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biotinylated cona  (Vector Laboratories)


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    Structured Review

    Vector Laboratories biotinylated cona
    Biotinylated Cona, supplied by Vector Laboratories, used in various techniques. Bioz Stars score: 94/100, based on 305 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/B-1005-5/Biotinylated+Concanavalin+A+(Con+A)/10__1038_slash_s41598___026___73033___5-84-0-5
    Average 94 stars, based on 305 article reviews
    biotinylated cona - by Bioz Stars, 2026-10
    94/100 stars

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    Recombinant:

    Article Title: OSTM1 is a ubiquitin E3 ligase that suppresses B-cell malignancy by activating the cAMP/PKA/CREB pathway
    Article Snippet: Flag-M2 (Millipore Sigma, F1804), Flag (Millipore Sigma, F7425), 6X-His (Thermo Fisher Scientific, MA1-21315), p-AKT Ser-473 (Cell Signaling Technology, 4060), t-AKT (Cell Signaling Technology, 9272), GAPDH (ProteinTech, 10494-1-AP), p-S6 Ser235/236 (Cell Signaling Technology, 4858), t-S6 (Cell Signaling Technology, 2217), p-STAT5 Y694 (Cell Signaling Technology, 9359), t-STAT5 (Cell Signaling Technology, 25656), p-p44/42 MAPK (Erk1/2) Thr202/Tyr204 (Cell Signaling Technology, 4376), t-p44/42 MAPK (Erk1/2) (Cell Signaling Technology, 9102), PDE3B (SMCP3B) (used for IB) (Novus Biologicals, NBP1-43333), PDE3B (used for IP) (Abcam, ab99290), Ubiquitin (P37) (Cell Signaling Technology, 58395), LC3B (Cell Signaling Technology, 2775), K48-linkage specific polyubiquitin (D9D5) (Cell Signaling Technology, 8081), GFP (Santa Cruz, sc-8334), BiP/GRP78 (BD Biosciences, 610978), calnexin (Transduction Labs, C45520-050), CLC7 (Thermo Fisher, A305-381A-T), p-CREB Ser133 (87G3) (Cell Signaling Technology, 9198), t-CREB (48H2) (Cell Signaling Technology, 9197), p-(Ser/Thr) PKA substrates (Cell Signaling Technology, 9621), OSTM1 (Millipore Sigma, ABN1365), goat anti-mouse IgG (H+L) cross-adsorbed secondary antibody, Alexa Fluor 680 (Thermo Fisher, A-21057), goat anti-rabbit IgG (H+L) cross-adsorbed secondary antibody, Alexa FluorTM 594 (Thermo Fisher, A11012), goat anti-rabbit IgG (H+L) cross-adsorbed secondary antibody, Alexa Fluor 488 (Thermo Fisher, A11008), goat anti-rabbit secondary antibody (LI-COR, 926-32211), goat anti-rat secondary antibody for 680 channel (Thermo Fisher, A-21096) .. 6-thioguanine (6-TG) (MedchemExpress, HY-13765), biotin (Millipore Sigma, PHR1233), brefeldin A (Thermo Fisher, 00-4506-51), chloroquine (Selleckchem, S6999), concanavilin A (Vector Labs, B1005-5), cycloheximide (Millipore Sigma, C4859), L-glutamine (Fisher Scientific, 25030081), IRDye 800CW streptavidin (LI-COR Bio, 926-32230), IL-3 (mouse recombinant, carrier-free. .. BioLegend, 575504), leupeptin hemisulfate (MedchemExpress, HY-18234A), MG132 (Selleckchem, S2619), MEM non-essential amino acids solution (Thermo Fisher, 11360070), NGI-1 (MedchemExpress, HY-117383), Protein G DynabeadsTM (Thermo Fisher, 10004D), sodium pyruvate (Thermo Fisher, 11360070), thapsigargin (Millipore Sigma, T9033), TRIzolTM Reagent (Thermo Fisher, 15596018), tunicamycin (Tocris Bioscience, 3516), polyethylenimine (PolySCIENCES, 23966-1), ubiquitylation kit (Enzo Life Sciences, BML-UW9920-0001).

    Incubation:

    Article Title: Chemical inhibition of α-mannosidase in S. mansoni schistosomula leads to reshaped N-glycosylation associated with developmental alterations
    Article Snippet: .. Next, the membranes were incubated with the in-house produced monoclonal antibody 100-4G11 which binds trimannosyl groups on N-glycans ( ; ) or Concanavalin A (Con A, 1:100,000; Vector Laboratories, Newark, CA, USA), followed by an anti-mouse polyvalent immunoglobulins (G,A,M)−alkaline phosphatase antibody (1:1,000, produced in goat; Sigma-Aldrich) or streptavidin-alkaline phosphatase conjugate (1:1,000; Roche). .. Antibody and lectin binding was visualised through incubation with 5-Bromo-4-chloro-3-indolyl-phosphate (BCIP; Roche) and 4-nitro blue tetrazolium chloride (NBT; Sigma-Aldrich).

    Article Title: Glucosamine induces apoptosis of cholangiocarcinoma cells by suppressing high-mannose type N -glycosylation and EGFR/STAT3 signaling
    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. .. The membranes were washed with TBST for 10 min, three times, and incubated with streptavidin-horseradish peroxidase conjugate (Invitrogen, Frederick, MD) for 1 h at room temperature.

    Produced:

    Article Title: Chemical inhibition of α-mannosidase in S. mansoni schistosomula leads to reshaped N-glycosylation associated with developmental alterations
    Article Snippet: .. Next, the membranes were incubated with the in-house produced monoclonal antibody 100-4G11 which binds trimannosyl groups on N-glycans ( ; ) or Concanavalin A (Con A, 1:100,000; Vector Laboratories, Newark, CA, USA), followed by an anti-mouse polyvalent immunoglobulins (G,A,M)−alkaline phosphatase antibody (1:1,000, produced in goat; Sigma-Aldrich) or streptavidin-alkaline phosphatase conjugate (1:1,000; Roche). .. Antibody and lectin binding was visualised through incubation with 5-Bromo-4-chloro-3-indolyl-phosphate (BCIP; Roche) and 4-nitro blue tetrazolium chloride (NBT; Sigma-Aldrich).

    Binding Assay:

    Article Title: Glucosamine induces apoptosis of cholangiocarcinoma cells by suppressing high-mannose type N -glycosylation and EGFR/STAT3 signaling
    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. .. The membranes were washed with TBST for 10 min, three times, and incubated with streptavidin-horseradish peroxidase conjugate (Invitrogen, Frederick, MD) for 1 h at room temperature.

    Whole Genome Amplification:

    Article Title: Glucosamine induces apoptosis of cholangiocarcinoma cells by suppressing high-mannose type N -glycosylation and EGFR/STAT3 signaling
    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. .. The membranes were washed with TBST for 10 min, three times, and incubated with streptavidin-horseradish peroxidase conjugate (Invitrogen, Frederick, MD) for 1 h at room temperature.



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    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 <t>lectin</t> blot analysis with concanavalin A <t>(ConA,</t> 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. .
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    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 <t>lectin</t> blot analysis with concanavalin A <t>(ConA,</t> 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. .
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    Image Search Results


    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