in both groups. Scale bars = 1 µm (left), 500 nm (right). Data represent the mean ± SEM. n = 3 mice per group for SEM (B, C, J–N); n = 6 mice per group for all other experiments. Statistical comparisons were conducted using unpaired Student's t‐test. ∗∗ p < 0.01, ∗∗∗ p < 0.001, ∗∗∗∗ P < 0.0001.
Biotinylated Erythrina Cristagalli Lectin, supplied by Vector Laboratories, used in various techniques. Bioz Stars score: 95/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/biotinylated+lectins/Biotinylated+Erythrina+Cristagalli+Lectin+(ECL%2C+ECA)/10__1038_slash_s41598___026___71900___9-103-33-39
Average 95 stars, based on 1 article reviews
biotinylated erythrina cristagalli lectin - by Bioz Stars, 2026-10
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marker isolectin b4  (Vector Laboratories)
95
Vector Laboratories marker isolectin b4
Neonatal sevoflurane exposure induces PNNs damage in the hippocampus. (A) Schematic of the experimental protocol for hippocampal extracellular matrix (ECM) analyses. (B) Representative scanning electron micrographs (SEM) of hippocampal ECM ultrastructure in Con and Sev ‑treated groups. Scale bars = 5 µm (5K×), 1.2 µm (20K×), and 500 nm (50K×). (C) Quantification of mean gray value (left) and fiber diameter (right) of hippocampal ECM in Con and Sev groups. (D, E) Wisteria <t>floribunda</t> <t>agglutinin</t> (WFA) staining and quantitative analysis of PNN intensity in the CA2 region at 7, 14, 30, and 60 days post‐exposure (dpe). Scale bar = 50 µm. (F, G) Western blotting and quantification of hapln1 and aggrecan protein levels in the hippocampus of Con and Sev groups. (H, I) Immunofluorescence staining and quantitative analysis of aggrecan in the hippocampus of Con and Sev groups at 60 dpe. Green: aggrecan. Blue: DAPI. Scale bar = 50 µm. (J–M) PNNs in the Con group exhibit bright, well‐organized mesh‐like architecture, whereas PNNs in the Sev group display reduced WFA intensity and a disrupted staining pattern. (J) Representative WFA staining. Purple: WFA. Scale bar = 10 µm. (K) Binary images of the regions in (J). (L) Quantification of black/white pixel ratio. (M) Representative surface intensity profiles of WFA‐positive PNNs. (N) Immunoelectron microscopy of PNNs in the Con and Sev groups. High‐magnification images (right panels) display immunogold labeling within WFA (red arrows) in both groups. Scale bars = 1 µm (left), 500 nm (right). Data represent the mean ± SEM. n = 3 mice per group for SEM (B, C, J–N); n = 6 mice per group for all other experiments. Statistical comparisons were conducted using unpaired Student's t‐test. ∗∗ p < 0.01, ∗∗∗ p < 0.001, ∗∗∗∗ P < 0.0001.
Marker Isolectin B4, supplied by Vector Laboratories, used in various techniques. Bioz Stars score: 95/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/biotinylated+lectins/Biotinylated+Griffonia+Simplicifolia+Lectin+I+(GSL+I)+isolectin+B4/pmc13133793-44-48-54
Average 95 stars, based on 1 article reviews
marker isolectin b4 - by Bioz Stars, 2026-10
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biotinylated tomato lectin  (Vector Laboratories)
95
Vector Laboratories biotinylated tomato lectin
Neonatal sevoflurane exposure induces PNNs damage in the hippocampus. (A) Schematic of the experimental protocol for hippocampal extracellular matrix (ECM) analyses. (B) Representative scanning electron micrographs (SEM) of hippocampal ECM ultrastructure in Con and Sev ‑treated groups. Scale bars = 5 µm (5K×), 1.2 µm (20K×), and 500 nm (50K×). (C) Quantification of mean gray value (left) and fiber diameter (right) of hippocampal ECM in Con and Sev groups. (D, E) Wisteria <t>floribunda</t> <t>agglutinin</t> (WFA) staining and quantitative analysis of PNN intensity in the CA2 region at 7, 14, 30, and 60 days post‐exposure (dpe). Scale bar = 50 µm. (F, G) Western blotting and quantification of hapln1 and aggrecan protein levels in the hippocampus of Con and Sev groups. (H, I) Immunofluorescence staining and quantitative analysis of aggrecan in the hippocampus of Con and Sev groups at 60 dpe. Green: aggrecan. Blue: DAPI. Scale bar = 50 µm. (J–M) PNNs in the Con group exhibit bright, well‐organized mesh‐like architecture, whereas PNNs in the Sev group display reduced WFA intensity and a disrupted staining pattern. (J) Representative WFA staining. Purple: WFA. Scale bar = 10 µm. (K) Binary images of the regions in (J). (L) Quantification of black/white pixel ratio. (M) Representative surface intensity profiles of WFA‐positive PNNs. (N) Immunoelectron microscopy of PNNs in the Con and Sev groups. High‐magnification images (right panels) display immunogold labeling within WFA (red arrows) in both groups. Scale bars = 1 µm (left), 500 nm (right). Data represent the mean ± SEM. n = 3 mice per group for SEM (B, C, J–N); n = 6 mice per group for all other experiments. Statistical comparisons were conducted using unpaired Student's t‐test. ∗∗ p < 0.01, ∗∗∗ p < 0.001, ∗∗∗∗ P < 0.0001.
Biotinylated Tomato Lectin, supplied by Vector Laboratories, used in various techniques. Bioz Stars score: 95/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/biotinylated+lectins/Biotinylated+Lycopersicon+Esculentum+(Tomato)+Lectin+(LEL%2C+TL)/pmc13005877-46-9-16
Average 95 stars, based on 1 article reviews
biotinylated tomato lectin - by Bioz Stars, 2026-10
95/100 stars
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biotinylated gsl i  (Vector Laboratories)
94
Vector Laboratories biotinylated gsl i
