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mbdnf  (Santa Cruz Biotechnology)


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    Santa Cruz Biotechnology mbdnf
    Mbdnf, supplied by Santa Cruz Biotechnology, used in various techniques. Bioz Stars score: 94/100, based on 257 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Average 94 stars, based on 257 article reviews
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    Related Articles

    Incubation:

    Article Title: The astrocytic sigma-1 receptor constitutes in the fast antidepressant action of hypidone hydrochloride (YL-0919) in rodents
    Article Snippet: .. The membranes were blocked with 5% skim milk for 1 h at room temperature, and incubated with the following primary antibodies against sigma-1R (1:1,000, Cell signaling technology, 61994S), pro-BDNF (1:1,000, Santa Cruz, sc-65514), BDNF (1:1,000, Abcam, ab108319) and β-actin (1:1,000, Proteintech, 60008-1-1) individually at 4°C overnight. .. Then secondary antibodies (1:5,000, Jackson ImmunoResearch) were incubated for 2 h at room temperature.

    Article Title: Memory impairment in the D2. mdx mouse model of Duchenne muscular dystrophy is prevented by the adiponectin receptor agonist ALY688
    Article Snippet: .. Membranes were incubated with the appropriate primary antibodies as follows: APP (BioLegend 825001), soluble APPα (IBL 11088), soluble APPβ (BioLegend 813401), BACE1 (CST 5606), ADAM10 (Abcam ab1997), p‐tau (serine 202; CST 11834), total tau (CST 4019), p‐Raptor (serine 792; CST 2083), total Raptor (CST 2280), p‐p70s6K (thr389; CST 9206S), total p70s6k (Santa Cruz SC‐230), NeuN (CST 24307) and pro‐BDNF (SC SC‐65514), diluted to 1:1000 in 5% bovine serum albumin, overnight at 4°C. ..

    Article Title: Hyperbaric oxygen therapy enhances hippocampal long-term potentiation via upregulation of BDNF and p-CREB1 in rats: Evidence outside pathological models.
    Article Snippet: Hyperbaric oxygen therapy (HBOT) is known to confer neuroprotective benefits in injury models, but its in vivo effects on synaptic plasticity in the healthy brain remain unclear.. This study investigates HBOT’s impact on hippocampal long-term potentiation (LTP) and underlying molecular mechanisms in adult male Wistar rats.. Animals were randomized into Control (ambient air) and HBOT (100 % O2 at 2.4 ATA for 1 h daily) groups for seven days.

    Article Title: Memory impairment in the D2.<i>mdx</i> mouse model of Duchenne muscular dystrophy is prevented by the adiponectin receptor agonist ALY688
    Article Snippet: All images were normalized to total protein from the samemembrane stained usingAmidoBlack total protein stain (A8181; Sigma). .. All remaining proteins were detected on 0.45 μmnitrocellulose and blockedwith 5%non-fat drymilk in TBS-T.Membraneswere incubated with the appropriate primary antibodies as follows: APP (BioLegend 825001), solubleAPPα (IBL11088), solubleAPPβ (BioLegend813401), BACE1 (CST 5606), ADAM10 (Abcam ab1997), p-tau (serine 202; CST 11834), total tau (CST 4019), p-Raptor (serine 792; CST 2083), total Raptor (CST 2280), p-p70s6K (thr389; CST 9206S), total p70s6k (Santa Cruz SC-230), NeuN (CST 24307) and pro-BDNF (SC SC-65514), diluted to 1:1000 in 5% bovine serum albumin, overnight at 4◦C. .. After primary antibody incubation and washing, membranes were incubated in horseradish peroxidase secondary antibodies diluted 1:5000 in 1% non-fat dry milk–TBS-T. Membranes were washed (3×5min in TBST), and protein bands were imaged using enhanced chemiluminescence (Western lightning Plus-ELC; PerkinElmer, 105001EA) and the ChemiDoc Imaging System (BioRad).

    Staining:

    Article Title: BDNF/Cyclin D1 Signaling System and Cognitive Performance After Perampanel and Lacosamide Treatment Singly or in Combination in an Experimental Model of Temporal Lobe Epilepsy
    Article Snippet: Lacosamide (Vimpat ® , USB Pharma, Brussels, Belgium), Perampanel (Fycompa ® , Eisai Ltd., Frankfurt am Main, Germany), and Diazepam (Sopharma, Sofia, Bulgaria) were obtained from the pharmaceutical companies. .. The following reagents were used in the study: Bouen’s Fluid Sigma, HT10132 (Aldrich Chemie GmbH, Taufkirchen, Germany); Gill’s Hematoxylin Solution, No. 2, sc-24973A (Santa Cruz Biotechnology, Inc., Dallas, TX, USA); ImmunoCruz goat ABC Staining, sc-2023 (Santa Cruz Biotechnology, Inc., Dallas, TX, USA); pro BDNF (5H8), sc-65514; Cyclin D1 (A-12), sc-8396 (Santa Cruz Biotechnology, Inc., Dallas, TX, USA); and VectaMount ® Express Mounting Medium, H-5700-60 (Vector Laboratories, Newark, CA, USA). ..

