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concanavalin a  (Vector Laboratories)


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    Structured Review

    Vector Laboratories concanavalin a
    Glucosamine (GlcN) interrupted intracellular signaling and suppressed glycosylation. (A) Glucosamine treatment resulted in a reduced molecular weight of epidermal growth factor receptor (EGFR). This led to (B) suppression of phosphorylation of signal transducer and activator of transcription 3 (STAT3) at Y705. (D) The Western blots demonstrated the molecular weight reduction of glycoprotein 130 (gp130), suggesting glucosamine inhibits the glycosylation of intracellular proteins. (D) <t>Concanavalin</t> <t>A</t> (con A) lectin blots confirmed that glucosamine can inhibit the global N -glycosylation of the intracellular proteins in CCA cells. Western blots are representative of three biological replications with the same trend of results. Graphs show the averaged band intensities of proteins from three biological replications. GAPDH was used as a loading control, and the control groups (0 mM glucosamine) were assigned a factor of 1. * p < .05, ** p < .01, *** p < .001.
    Concanavalin A, supplied by Vector Laboratories, used in various techniques. Bioz Stars score: 94/100, based on 302 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Images

    1) Product Images from "Glucosamine induces apoptosis of cholangiocarcinoma cells by suppressing high-mannose type N -glycosylation and EGFR/STAT3 signaling"

    Article Title: Glucosamine induces apoptosis of cholangiocarcinoma cells by suppressing high-mannose type N -glycosylation and EGFR/STAT3 signaling

    Journal: Future Science OA

    doi: 10.1080/20565623.2026.2641244

    Glucosamine (GlcN) interrupted intracellular signaling and suppressed glycosylation. (A) Glucosamine treatment resulted in a reduced molecular weight of epidermal growth factor receptor (EGFR). This led to (B) suppression of phosphorylation of signal transducer and activator of transcription 3 (STAT3) at Y705. (D) The Western blots demonstrated the molecular weight reduction of glycoprotein 130 (gp130), suggesting glucosamine inhibits the glycosylation of intracellular proteins. (D) Concanavalin A (con A) lectin blots confirmed that glucosamine can inhibit the global N -glycosylation of the intracellular proteins in CCA cells. Western blots are representative of three biological replications with the same trend of results. Graphs show the averaged band intensities of proteins from three biological replications. GAPDH was used as a loading control, and the control groups (0 mM glucosamine) were assigned a factor of 1. * p < .05, ** p < .01, *** p < .001.
    Figure Legend Snippet: Glucosamine (GlcN) interrupted intracellular signaling and suppressed glycosylation. (A) Glucosamine treatment resulted in a reduced molecular weight of epidermal growth factor receptor (EGFR). This led to (B) suppression of phosphorylation of signal transducer and activator of transcription 3 (STAT3) at Y705. (D) The Western blots demonstrated the molecular weight reduction of glycoprotein 130 (gp130), suggesting glucosamine inhibits the glycosylation of intracellular proteins. (D) Concanavalin A (con A) lectin blots confirmed that glucosamine can inhibit the global N -glycosylation of the intracellular proteins in CCA cells. Western blots are representative of three biological replications with the same trend of results. Graphs show the averaged band intensities of proteins from three biological replications. GAPDH was used as a loading control, and the control groups (0 mM glucosamine) were assigned a factor of 1. * p < .05, ** p < .01, *** p < .001.

    Techniques Used: Glycoproteomics, Molecular Weight, Phospho-proteomics, Western Blot, Control

    Related Articles

    other:

    Article Title: Rescue of α-synuclein aggregation in Parkinson's patient neurons by synergistic enhancement of ER proteostasis and protein trafficking.
    Article Snippet: To recover CON-A bound proteins, 25 ml neutrAvidin agarose beads (Thermo Fisher Scientific) were added to the reaction mix and samples were incubated at 4 C for 1 hour.

    Incubation:

    Article Title: Rescue of α-synuclein aggregation in Parkinson's patient neurons by synergistic enhancement of ER proteostasis and protein trafficking.
    Article Snippet: Assessment of calnexin activity by Concanavalin-A pulldown H4 neuroglioma cells were treated with vehicle or 25uM Diltiazem (Sigma) for 4 days, harvested, and extracted in 0.3% CHAPS lysis buffer (0.3%CHAPS, 40mMHEPES pH 7.4, 120mMNaCl, 1mMEDTA, 10%v/v glycerol). .. For pulldown of total N-linked glycosylated proteins, 1500 mg lysate wasmixedwith 20 mg/ml biotinylated Concanavalin A (CON-A) (Vector Laboratories) and the reactionmixture was incubated overnight at 4 C under gentle rotation. .. To recover CON-A bound proteins, 25 ml neutrAvidin agarose beads (Thermo Fisher Scientific) were added to the reaction mix and samples were incubated at 4 C for 1 hour.