Neonatal sevoflurane exposure induces PNNs damage in the hippocampus. (A) Schematic of the experimental protocol for hippocampal extracellular matrix (ECM) analyses. (B) Representative scanning electron micrographs (SEM) of hippocampal ECM ultrastructure in Con and Sev ‑treated groups. Scale bars = 5 µm (5K×), 1.2 µm (20K×), and 500 nm (50K×). (C) Quantification of mean gray value (left) and fiber diameter (right) of hippocampal ECM in Con and Sev groups. (D, E) Wisteria <t>floribunda</t> <t>agglutinin</t> (WFA) staining and quantitative analysis of PNN intensity in the CA2 region at 7, 14, 30, and 60 days post‐exposure (dpe). Scale bar = 50 µm. (F, G) Western blotting and quantification of hapln1 and aggrecan protein levels in the hippocampus of Con and Sev groups. (H, I) Immunofluorescence staining and quantitative analysis of aggrecan in the hippocampus of Con and Sev groups at 60 dpe. Green: aggrecan. Blue: DAPI. Scale bar = 50 µm. (J–M) PNNs in the Con group exhibit bright, well‐organized mesh‐like architecture, whereas PNNs in the Sev group display reduced WFA intensity and a disrupted staining pattern. (J) Representative WFA staining. Purple: WFA. Scale bar = 10 µm. (K) Binary images of the regions in (J). (L) Quantification of black/white pixel ratio. (M) Representative surface intensity profiles of WFA‐positive PNNs. (N) Immunoelectron microscopy of PNNs in the Con and Sev groups. High‐magnification images (right panels) display immunogold labeling within WFA (red arrows) in both groups. Scale bars = 1 µm (left), 500 nm (right). Data represent the mean ± SEM. n = 3 mice per group for SEM (B, C, J–N); n = 6 mice per group for all other experiments. Statistical comparisons were conducted using unpaired Student's t‐test. ∗∗ p < 0.01, ∗∗∗ p < 0.001, ∗∗∗∗ P < 0.0001.
Biotinylated Gsl I, supplied by Vector Laboratories, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/biotinylated+lectins/Biotinylated+Griffonia+(Bandeiraea)+Simplicifolia+Lectin+I+(GSL+I%2C+BSL+I)/pm36156798-63-12-29
Average 94 stars, based on 1 article reviews
biotinylated gsl i - by Bioz Stars, 2026-10
94/100 stars
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ltl  (Vector Laboratories)
96
Vector Laboratories ltl
Neonatal sevoflurane exposure induces PNNs damage in the hippocampus. (A) Schematic of the experimental protocol for hippocampal extracellular matrix (ECM) analyses. (B) Representative scanning electron micrographs (SEM) of hippocampal ECM ultrastructure in Con and Sev ‑treated groups. Scale bars = 5 µm (5K×), 1.2 µm (20K×), and 500 nm (50K×). (C) Quantification of mean gray value (left) and fiber diameter (right) of hippocampal ECM in Con and Sev groups. (D, E) Wisteria <t>floribunda</t> <t>agglutinin</t> (WFA) staining and quantitative analysis of PNN intensity in the CA2 region at 7, 14, 30, and 60 days post‐exposure (dpe). Scale bar = 50 µm. (F, G) Western blotting and quantification of hapln1 and aggrecan protein levels in the hippocampus of Con and Sev groups. (H, I) Immunofluorescence staining and quantitative analysis of aggrecan in the hippocampus of Con and Sev groups at 60 dpe. Green: aggrecan. Blue: DAPI. Scale bar = 50 µm. (J–M) PNNs in the Con group exhibit bright, well‐organized mesh‐like architecture, whereas PNNs in the Sev group display reduced WFA intensity and a disrupted staining pattern. (J) Representative WFA staining. Purple: WFA. Scale bar = 10 µm. (K) Binary images of the regions in (J). (L) Quantification of black/white pixel ratio. (M) Representative surface intensity profiles of WFA‐positive PNNs. (N) Immunoelectron microscopy of PNNs in the Con and Sev groups. High‐magnification images (right panels) display immunogold labeling within WFA (red arrows) in both groups. Scale bars = 1 µm (left), 500 nm (right). Data represent the mean ± SEM. n = 3 mice per group for SEM (B, C, J–N); n = 6 mice per group for all other experiments. Statistical comparisons were conducted using unpaired Student's t‐test. ∗∗ p < 0.01, ∗∗∗ p < 0.001, ∗∗∗∗ P < 0.0001.
Ltl, supplied by Vector Laboratories, used in various techniques. Bioz Stars score: 96/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/biotinylated+lectins/Biotinylated+Lotus+Tetragonolobus+Lectin+(LTL)/pm41981279-221-9-13
Average 96 stars, based on 1 article reviews
ltl - by Bioz Stars, 2026-10
96/100 stars
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sambucus nigra lectin biotinylated  (MedChemExpress)
93
MedChemExpress sambucus nigra lectin biotinylated
Neonatal sevoflurane exposure induces PNNs damage in the hippocampus. (A) Schematic of the experimental protocol for hippocampal extracellular matrix (ECM) analyses. (B) Representative scanning electron micrographs (SEM) of hippocampal ECM ultrastructure in Con and Sev ‑treated groups. Scale bars = 5 µm (5K×), 1.2 µm (20K×), and 500 nm (50K×). (C) Quantification of mean gray value (left) and fiber diameter (right) of hippocampal ECM in Con and Sev groups. (D, E) Wisteria <t>floribunda</t> <t>agglutinin</t> (WFA) staining and quantitative analysis of PNN intensity in the CA2 region at 7, 14, 30, and 60 days post‐exposure (dpe). Scale bar = 50 µm. (F, G) Western blotting and quantification of hapln1 and aggrecan protein levels in the hippocampus of Con and Sev groups. (H, I) Immunofluorescence staining and quantitative analysis of aggrecan in the hippocampus of Con and Sev groups at 60 dpe. Green: aggrecan. Blue: DAPI. Scale bar = 50 µm. (J–M) PNNs in the Con group exhibit bright, well‐organized mesh‐like architecture, whereas PNNs in the Sev group display reduced WFA intensity and a disrupted staining pattern. (J) Representative WFA staining. Purple: WFA. Scale bar = 10 µm. (K) Binary images of the regions in (J). (L) Quantification of black/white pixel ratio. (M) Representative surface intensity profiles of WFA‐positive PNNs. (N) Immunoelectron microscopy of PNNs in the Con and Sev groups. High‐magnification images (right panels) display immunogold labeling within WFA (red arrows) in both groups. Scale bars = 1 µm (left), 500 nm (right). Data represent the mean ± SEM. n = 3 mice per group for SEM (B, C, J–N); n = 6 mice per group for all other experiments. Statistical comparisons were conducted using unpaired Student's t‐test. ∗∗ p < 0.01, ∗∗∗ p < 0.001, ∗∗∗∗ P < 0.0001.