    Article Title: BDNF/Cyclin D1 Signaling System and Cognitive Performance After Perampanel and Lacosamide Treatment Singly or in Combination in an Experimental Model of Temporal Lobe Epilepsy.
    Article Snippet: Lacosamide (Vimpat®, USB Pharma, Brussels, Belgium), Perampanel (Fycompa®, Eisai Ltd., Frankfurt am Main, Germany), and Diazepam (Sopharma, Sofia, Bulgaria) were obtained from the pharmaceutical companies. .. The following reagents were used in the study: Bouen’s Fluid Sigma, HT10132 (Aldrich Chemie GmbH, Taufkirchen, Germany); Gill’s Hematoxylin Solution, No. 2, sc-24973A (Santa Cruz Biotechnology, Inc., Dallas, TX, USA); ImmunoCruz goat ABC Staining, sc-2023 (Santa Cruz Biotechnology, Inc., Dallas, TX, USA); pro BDNF (5H8), sc-65514; Cyclin D1 (A-12), sc-8396 (Santa Cruz Biotechnology, Inc., Dallas, TX, USA); and VectaMount® Express Mounting Medium, H-5700-60 (Vector Laboratories, Newark, CA, USA). ..

    Binding Assay:

    Article Title: Hyperbaric oxygen therapy enhances hippocampal long-term potentiation via upregulation of BDNF and p-CREB1 in rats: Evidence outside pathological models.
    Article Snippet: Hyperbaric oxygen therapy (HBOT) is known to confer neuroprotective benefits in injury models, but its in vivo effects on synaptic plasticity in the healthy brain remain unclear.. This study investigates HBOT’s impact on hippocampal long-term potentiation (LTP) and underlying molecular mechanisms in adult male Wistar rats.. Animals were randomized into Control (ambient air) and HBOT (100 % O2 at 2.4 ATA for 1 h daily) groups for seven days.

    Blocking Assay:

    Article Title: Hyperbaric oxygen therapy enhances hippocampal long-term potentiation via upregulation of BDNF and p-CREB1 in rats: Evidence outside pathological models.
    Article Snippet: Hyperbaric oxygen therapy (HBOT) is known to confer neuroprotective benefits in injury models, but its in vivo effects on synaptic plasticity in the healthy brain remain unclear.. This study investigates HBOT’s impact on hippocampal long-term potentiation (LTP) and underlying molecular mechanisms in adult male Wistar rats.. Animals were randomized into Control (ambient air) and HBOT (100 % O2 at 2.4 ATA for 1 h daily) groups for seven days.

    Bioprocessing:

    Article Title: Hyperbaric oxygen therapy enhances hippocampal long-term potentiation via upregulation of BDNF and p-CREB1 in rats: Evidence outside pathological models.
    Article Snippet: Hyperbaric oxygen therapy (HBOT) is known to confer neuroprotective benefits in injury models, but its in vivo effects on synaptic plasticity in the healthy brain remain unclear.. This study investigates HBOT’s impact on hippocampal long-term potentiation (LTP) and underlying molecular mechanisms in adult male Wistar rats.. Animals were randomized into Control (ambient air) and HBOT (100 % O2 at 2.4 ATA for 1 h daily) groups for seven days.

    Methylation:

    Article Title: Synergistic suppression of BDNF via epigenetic mechanism deteriorating learning and memory impairment caused by Mn and Pb co-exposure.
    Article Snippet: Microglia, the resident immune cells of the central nervous system (CNS), play a dual role in neurotoxicity by releasing the NLR Family Pyrin Domain Containing 3 (NLRP3) inflammasome and brain-derived neurotrophic factor (BDNF) in response to environmental stress.. Suppression of BDNF is implicated in learning and memory impairment induced by exposure to manganese (Mn) or lead (Pb) individually.. Methyl CpG Binding Protein 2 (MeCp2) and its phosphorylation status are related to BDNF suppression.