    Article Title: The hexosamine biosynthetic pathway rescues lysosomal dysfunction in Parkinson’s disease patient iPSC derived midbrain neurons
    Article Snippet: SNCA -3X and A53T iPSn were infected with GFP or GFPT2 at MOI3, dpi 15, harvested, and extracted in 0.3% CHAPS buffer containing 40 mM HEPES pH 7.4, 120 mM NaCl, 1 mM EDTA, 10% vol/vol glycerol, protease inhibitor cocktail (PIC) (Roche), phenylmethylsulfonyl fluoride (PMSF) (Sigma), sodium orthovanadate (Na3VO4) (Sigma) and sodium fluoride (NaF) (Sigma). .. For pulldown of total N-linked glycosylated proteins, 400 μg lysate was mixed with 20 μg/ml biotinylated Concanavalin A (CON-A) (Vector Laboratories) and the reaction mixture was incubated overnight at 4 °C under gentle rotation. .. To recover CON-A bound proteins, 25 μl neutrAvidin agarose beads (Thermo Fisher Scientific) were added to the reaction mix and samples were incubated at 4 °C for 1 h. The beads were collected by centrifugation at 2500 × g for 2 min, followed by three washes with lysis buffer.

    Gentle:

    Article Title: Rescue of α-synuclein aggregation in Parkinson's patient neurons by synergistic enhancement of ER proteostasis and protein trafficking.
    Article Snippet: Assessment of calnexin activity by Concanavalin-A pulldown H4 neuroglioma cells were treated with vehicle or 25uM Diltiazem (Sigma) for 4 days, harvested, and extracted in 0.3% CHAPS lysis buffer (0.3%CHAPS, 40mMHEPES pH 7.4, 120mMNaCl, 1mMEDTA, 10%v/v glycerol). .. For pulldown of total N-linked glycosylated proteins, 1500 mg lysate wasmixedwith 20 mg/ml biotinylated Concanavalin A (CON-A) (Vector Laboratories) and the reactionmixture was incubated overnight at 4 C under gentle rotation. .. To recover CON-A bound proteins, 25 ml neutrAvidin agarose beads (Thermo Fisher Scientific) were added to the reaction mix and samples were incubated at 4 C for 1 hour.

    Article Title: The hexosamine biosynthetic pathway rescues lysosomal dysfunction in Parkinson’s disease patient iPSC derived midbrain neurons
    Article Snippet: SNCA -3X and A53T iPSn were infected with GFP or GFPT2 at MOI3, dpi 15, harvested, and extracted in 0.3% CHAPS buffer containing 40 mM HEPES pH 7.4, 120 mM NaCl, 1 mM EDTA, 10% vol/vol glycerol, protease inhibitor cocktail (PIC) (Roche), phenylmethylsulfonyl fluoride (PMSF) (Sigma), sodium orthovanadate (Na3VO4) (Sigma) and sodium fluoride (NaF) (Sigma). .. For pulldown of total N-linked glycosylated proteins, 400 μg lysate was mixed with 20 μg/ml biotinylated Concanavalin A (CON-A) (Vector Laboratories) and the reaction mixture was incubated overnight at 4 °C under gentle rotation. .. To recover CON-A bound proteins, 25 μl neutrAvidin agarose beads (Thermo Fisher Scientific) were added to the reaction mix and samples were incubated at 4 °C for 1 h. The beads were collected by centrifugation at 2500 × g for 2 min, followed by three washes with lysis buffer.