Sambucus Nigra Lectin Biotinylated, supplied by MedChemExpress, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/biotinylated+lectins/Sambucus+Nigra+Lectin/pm40185397-251-20-24
Average 93 stars, based on 1 article reviews
sambucus nigra lectin biotinylated - by Bioz Stars, 2026-10
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biotinylated plant lectins sna  (Vector Laboratories)
96
Vector Laboratories biotinylated plant lectins sna
Neonatal sevoflurane exposure induces PNNs damage in the hippocampus. (A) Schematic of the experimental protocol for hippocampal extracellular matrix (ECM) analyses. (B) Representative scanning electron micrographs (SEM) of hippocampal ECM ultrastructure in Con and Sev ‑treated groups. Scale bars = 5 µm (5K×), 1.2 µm (20K×), and 500 nm (50K×). (C) Quantification of mean gray value (left) and fiber diameter (right) of hippocampal ECM in Con and Sev groups. (D, E) Wisteria <t>floribunda</t> <t>agglutinin</t> (WFA) staining and quantitative analysis of PNN intensity in the CA2 region at 7, 14, 30, and 60 days post‐exposure (dpe). Scale bar = 50 µm. (F, G) Western blotting and quantification of hapln1 and aggrecan protein levels in the hippocampus of Con and Sev groups. (H, I) Immunofluorescence staining and quantitative analysis of aggrecan in the hippocampus of Con and Sev groups at 60 dpe. Green: aggrecan. Blue: DAPI. Scale bar = 50 µm. (J–M) PNNs in the Con group exhibit bright, well‐organized mesh‐like architecture, whereas PNNs in the Sev group display reduced WFA intensity and a disrupted staining pattern. (J) Representative WFA staining. Purple: WFA. Scale bar = 10 µm. (K) Binary images of the regions in (J). (L) Quantification of black/white pixel ratio. (M) Representative surface intensity profiles of WFA‐positive PNNs. (N) Immunoelectron microscopy of PNNs in the Con and Sev groups. High‐magnification images (right panels) display immunogold labeling within WFA (red arrows) in both groups. Scale bars = 1 µm (left), 500 nm (right). Data represent the mean ± SEM. n = 3 mice per group for SEM (B, C, J–N); n = 6 mice per group for all other experiments. Statistical comparisons were conducted using unpaired Student's t‐test. ∗∗ p < 0.01, ∗∗∗ p < 0.001, ∗∗∗∗ P < 0.0001.
Biotinylated Plant Lectins Sna, supplied by Vector Laboratories, used in various techniques. Bioz Stars score: 96/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/biotinylated+lectins/Biotinylated+Sambucus+Nigra+Lectin+(SNA%2C+EBL)/10__1155_slash_2012_slash_309203-37-0-24
Average 96 stars, based on 1 article reviews
biotinylated plant lectins sna - by Bioz Stars, 2026-10
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maackia amurensis  (Vector Laboratories)
95
Vector Laboratories maackia amurensis
Neonatal sevoflurane exposure induces PNNs damage in the hippocampus. (A) Schematic of the experimental protocol for hippocampal extracellular matrix (ECM) analyses. (B) Representative scanning electron micrographs (SEM) of hippocampal ECM ultrastructure in Con and Sev ‑treated groups. Scale bars = 5 µm (5K×), 1.2 µm (20K×), and 500 nm (50K×). (C) Quantification of mean gray value (left) and fiber diameter (right) of hippocampal ECM in Con and Sev groups. (D, E) Wisteria <t>floribunda</t> <t>agglutinin</t> (WFA) staining and quantitative analysis of PNN intensity in the CA2 region at 7, 14, 30, and 60 days post‐exposure (dpe). Scale bar = 50 µm. (F, G) Western blotting and quantification of hapln1 and aggrecan protein levels in the hippocampus of Con and Sev groups. (H, I) Immunofluorescence staining and quantitative analysis of aggrecan in the hippocampus of Con and Sev groups at 60 dpe. Green: aggrecan. Blue: DAPI. Scale bar = 50 µm. (J–M) PNNs in the Con group exhibit bright, well‐organized mesh‐like architecture, whereas PNNs in the Sev group display reduced WFA intensity and a disrupted staining pattern. (J) Representative WFA staining. Purple: WFA. Scale bar = 10 µm. (K) Binary images of the regions in (J). (L) Quantification of black/white pixel ratio. (M) Representative surface intensity profiles of WFA‐positive PNNs. (N) Immunoelectron microscopy of PNNs in the Con and Sev groups. High‐magnification images (right panels) display immunogold labeling within WFA (red arrows) in both groups. Scale bars = 1 µm (left), 500 nm (right). Data represent the mean ± SEM. n = 3 mice per group for SEM (B, C, J–N); n = 6 mice per group for all other experiments. Statistical comparisons were conducted using unpaired Student's t‐test. ∗∗ p < 0.01, ∗∗∗ p < 0.001, ∗∗∗∗ P < 0.0001.
Maackia Amurensis, supplied by Vector Laboratories, used in various techniques. Bioz Stars score: 95/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/biotinylated+lectins/Biotinylated+Maackia+Amurensis+Lectin+I+(MAL+I)/10__1128_slash_jvi__02489___09-94-11-22
Average 95 stars, based on 1 article reviews
maackia amurensis - by Bioz Stars, 2026-10
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biotinylated aleuria aurantia lectin  (Vector Laboratories)
94
Vector Laboratories biotinylated aleuria aurantia lectin