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    Pro-NGF/p75NTR axis is up-regulated in glucose neurotoxicity in DA neurons. a Western blot analysis and quantification of TrkA and TrkB in Control and HG- (100mM) treated neurons for 48 h. Protein levels were normalized to β-Actin. b Western blot analysis and quantification of p75NTR in Control and HG (50mM, 100mM) treated neurons for 48 h. Protein levels were normalized to β-Actin. c Celltox cytotoxicity assay. Representative photos and quantification of dead (green) neurons after treatment with HG (50mM, 100mM) and/or p75NTR inhibitor (2.5 ng/ml, anti-p75 Receptor antibody (MC-192) Abcam) for 48 h. Scale bar 50 μm. d , e <t>ELISA</t> quantification of d pro-NGF protein levels in the cell lysate and e the secreted pro-NGF protein levels in the supernatant of DA neurons treated with HG (100mM) for 48 h. f Schematics of the up-regulated pro-NGF/p75NTR axis in DA neurons upon treatment with HG. For a – e data are presented as mean ± SEM of three biological replicates derived from three independent iPSC lines. For a and c statistical significance was assessed with a two-way ANOVA and Sidak’s multiple comparisons test (** P < 0.01). For b statistical significance was assessed with an ordinary one-way ANOVA and Turkey’s multiple comparisons test (** P < 0.01). For d and e statistical significance was evaluated with an unpaired t-test (* P < 0.05). Full-length blots are presented in Figure S5
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    Pro-NGF/p75NTR axis is up-regulated in glucose neurotoxicity in DA neurons. a Western blot analysis and quantification of TrkA and TrkB in Control and HG- (100mM) treated neurons for 48 h. Protein levels were normalized to β-Actin. b Western blot analysis and quantification of p75NTR in Control and HG (50mM, 100mM) treated neurons for 48 h. Protein levels were normalized to β-Actin. c Celltox cytotoxicity assay. Representative photos and quantification of dead (green) neurons after treatment with HG (50mM, 100mM) and/or p75NTR inhibitor (2.5 ng/ml, anti-p75 Receptor antibody (MC-192) Abcam) for 48 h. Scale bar 50 μm. d , e <t>ELISA</t> quantification of d pro-NGF protein levels in the cell lysate and e the secreted pro-NGF protein levels in the supernatant of DA neurons treated with HG (100mM) for 48 h. f Schematics of the up-regulated pro-NGF/p75NTR axis in DA neurons upon treatment with HG. For a – e data are presented as mean ± SEM of three biological replicates derived from three independent iPSC lines. For a and c statistical significance was assessed with a two-way ANOVA and Sidak’s multiple comparisons test (** P < 0.01). For b statistical significance was assessed with an ordinary one-way ANOVA and Turkey’s multiple comparisons test (** P < 0.01). For d and e statistical significance was evaluated with an unpaired t-test (* P < 0.05). Full-length blots are presented in Figure S5
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    Pro-NGF/p75NTR axis is up-regulated in glucose neurotoxicity in DA neurons. a Western blot analysis and quantification of TrkA and TrkB in Control and HG- (100mM) treated neurons for 48 h. Protein levels were normalized to β-Actin. b Western blot analysis and quantification of p75NTR in Control and HG (50mM, 100mM) treated neurons for 48 h. Protein levels were normalized to β-Actin. c Celltox cytotoxicity assay. Representative photos and quantification of dead (green) neurons after treatment with HG (50mM, 100mM) and/or p75NTR inhibitor (2.5 ng/ml, anti-p75 Receptor antibody (MC-192) Abcam) for 48 h. Scale bar 50 μm. d , e <t>ELISA</t> quantification of d pro-NGF protein levels in the cell lysate and e the secreted pro-NGF protein levels in the supernatant of DA neurons treated with HG (100mM) for 48 h. f Schematics of the up-regulated pro-NGF/p75NTR axis in DA neurons upon treatment with HG. For a – e data are presented as mean ± SEM of three biological replicates derived from three independent iPSC lines. For a and c statistical significance was assessed with a two-way ANOVA and Sidak’s multiple comparisons test (** P < 0.01). For b statistical significance was assessed with an ordinary one-way ANOVA and Turkey’s multiple comparisons test (** P < 0.01). For d and e statistical significance was evaluated with an unpaired t-test (* P < 0.05). Full-length blots are presented in Figure S5
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    Pro-NGF/p75NTR axis is up-regulated in glucose neurotoxicity in DA neurons. a Western blot analysis and quantification of TrkA and TrkB in Control and HG- (100mM) treated neurons for 48 h. Protein levels were normalized to β-Actin. b Western blot analysis and quantification of p75NTR in Control and HG (50mM, 100mM) treated neurons for 48 h. Protein levels were normalized to β-Actin. c Celltox cytotoxicity assay. Representative photos and quantification of dead (green) neurons after treatment with HG (50mM, 100mM) and/or p75NTR inhibitor (2.5 ng/ml, anti-p75 Receptor antibody (MC-192) Abcam) for 48 h. Scale bar 50 μm. d , e <t>ELISA</t> quantification of d pro-NGF protein levels in the cell lysate and e the secreted pro-NGF protein levels in the supernatant of DA neurons treated with HG (100mM) for 48 h. f Schematics of the up-regulated pro-NGF/p75NTR axis in DA neurons upon treatment with HG. For a – e data are presented as mean ± SEM of three biological replicates derived from three independent iPSC lines. For a and c statistical significance was assessed with a two-way ANOVA and Sidak’s multiple comparisons test (** P < 0.01). For b statistical significance was assessed with an ordinary one-way ANOVA and Turkey’s multiple comparisons test (** P < 0.01). For d and e statistical significance was evaluated with an unpaired t-test (* P < 0.05). Full-length blots are presented in Figure S5
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    Image Search Results