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    Image Search Results


    Glucosamine (GlcN) interrupted intracellular signaling and suppressed glycosylation. (A) Glucosamine treatment resulted in a reduced molecular weight of epidermal growth factor receptor (EGFR). This led to (B) suppression of phosphorylation of signal transducer and activator of transcription 3 (STAT3) at Y705. (D) The Western blots demonstrated the molecular weight reduction of glycoprotein 130 (gp130), suggesting glucosamine inhibits the glycosylation of intracellular proteins. (D) Concanavalin A (con A) lectin blots confirmed that glucosamine can inhibit the global N -glycosylation of the intracellular proteins in CCA cells. Western blots are representative of three biological replications with the same trend of results. Graphs show the averaged band intensities of proteins from three biological replications. GAPDH was used as a loading control, and the control groups (0 mM glucosamine) were assigned a factor of 1. * p < .05, ** p < .01, *** p < .001.

    Journal: Future Science OA

    Article Title: Glucosamine induces apoptosis of cholangiocarcinoma cells by suppressing high-mannose type N -glycosylation and EGFR/STAT3 signaling

    doi: 10.1080/20565623.2026.2641244

    Figure Lengend Snippet: Glucosamine (GlcN) interrupted intracellular signaling and suppressed glycosylation. (A) Glucosamine treatment resulted in a reduced molecular weight of epidermal growth factor receptor (EGFR). This led to (B) suppression of phosphorylation of signal transducer and activator of transcription 3 (STAT3) at Y705. (D) The Western blots demonstrated the molecular weight reduction of glycoprotein 130 (gp130), suggesting glucosamine inhibits the glycosylation of intracellular proteins. (D) Concanavalin A (con A) lectin blots confirmed that glucosamine can inhibit the global N -glycosylation of the intracellular proteins in CCA cells. Western blots are representative of three biological replications with the same trend of results. Graphs show the averaged band intensities of proteins from three biological replications. GAPDH was used as a loading control, and the control groups (0 mM glucosamine) were assigned a factor of 1. * p < .05, ** p < .01, *** p < .001.

    Article Snippet: The membranes were blocked for nonspecific binding with 5% bovine serum albumin (w/v) in TBST for 1 h at room temperature, and then incubated with 0.25 μg/mL biotinylated lectins as follows; concanavalin A (Con A) (Vector Laboratories, Newark, NJ), wheat germ agglutinin (WGA) (Vector Laboratories), and Phaseolus Vulgaris erythroagglutinin (PHA-E) (Vector Laboratories), for 1 h at room temperature.

    Techniques: Glycoproteomics, Molecular Weight, Phospho-proteomics, Western Blot, Control

    a , Experimental design (created with BioRender.com ). Inhibition of PYGL-mediated glycogenolysis by CP-91149 in vivo. WT mice under a regular 12 h light–dark cycle and NR feeding were subcutaneously injected with either vehicle (Veh) or CP-91149 at ZT0 for tissue collections at ZT3, ZT6, ZT9, ZT12 and ZT24. b , Average food consumption of WT mice ( n = 4 biological replicates) 24 h after CP-91149 injection. c , Temporal profiles of glycogen in the liver of Veh-injected and CP-91149-injected mice ( n = 20 (5 timepoints × 4 biological replicates)). d , Glycosylation levels of proteins in CP-91149-treated and vehicle-treated mouse liver were determined by lectin blot analysis with concanavalin A (ConA, n = 20 (5 timepoints × 4 biological replicates)). Amido black staining of the membranes was used as a loading control and serves as a reference for normalization of the quantified values (right). e , C3 levels in mouse serum as assessed by ELISA ( n = 20 (5 timepoints × 4 biological replicates)). f , Experimental design (created with BioRender.com ). Inhibition of PYGL-mediated glycogenolysis by CP-91149 in AML12 mouse hepatocytes. Treatment with Veh or CP-91149 (67 µM) was performed for 3, 6, 12 and 24 h. g , h , Kinetic profiles of UDP-glucose + UDP-galactose levels ( g ), cytidine 5′-monophospho-N-acetyl neuraminic acid (CMP-Neu5Ac) ( h , left) and uridine diphosphate N-acetylglucosamine (UDP-GlcNAc) ( h , right) in AML12 cells upon CP-91149 treatment ( n = 16 (4 timepoints × 4 biological replicates)). i , Glycosylation levels of proteins in CP-91149-treated and vehicle-treated AML12 cells were determined by lectin blot analysis with ConA ( n = 16 (4 timepoints × 4 biological replicates)). Amido black staining of the membranes was used as a loading control and serves as a reference for normalization of the quantified values (bottom). j , ALB, FN1 and C3 levels in cell medium determined by ELISA ( n = 22–24 (4 timepoints × 6 biological replicates, with ALB 14 h Veh and 24 h CP-91149 n = 5)). k , Experimental design (created with BioRender.com ). AML12 cells were treated with Veh or CP-91149 for 14 h in the absence or presence of supplemental UDP-glucose (UDPG; 2 mM). l , m , ALB and C3 levels in cell medium ( l ) and lysates ( m ) as determined by ELISA ( n = 6 biological replicates, except for ALB under CP-91149 treatment ( n = 5)). Data are displayed as means; error bars, s.e.m. Boxplots show the median (centre line), interquartile range (box) and minimum to maximum values (whiskers). A detailed description of the statistical analysis is available in Source Data Fig. . See also Extended Data Fig. .