(A) TIM-3 expression on KASUMI-3 cells, primary AML blasts, and healthy immune subsets (CIK cells, monocytes, NK cells) assessed by flow cytometry using QuantiBRITE beads. REH (ALL cell line) served as negative control. (B) Short-term killing assay of TIM-3.CAR-CIK cells against CIK (n = 11) or KASUMI-3 (n = 8) cells compared with NT cells. Target cell lysis was evaluated by flow cytometry (E:T 5:1). (C) Short-term killing assay of TIM-3.CAR-CIK cells against monocytes (n = 8) or NK cells (n = 8) compared with NT (E:T 5:1). KASUMI-3 (n = 4) were included as positive control. (D) Immunoblot analysis of TIM-3 in lysates from monocytes, CIK cells, and KASUMI-3 cells following enzymatic treatment with PNGase F or broad neuraminidase, probed with a commercial anti–TIM-3 antibody (TIM-3-cmAb). GAPDH, loading control. Glycan symbols follow SNFG. (E) TIM-3 immunoprecipitates from monocytes, CIK cells, and KASUMI-3 cells treated with PNGase F or O- glycosidase and analyzed by immunoblot with TIM-3-cmAb and <t>lectin</t> far-western with <t>Aleuria</t> aurantia lectin (AAL; fucosylated epitopes). TGX stain-free total protein signal is shown as a loading/normalization control. (F) KASUMI-3 cells treated with vehicle (mock) or the fucosylation inhibitor 2F-peracetyl-fucose (SGN-2FF), followed by PNGase F or neuraminidase treatment and immunoblot/lectin probing with TIM-3-cmAb and AAL. See also Figure S3A . (G) Short-term killing assay of TIM-3.CAR-CIK cells against untreated or SGN-2FF-treated KASUMI-3 cells at various E:T ratios (5:1, 1:1, 0.5:1, 0.25:1 and 0.125:1, n = 8). (H) Affinity kinetics (left) and binding avidity at 1000 pN force (right) of TIM-3.CAR-CIK cells to untreated or defucosylated KASUMI-3 by LUMICKS analysis (n = 6). Immunoblot experiments (D-F) were repeated in three independent biological replicates with similar results. Data are presented as individual values and mean ± SD. Statistical significance was determined with repeated-measures two-way ANOVA with Bonferroni’s post hoc test (B, C) or using paired t test (G, H). ns, not significant; *p = 0.01, **p < 0.001, ***p = 0.0001 and ****p < 0.0001. Illustrations were created with Biorender.com. See also Figure S3 for loading-matched TIM-3 immunoprecipitation controls.
Biotinylated Aleuria Aurantia Lectin, supplied by Vector Laboratories, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/biotinylated+lectins/Biotinylated+Aleuria+Aurantia+Lectin+(AAL)/bio_rxiv__64898__2026__04__22__719217-335-25-31
Average 94 stars, based on 1 article reviews
biotinylated aleuria aurantia lectin - by Bioz Stars, 2026-10
94/100 stars
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biotinylated dsl  (Vector Laboratories)
93
Vector Laboratories biotinylated dsl
(A) TIM-3 expression on KASUMI-3 cells, primary AML blasts, and healthy immune subsets (CIK cells, monocytes, NK cells) assessed by flow cytometry using QuantiBRITE beads. REH (ALL cell line) served as negative control. (B) Short-term killing assay of TIM-3.CAR-CIK cells against CIK (n = 11) or KASUMI-3 (n = 8) cells compared with NT cells. Target cell lysis was evaluated by flow cytometry (E:T 5:1). (C) Short-term killing assay of TIM-3.CAR-CIK cells against monocytes (n = 8) or NK cells (n = 8) compared with NT (E:T 5:1). KASUMI-3 (n = 4) were included as positive control. (D) Immunoblot analysis of TIM-3 in lysates from monocytes, CIK cells, and KASUMI-3 cells following enzymatic treatment with PNGase F or broad neuraminidase, probed with a commercial anti–TIM-3 antibody (TIM-3-cmAb). GAPDH, loading control. Glycan symbols follow SNFG. (E) TIM-3 immunoprecipitates from monocytes, CIK cells, and KASUMI-3 cells treated with PNGase F or O- glycosidase and analyzed by immunoblot with TIM-3-cmAb and <t>lectin</t> far-western with <t>Aleuria</t> aurantia lectin (AAL; fucosylated epitopes). TGX stain-free total protein signal is shown as a loading/normalization control. (F) KASUMI-3 cells treated with vehicle (mock) or the fucosylation inhibitor 2F-peracetyl-fucose (SGN-2FF), followed by PNGase F or neuraminidase treatment and immunoblot/lectin probing with TIM-3-cmAb and AAL. See also Figure S3A . (G) Short-term killing assay of TIM-3.CAR-CIK cells against untreated or SGN-2FF-treated KASUMI-3 cells at various E:T ratios (5:1, 1:1, 0.5:1, 0.25:1 and 0.125:1, n = 8). (H) Affinity kinetics (left) and binding avidity at 1000 pN force (right) of TIM-3.CAR-CIK cells to untreated or defucosylated KASUMI-3 by LUMICKS analysis (n = 6). Immunoblot experiments (D-F) were repeated in three independent biological replicates with similar results. Data are presented as individual values and mean ± SD. Statistical significance was determined with repeated-measures two-way ANOVA with Bonferroni’s post hoc test (B, C) or using paired t test (G, H). ns, not significant; *p = 0.01, **p < 0.001, ***p = 0.0001 and ****p < 0.0001. Illustrations were created with Biorender.com. See also Figure S3 for loading-matched TIM-3 immunoprecipitation controls.
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α2,3-sialylation is required for BCG-induced osteoclast differentiation and activity (A) Comparison of differentially expressed genes (DEGs) between BCG-infected osteoclasts (RB) and uninfected controls (R). (n = 3 biological replicates per group, differential expression was defined as |FoldChange| > 2 and padj <0.05). (B) Volcano plot of DEGs highlighting genes related to sialic acid biosynthesis. (C) KEGG pathway enrichment analysis of upregulated DEGs in RB cells. (D,E) Immunofluorescence staining of α2,3-SA in mouse calvarial sections using MAL II lectin, with quantification of α2,3-SA fluorescence intensity (n = 5). Intensity density was normalized to the PBS group mean. (F) In vitro osteoclasts subjected to MAL II lectin staining and TRAP staining, with or without sialidase treatment to enzymatically remove α2,3-SA. (G) Quantification of α2,3-SA fluorescence intensity in cultured osteoclasts (n = 5). Intensity density was measured in cellular ROIs after background subtraction and normalized to the RANKL group mean. (H) Quantification of TRAP + multinucleated cells (≥3 nuclei) per field (randomly selected fields, fixed magnification) in vitro (n = 5). (I) mRNA expression levels of osteoclast differentiation markers ( Fos, Mmp9, Nfatc1, and Ocstamp ) in osteoclasts (n = 3). Data are presented as mean ± SD. Statistical significance was determined by two-tailed unpaired Student’s t-test for two-group comparisons (E) and one-way ANOVA followed by Tukey’s post hoc test for three-group comparisons (G–I) .

