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    Alomone Labs probdnf
    Blockage of <t>proBDNF</t> expression during the postnatal period induces spatial learning impairments. (A) The level of proBDNF in the hippocampus. (* p
    Probdnf, supplied by Alomone Labs, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    80
    Santa Cruz Biotechnology probdnf
    The BDNF prodomain is secreted from cultured neurons. (a) Prodomain was detected in the media of day 6 in vitro rat hippocampal cultures. Cultures were treated with or without α-2 anti-plasmin and/or MMP inhibitor II (MMP1, 3, 7 and 9 inhibitor) in order to prevent extracellular cleavage of secreted <t>proBDNF.</t> Activity-dependent secretion was achieved by depolarization with KCl. (b) Quantification of (a). Bars represent mean ± s.e.m. of prodomain densitometry data. n=3 per group. (c) Treatment with N-glycanase reduced the molecular mass of the secreted prodomain. (d) Prodomain was detected in the media of day 6 in vitro hippocampal-cortical neurons from E18 pups obtained from Bdnf Met/+ × Bdnf Met/+ mice litters. Level of secreted prodomain differ between Bdnf Val/Val and Bdnf Met/Met cultures. (e) Quantification of (d). Bars represent mean ± s.e.m. of prodomain densitometry data. n=4 per group. Statistical comparisons were made by one way analysis of variance test. * p
    Probdnf, supplied by Santa Cruz Biotechnology, used in various techniques. Bioz Stars score: 80/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/probdnf/product/Santa Cruz Biotechnology
    Average 80 stars, based on 1 article reviews
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    Image Search Results


    Blockage of proBDNF expression during the postnatal period induces spatial learning impairments. (A) The level of proBDNF in the hippocampus. (* p

    Journal: Frontiers in Cell and Developmental Biology

    Article Title: Requirements of Postnatal proBDNF in the Hippocampus for Spatial Memory Consolidation and Neural Function

    doi: 10.3389/fcell.2021.678182

    Figure Lengend Snippet: Blockage of proBDNF expression during the postnatal period induces spatial learning impairments. (A) The level of proBDNF in the hippocampus. (* p

    Article Snippet: Anti-proBDNF antibody was purchased from Alomone Labs, Ltd. (Jerusalem, Israel; Cat. No. ANT-006).

    Techniques: Expressing

    Schematic representations of the cannulae and electrode placements and morphological alterations in the CA1 region. (A) Histological (left) and schematic (right) representations of the cannula placements. The control group infused with ACSF throughout the whole PD4w; the Anti@2w and Anti@4w groups were infused with anti-proBDNF antibody throughout the whole second and fourth postnatal weeks, respectively. The yellow arrows indicated the top of the cannulae. (B) Histological and schematic representations of electrode placements. (C) Following the open field test, infusion-induced neuronal damage was assessed by Silver staining (see Supplementary Methods ). The white scale bar presented at the bottom of the photomicrograph indicated 25 μm. The yellow arrows indicated the electrode tips. There was no statistical difference in the quantification of neurodegeneration in CA1 neurons between the control (top) and anti-proBDNF (bottom) groups. The anti-proBDNF group was infused with anti-proBDNF antibody throughout the whole fourth postnatal week. The control group was treated with the same volume of the vehicle (ACSF) throughout the whole the fourth postnatal week. The treatment was conducted twice a day in a 12-h interval. n = 6 for each group.

    Journal: Frontiers in Cell and Developmental Biology

    Article Title: Requirements of Postnatal proBDNF in the Hippocampus for Spatial Memory Consolidation and Neural Function

    doi: 10.3389/fcell.2021.678182

    Figure Lengend Snippet: Schematic representations of the cannulae and electrode placements and morphological alterations in the CA1 region. (A) Histological (left) and schematic (right) representations of the cannula placements. The control group infused with ACSF throughout the whole PD4w; the Anti@2w and Anti@4w groups were infused with anti-proBDNF antibody throughout the whole second and fourth postnatal weeks, respectively. The yellow arrows indicated the top of the cannulae. (B) Histological and schematic representations of electrode placements. (C) Following the open field test, infusion-induced neuronal damage was assessed by Silver staining (see Supplementary Methods ). The white scale bar presented at the bottom of the photomicrograph indicated 25 μm. The yellow arrows indicated the electrode tips. There was no statistical difference in the quantification of neurodegeneration in CA1 neurons between the control (top) and anti-proBDNF (bottom) groups. The anti-proBDNF group was infused with anti-proBDNF antibody throughout the whole fourth postnatal week. The control group was treated with the same volume of the vehicle (ACSF) throughout the whole the fourth postnatal week. The treatment was conducted twice a day in a 12-h interval. n = 6 for each group.