    Pro-NGF/p75NTR axis is up-regulated in glucose neurotoxicity in DA neurons. a Western blot analysis and quantification of TrkA and TrkB in Control and HG- (100mM) treated neurons for 48 h. Protein levels were normalized to β-Actin. b Western blot analysis and quantification of p75NTR in Control and HG (50mM, 100mM) treated neurons for 48 h. Protein levels were normalized to β-Actin. c Celltox cytotoxicity assay. Representative photos and quantification of dead (green) neurons after treatment with HG (50mM, 100mM) and/or p75NTR inhibitor (2.5 ng/ml, anti-p75 Receptor antibody (MC-192) Abcam) for 48 h. Scale bar 50 μm. d , e ELISA quantification of d pro-NGF protein levels in the cell lysate and e the secreted pro-NGF protein levels in the supernatant of DA neurons treated with HG (100mM) for 48 h. f Schematics of the up-regulated pro-NGF/p75NTR axis in DA neurons upon treatment with HG. For a – e data are presented as mean ± SEM of three biological replicates derived from three independent iPSC lines. For a and c statistical significance was assessed with a two-way ANOVA and Sidak’s multiple comparisons test (** P < 0.01). For b statistical significance was assessed with an ordinary one-way ANOVA and Turkey’s multiple comparisons test (** P < 0.01). For d and e statistical significance was evaluated with an unpaired t-test (* P < 0.05). Full-length blots are presented in Figure S5

    Journal: Stem Cell Research & Therapy

    Article Title: Targeting p75NTR activity alleviates the neurotoxic effect of high glucose on iPSC-derived dopaminergic neurons

    doi: 10.1186/s13287-026-04965-y

    Figure Lengend Snippet: Pro-NGF/p75NTR axis is up-regulated in glucose neurotoxicity in DA neurons. a Western blot analysis and quantification of TrkA and TrkB in Control and HG- (100mM) treated neurons for 48 h. Protein levels were normalized to β-Actin. b Western blot analysis and quantification of p75NTR in Control and HG (50mM, 100mM) treated neurons for 48 h. Protein levels were normalized to β-Actin. c Celltox cytotoxicity assay. Representative photos and quantification of dead (green) neurons after treatment with HG (50mM, 100mM) and/or p75NTR inhibitor (2.5 ng/ml, anti-p75 Receptor antibody (MC-192) Abcam) for 48 h. Scale bar 50 μm. d , e ELISA quantification of d pro-NGF protein levels in the cell lysate and e the secreted pro-NGF protein levels in the supernatant of DA neurons treated with HG (100mM) for 48 h. f Schematics of the up-regulated pro-NGF/p75NTR axis in DA neurons upon treatment with HG. For a – e data are presented as mean ± SEM of three biological replicates derived from three independent iPSC lines. For a and c statistical significance was assessed with a two-way ANOVA and Sidak’s multiple comparisons test (** P < 0.01). For b statistical significance was assessed with an ordinary one-way ANOVA and Turkey’s multiple comparisons test (** P < 0.01). For d and e statistical significance was evaluated with an unpaired t-test (* P < 0.05). Full-length blots are presented in Figure S5

    Article Snippet: Pro-NGF and pro-BDNF protein levels were quantified in the cell lysis and the supernatant of neurons cultured in 12 well plate format (one well per condition) by using the human pro-NGF and the human pro-BDNF Rapid ELISA kits (Biosensis, BEK-2226-1P/2P for pro-NGF and BEK-2237-2P for pro-BDNF), respectively.

    Techniques: Western Blot, Control, CellTox Assay, Cytotoxicity Assay, Enzyme-linked Immunosorbent Assay, Derivative Assay