Journal: Frontiers in Pharmacology

Article Title: Mycobacterium tuberculosis infection drives osteoclast overactivation via α2,3-Sialylation to promote pathological bone destruction

doi: 10.3389/fphar.2026.1738896

Figure Lengend Snippet: α2,3-sialylation is required for BCG-induced osteoclast differentiation and activity (A) Comparison of differentially expressed genes (DEGs) between BCG-infected osteoclasts (RB) and uninfected controls (R). (n = 3 biological replicates per group, differential expression was defined as |FoldChange| > 2 and padj <0.05). (B) Volcano plot of DEGs highlighting genes related to sialic acid biosynthesis. (C) KEGG pathway enrichment analysis of upregulated DEGs in RB cells. (D,E) Immunofluorescence staining of α2,3-SA in mouse calvarial sections using MAL II lectin, with quantification of α2,3-SA fluorescence intensity (n = 5). Intensity density was normalized to the PBS group mean. (F) In vitro osteoclasts subjected to MAL II lectin staining and TRAP staining, with or without sialidase treatment to enzymatically remove α2,3-SA. (G) Quantification of α2,3-SA fluorescence intensity in cultured osteoclasts (n = 5). Intensity density was measured in cellular ROIs after background subtraction and normalized to the RANKL group mean. (H) Quantification of TRAP + multinucleated cells (≥3 nuclei) per field (randomly selected fields, fixed magnification) in vitro (n = 5). (I) mRNA expression levels of osteoclast differentiation markers ( Fos, Mmp9, Nfatc1, and Ocstamp ) in osteoclasts (n = 3). Data are presented as mean ± SD. Statistical significance was determined by two-tailed unpaired Student’s t-test for two-group comparisons (E) and one-way ANOVA followed by Tukey’s post hoc test for three-group comparisons (G–I) .

Article Snippet: Biotin MAL-II , Vector laboratories , Cat# B-1265-1.