    Journal: Nature Metabolism

    Article Title: Feeding-regulated glycogen metabolism drives rhythmic liver protein secretion

    doi: 10.1038/s42255-026-01453-8

    Figure Lengend Snippet: a , Experimental design (created with BioRender.com ). Inhibition of PYGL-mediated glycogenolysis by CP-91149 in vivo. WT mice under a regular 12 h light–dark cycle and NR feeding were subcutaneously injected with either vehicle (Veh) or CP-91149 at ZT0 for tissue collections at ZT3, ZT6, ZT9, ZT12 and ZT24. b , Average food consumption of WT mice ( n = 4 biological replicates) 24 h after CP-91149 injection. c , Temporal profiles of glycogen in the liver of Veh-injected and CP-91149-injected mice ( n = 20 (5 timepoints × 4 biological replicates)). d , Glycosylation levels of proteins in CP-91149-treated and vehicle-treated mouse liver were determined by lectin blot analysis with concanavalin A (ConA, n = 20 (5 timepoints × 4 biological replicates)). Amido black staining of the membranes was used as a loading control and serves as a reference for normalization of the quantified values (right). e , C3 levels in mouse serum as assessed by ELISA ( n = 20 (5 timepoints × 4 biological replicates)). f , Experimental design (created with BioRender.com ). Inhibition of PYGL-mediated glycogenolysis by CP-91149 in AML12 mouse hepatocytes. Treatment with Veh or CP-91149 (67 µM) was performed for 3, 6, 12 and 24 h. g , h , Kinetic profiles of UDP-glucose + UDP-galactose levels ( g ), cytidine 5′-monophospho-N-acetyl neuraminic acid (CMP-Neu5Ac) ( h , left) and uridine diphosphate N-acetylglucosamine (UDP-GlcNAc) ( h , right) in AML12 cells upon CP-91149 treatment ( n = 16 (4 timepoints × 4 biological replicates)). i , Glycosylation levels of proteins in CP-91149-treated and vehicle-treated AML12 cells were determined by lectin blot analysis with ConA ( n = 16 (4 timepoints × 4 biological replicates)). Amido black staining of the membranes was used as a loading control and serves as a reference for normalization of the quantified values (bottom). j , ALB, FN1 and C3 levels in cell medium determined by ELISA ( n = 22–24 (4 timepoints × 6 biological replicates, with ALB 14 h Veh and 24 h CP-91149 n = 5)). k , Experimental design (created with BioRender.com ). AML12 cells were treated with Veh or CP-91149 for 14 h in the absence or presence of supplemental UDP-glucose (UDPG; 2 mM). l , m , ALB and C3 levels in cell medium ( l ) and lysates ( m ) as determined by ELISA ( n = 6 biological replicates, except for ALB under CP-91149 treatment ( n = 5)). Data are displayed as means; error bars, s.e.m. Boxplots show the median (centre line), interquartile range (box) and minimum to maximum values (whiskers). A detailed description of the statistical analysis is available in Source Data Fig. . See also Extended Data Fig. .

    Article Snippet: Primary antibodies were used at the following dilutions: 1:1,000 for ATF4 (Cell Signaling Technologies, 11815), ARFGAP1 (Cell Signaling Technologies, 14608), Phospho-RPS6 (Cell Signaling Technologies, 2211), Total-RPS6 (Cell Signaling Technologies, 2217), GABARAPL1 (Genetex, GTX132664) and ConA Lectin (Vector Laboratories, B-1005) and 1:2,000 for STX4 (ProteinTech, 14988-1-AP).

    Techniques: Inhibition, In Vivo, Injection, Glycoproteomics, Staining, Control, Enzyme-linked Immunosorbent Assay