Techniques: Activity Assay, Comparison, Infection, Quantitative Proteomics, Immunofluorescence, Staining, Fluorescence, In Vitro, Cell Culture, Expressing, Two Tailed Test

Neonatal sevoflurane exposure induces PNNs damage in the hippocampus. (A) Schematic of the experimental protocol for hippocampal extracellular matrix (ECM) analyses. (B) Representative scanning electron micrographs (SEM) of hippocampal ECM ultrastructure in Con and Sev ‑treated groups. Scale bars = 5 µm (5K×), 1.2 µm (20K×), and 500 nm (50K×). (C) Quantification of mean gray value (left) and fiber diameter (right) of hippocampal ECM in Con and Sev groups. (D, E) Wisteria floribunda agglutinin (WFA) staining and quantitative analysis of PNN intensity in the CA2 region at 7, 14, 30, and 60 days post‐exposure (dpe). Scale bar = 50 µm. (F, G) Western blotting and quantification of hapln1 and aggrecan protein levels in the hippocampus of Con and Sev groups. (H, I) Immunofluorescence staining and quantitative analysis of aggrecan in the hippocampus of Con and Sev groups at 60 dpe. Green: aggrecan. Blue: DAPI. Scale bar = 50 µm. (J–M) PNNs in the Con group exhibit bright, well‐organized mesh‐like architecture, whereas PNNs in the Sev group display reduced WFA intensity and a disrupted staining pattern. (J) Representative WFA staining. Purple: WFA. Scale bar = 10 µm. (K) Binary images of the regions in (J). (L) Quantification of black/white pixel ratio. (M) Representative surface intensity profiles of WFA‐positive PNNs. (N) Immunoelectron microscopy of PNNs in the Con and Sev groups. High‐magnification images (right panels) display immunogold labeling within WFA (red arrows) in both groups. Scale bars = 1 µm (left), 500 nm (right). Data represent the mean ± SEM. n = 3 mice per group for SEM (B, C, J–N); n = 6 mice per group for all other experiments. Statistical comparisons were conducted using unpaired Student's t‐test. ∗∗ p < 0.01, ∗∗∗ p < 0.001, ∗∗∗∗ P < 0.0001.

Journal: Advanced Science

Article Title: Neonatal Sevoflurane Exposure Induces Long‐Term Cognitive Impairment via Epigenetically Mediated MMP9 Activation and Perineuronal Net Disruption in the Hippocampal CA2

doi: 10.1002/advs.78006

Figure Lengend Snippet: Neonatal sevoflurane exposure induces PNNs damage in the hippocampus. (A) Schematic of the experimental protocol for hippocampal extracellular matrix (ECM) analyses. (B) Representative scanning electron micrographs (SEM) of hippocampal ECM ultrastructure in Con and Sev ‑treated groups. Scale bars = 5 µm (5K×), 1.2 µm (20K×), and 500 nm (50K×). (C) Quantification of mean gray value (left) and fiber diameter (right) of hippocampal ECM in Con and Sev groups. (D, E) Wisteria floribunda agglutinin (WFA) staining and quantitative analysis of PNN intensity in the CA2 region at 7, 14, 30, and 60 days post‐exposure (dpe). Scale bar = 50 µm. (F, G) Western blotting and quantification of hapln1 and aggrecan protein levels in the hippocampus of Con and Sev groups. (H, I) Immunofluorescence staining and quantitative analysis of aggrecan in the hippocampus of Con and Sev groups at 60 dpe. Green: aggrecan. Blue: DAPI. Scale bar = 50 µm. (J–M) PNNs in the Con group exhibit bright, well‐organized mesh‐like architecture, whereas PNNs in the Sev group display reduced WFA intensity and a disrupted staining pattern. (J) Representative WFA staining. Purple: WFA. Scale bar = 10 µm. (K) Binary images of the regions in (J). (L) Quantification of black/white pixel ratio. (M) Representative surface intensity profiles of WFA‐positive PNNs. (N) Immunoelectron microscopy of PNNs in the Con and Sev groups. High‐magnification images (right panels) display immunogold labeling within WFA (red arrows) in both groups. Scale bars = 1 µm (left), 500 nm (right). Data represent the mean ± SEM. n = 3 mice per group for SEM (B, C, J–N); n = 6 mice per group for all other experiments. Statistical comparisons were conducted using unpaired Student's t‐test. ∗∗ p < 0.01, ∗∗∗ p < 0.001, ∗∗∗∗ P < 0.0001.

Article Snippet: Serial coronal brain sections were blocked in PBS containing 3% BSA and 0.3% Triton X‐100, then incubated overnight at room temperature with the following primary antibodies: biotinylated Wisteria floribunda agglutinin (WFA; Vector Laboratories, 1:300), rabbit anti‐Aggrecan (Merck‐Millipore, MABT83, 1:200), rabbit anti‐NeuN (Merck Millipore, ABN78, 1:600), rabbit anti‐GFAP (GeneTex, GTX108711, 1:200), mouse anti‐CC1 (Sigma–Aldrich, OP80, 1:100), rabbit anti‐Iba1 (WAKO, Lek0542, 1:200), rabbit anti‐Camk2 (GeneTex, GTX135117, 1:200), mouse anti‐CaMKIIα (Abcam, ab22609, 1:200), goat anti‐BDNF (Vector Laboratories, EB08117, 1:500), rabbit anti‐VGlut2 (Abcam, ab216463, 1:200), chicken anti‐MAP2 (Abcam, ab5392, 1:500), and rabbit anti‐MMP9 (Abclonal, A25299, 1:200).After PBS washes, sections were incubated for 3 h at room temperature in the dark with corresponding Alexa Fluor 488‐ or 594‐conjugated secondary antibodies (donkey anti‐rabbit, donkey anti‐mouse, donkey anti‐chicken, and donkey anti‐goat; Jackson ImmunoResearch, 1:500) or Alexa Fluor 488‐conjugated streptavidin (Cell Signaling Technology, 89067S, 1:500).

Techniques: Staining, Analysis, Western Blot, Immunofluorescence, Immuno-Electron Microscopy, Labeling

(A) TIM-3 expression on KASUMI-3 cells, primary AML blasts, and healthy immune subsets (CIK cells, monocytes, NK cells) assessed by flow cytometry using QuantiBRITE beads. REH (ALL cell line) served as negative control. (B) Short-term killing assay of TIM-3.CAR-CIK cells against CIK (n = 11) or KASUMI-3 (n = 8) cells compared with NT cells. Target cell lysis was evaluated by flow cytometry (E:T 5:1). (C) Short-term killing assay of TIM-3.CAR-CIK cells against monocytes (n = 8) or NK cells (n = 8) compared with NT (E:T 5:1). KASUMI-3 (n = 4) were included as positive control. (D) Immunoblot analysis of TIM-3 in lysates from monocytes, CIK cells, and KASUMI-3 cells following enzymatic treatment with PNGase F or broad neuraminidase, probed with a commercial anti–TIM-3 antibody (TIM-3-cmAb). GAPDH, loading control. Glycan symbols follow SNFG. (E) TIM-3 immunoprecipitates from monocytes, CIK cells, and KASUMI-3 cells treated with PNGase F or O- glycosidase and analyzed by immunoblot with TIM-3-cmAb and lectin far-western with Aleuria aurantia lectin (AAL; fucosylated epitopes). TGX stain-free total protein signal is shown as a loading/normalization control. (F) KASUMI-3 cells treated with vehicle (mock) or the fucosylation inhibitor 2F-peracetyl-fucose (SGN-2FF), followed by PNGase F or neuraminidase treatment and immunoblot/lectin probing with TIM-3-cmAb and AAL. See also Figure S3A . (G) Short-term killing assay of TIM-3.CAR-CIK cells against untreated or SGN-2FF-treated KASUMI-3 cells at various E:T ratios (5:1, 1:1, 0.5:1, 0.25:1 and 0.125:1, n = 8). (H) Affinity kinetics (left) and binding avidity at 1000 pN force (right) of TIM-3.CAR-CIK cells to untreated or defucosylated KASUMI-3 by LUMICKS analysis (n = 6). Immunoblot experiments (D-F) were repeated in three independent biological replicates with similar results. Data are presented as individual values and mean ± SD. Statistical significance was determined with repeated-measures two-way ANOVA with Bonferroni’s post hoc test (B, C) or using paired t test (G, H). ns, not significant; *p = 0.01, **p < 0.001, ***p = 0.0001 and ****p < 0.0001. Illustrations were created with Biorender.com. See also Figure S3 for loading-matched TIM-3 immunoprecipitation controls.

Journal: bioRxiv

Article Title: Differential TIM-3 glycosylation enables specific dual targeting CAR-T therapy in acute myeloid leukemia

doi: 10.64898/2026.04.22.719217

Figure Lengend Snippet: (A) TIM-3 expression on KASUMI-3 cells, primary AML blasts, and healthy immune subsets (CIK cells, monocytes, NK cells) assessed by flow cytometry using QuantiBRITE beads. REH (ALL cell line) served as negative control. (B) Short-term killing assay of TIM-3.CAR-CIK cells against CIK (n = 11) or KASUMI-3 (n = 8) cells compared with NT cells. Target cell lysis was evaluated by flow cytometry (E:T 5:1). (C) Short-term killing assay of TIM-3.CAR-CIK cells against monocytes (n = 8) or NK cells (n = 8) compared with NT (E:T 5:1). KASUMI-3 (n = 4) were included as positive control. (D) Immunoblot analysis of TIM-3 in lysates from monocytes, CIK cells, and KASUMI-3 cells following enzymatic treatment with PNGase F or broad neuraminidase, probed with a commercial anti–TIM-3 antibody (TIM-3-cmAb). GAPDH, loading control. Glycan symbols follow SNFG. (E) TIM-3 immunoprecipitates from monocytes, CIK cells, and KASUMI-3 cells treated with PNGase F or O- glycosidase and analyzed by immunoblot with TIM-3-cmAb and lectin far-western with Aleuria aurantia lectin (AAL; fucosylated epitopes). TGX stain-free total protein signal is shown as a loading/normalization control. (F) KASUMI-3 cells treated with vehicle (mock) or the fucosylation inhibitor 2F-peracetyl-fucose (SGN-2FF), followed by PNGase F or neuraminidase treatment and immunoblot/lectin probing with TIM-3-cmAb and AAL. See also Figure S3A . (G) Short-term killing assay of TIM-3.CAR-CIK cells against untreated or SGN-2FF-treated KASUMI-3 cells at various E:T ratios (5:1, 1:1, 0.5:1, 0.25:1 and 0.125:1, n = 8). (H) Affinity kinetics (left) and binding avidity at 1000 pN force (right) of TIM-3.CAR-CIK cells to untreated or defucosylated KASUMI-3 by LUMICKS analysis (n = 6). Immunoblot experiments (D-F) were repeated in three independent biological replicates with similar results. Data are presented as individual values and mean ± SD. Statistical significance was determined with repeated-measures two-way ANOVA with Bonferroni’s post hoc test (B, C) or using paired t test (G, H). ns, not significant; *p = 0.01, **p < 0.001, ***p = 0.0001 and ****p < 0.0001. Illustrations were created with Biorender.com. See also Figure S3 for loading-matched TIM-3 immunoprecipitation controls.

Article Snippet: Membranes were probed with anti-human TIM-3 antibody (TIM-3-cmAb) (1:250; R&D Systems, MAB23652), a recombinant monoclonal antibody derived from the TIM-3.CAR scFv (TIM-3 scFv-mAb) (1:500; GENEWIZ), biotinylated Aleuria aurantia lectin (AAL; 1:3000; Vector Laboratories, B-1395-1), and biotinylated Ricinus communis agglutinin I (RCA I; 1:3000; Vector Laboratories, B-1085-1).

Techniques: Expressing, Flow Cytometry, Negative Control, Lysis, Positive Control, Western Blot, Control, Glycoproteomics, Staining, Binding Assay, Immunoprecipitation

(A) Immunoblot profiling of TIM-3 glycoforms in monocytes, CIK cells, and KASUMI-3 lysates using a recombinant scFv-derived monoclonal antibody (TIM-3scFv-mAb) following enzymatic treatment with PNGase F or broad neuraminidase. GAPDH, loading control. (B) TIM-3 immunoprecipitates from healthy monocytes, KASUMI-3 cells, and primary AML blasts treated with neuraminidase and/or PNGase F and analyzed by lectin and antibody probing: Ricinus communis agglutinin I (RCA-I; terminal β-galactose/LacNAc motifs), CA19-9 (sialyl-Lewis A), CSLEX1 (sialyl-Lewis X), and TIM-3scFv-mAb. See also Figure S3B . (C) High-resolution immunoblot of TIM-3 species detected by TIM-3scFv-mAb in CIK cells, primary AML blasts, and KASUMI-3 cells. GAPDH, loading control. See also Figure S3C . (D) RT-qPCR expression profiling of glycosyltransferases (FUT7, FUT8, ST3GAL3, ST3GAL4, ST3GAL6) in monocytes, KASUMI-3 cells, and primary AML blasts. Data are plotted as fold-change relative to monocytes and normalized to 18S RNA; individual points denote biological samples where applicable. (E) Schematic model summarizing a glycoform-biased recognition framework in which AML-associated remodeling of TIM-3 N -glycans contributes to preferential TIM-3.CAR recognition of AML-enriched TIM-3 glycoforms. Representative N -glycan structures are proposed for TIM-3 in AML blasts, monocytes and CIK cells based on enzymatic perturbation and lectin/antibody probing. Sugar moieties drawn with dashed outlines indicate features not directly resolved/assigned. Glycan symbols follow SNFG. Immunoblot and lectin/antibody blot experiments (A-C) were repeated in three independent biological replicates with similar results. Illustrations were created with Biorender.com. See also Figure S3 for additional lectin/antibody probing of TIM-3 glycoforms and terminal galactose exposure.

Journal: bioRxiv

Article Title: Differential TIM-3 glycosylation enables specific dual targeting CAR-T therapy in acute myeloid leukemia

doi: 10.64898/2026.04.22.719217

Figure Lengend Snippet: (A) Immunoblot profiling of TIM-3 glycoforms in monocytes, CIK cells, and KASUMI-3 lysates using a recombinant scFv-derived monoclonal antibody (TIM-3scFv-mAb) following enzymatic treatment with PNGase F or broad neuraminidase. GAPDH, loading control. (B) TIM-3 immunoprecipitates from healthy monocytes, KASUMI-3 cells, and primary AML blasts treated with neuraminidase and/or PNGase F and analyzed by lectin and antibody probing: Ricinus communis agglutinin I (RCA-I; terminal β-galactose/LacNAc motifs), CA19-9 (sialyl-Lewis A), CSLEX1 (sialyl-Lewis X), and TIM-3scFv-mAb. See also Figure S3B . (C) High-resolution immunoblot of TIM-3 species detected by TIM-3scFv-mAb in CIK cells, primary AML blasts, and KASUMI-3 cells. GAPDH, loading control. See also Figure S3C . (D) RT-qPCR expression profiling of glycosyltransferases (FUT7, FUT8, ST3GAL3, ST3GAL4, ST3GAL6) in monocytes, KASUMI-3 cells, and primary AML blasts. Data are plotted as fold-change relative to monocytes and normalized to 18S RNA; individual points denote biological samples where applicable. (E) Schematic model summarizing a glycoform-biased recognition framework in which AML-associated remodeling of TIM-3 N -glycans contributes to preferential TIM-3.CAR recognition of AML-enriched TIM-3 glycoforms. Representative N -glycan structures are proposed for TIM-3 in AML blasts, monocytes and CIK cells based on enzymatic perturbation and lectin/antibody probing. Sugar moieties drawn with dashed outlines indicate features not directly resolved/assigned. Glycan symbols follow SNFG. Immunoblot and lectin/antibody blot experiments (A-C) were repeated in three independent biological replicates with similar results. Illustrations were created with Biorender.com. See also Figure S3 for additional lectin/antibody probing of TIM-3 glycoforms and terminal galactose exposure.

Article Snippet: Membranes were probed with anti-human TIM-3 antibody (TIM-3-cmAb) (1:250; R&D Systems, MAB23652), a recombinant monoclonal antibody derived from the TIM-3.CAR scFv (TIM-3 scFv-mAb) (1:500; GENEWIZ), biotinylated Aleuria aurantia lectin (AAL; 1:3000; Vector Laboratories, B-1395-1), and biotinylated Ricinus communis agglutinin I (RCA I; 1:3000; Vector Laboratories, B-1085-1).

Techniques: Western Blot, Recombinant, Derivative Assay, Control, Quantitative RT-PCR, Expressing, Glycoproteomics