    Article Snippet: Anti-proBDNF antibody was purchased from Alomone Labs, Ltd. (Jerusalem, Israel; Cat. No. ANT-006).

    Techniques: Silver Staining

    Blocking proBDNF reduces spine number and learning-related GluN2B expression. The samples from rats that performed spatial training in the MWM task were collected immediately following the training phase and selected for detecting spine density and the expression of glutamatergic receptor subunits. (A) Spine alteration in naive, untrained-antiproBDNF, trained control, and trained-antiproBDNF rats (top). Quantification of spine density (middle) and the proportion of spine (bottom). Scale bars, 5 μm. n = 6 per group. Sample images were projected at minimal intensity and inverted, background was then subtracted, followed by brightness/contrast adjustment. The expression and phosphorylation of GluA1 (B) and the expression of GluG2/3 and the phosphorylation of GluA2 (C) of AMPAR subunits. n = 10 per group. The expression and phosphorylation of GluN2A (D) and GluN2B (E) of NMDAR subunits. (* p

    Journal: Frontiers in Cell and Developmental Biology

    Article Title: Requirements of Postnatal proBDNF in the Hippocampus for Spatial Memory Consolidation and Neural Function

    doi: 10.3389/fcell.2021.678182

    Figure Lengend Snippet: Blocking proBDNF reduces spine number and learning-related GluN2B expression. The samples from rats that performed spatial training in the MWM task were collected immediately following the training phase and selected for detecting spine density and the expression of glutamatergic receptor subunits. (A) Spine alteration in naive, untrained-antiproBDNF, trained control, and trained-antiproBDNF rats (top). Quantification of spine density (middle) and the proportion of spine (bottom). Scale bars, 5 μm. n = 6 per group. Sample images were projected at minimal intensity and inverted, background was then subtracted, followed by brightness/contrast adjustment. The expression and phosphorylation of GluA1 (B) and the expression of GluG2/3 and the phosphorylation of GluA2 (C) of AMPAR subunits. n = 10 per group. The expression and phosphorylation of GluN2A (D) and GluN2B (E) of NMDAR subunits. (* p

    Article Snippet: Anti-proBDNF antibody was purchased from Alomone Labs, Ltd. (Jerusalem, Israel; Cat. No. ANT-006).

    Techniques: Blocking Assay, Expressing

    Activation of GluN2B can rescue memory consolidation induced by blocking postnatal proBDNF. The infusion of TBOA was conducted 0.5 (Anti+TBOA0.5(a)) or 2.5 h (Anti+TBOA2.5(a)) before spatial training (acquisition), immediately following training (consolidation; Anti+TBOA(b)), and 30 min prior to probe memory test (retrieval; Anti+TBOA(c)), respectively. (A) Schematic description of the experimental timeline. (B) Escape latency in the training phase and (C) the swim proximity score during the probe trial. Note the sample swimming traces demonstrating the swimming trajectories of the control, Anti+TBOA(b), and TBOA(b) groups rather than the Anti group superimposed on target quadrant. The triangle indicated the start point during probe trial. (* p

    Journal: Frontiers in Cell and Developmental Biology

    Article Title: Requirements of Postnatal proBDNF in the Hippocampus for Spatial Memory Consolidation and Neural Function

    doi: 10.3389/fcell.2021.678182

    Figure Lengend Snippet: Activation of GluN2B can rescue memory consolidation induced by blocking postnatal proBDNF. The infusion of TBOA was conducted 0.5 (Anti+TBOA0.5(a)) or 2.5 h (Anti+TBOA2.5(a)) before spatial training (acquisition), immediately following training (consolidation; Anti+TBOA(b)), and 30 min prior to probe memory test (retrieval; Anti+TBOA(c)), respectively. (A) Schematic description of the experimental timeline. (B) Escape latency in the training phase and (C) the swim proximity score during the probe trial. Note the sample swimming traces demonstrating the swimming trajectories of the control, Anti+TBOA(b), and TBOA(b) groups rather than the Anti group superimposed on target quadrant. The triangle indicated the start point during probe trial. (* p

    Article Snippet: Anti-proBDNF antibody was purchased from Alomone Labs, Ltd. (Jerusalem, Israel; Cat. No. ANT-006).

    Techniques: Activation Assay, Blocking Assay

    GluN2B-dependent neural function is enhanced by TBOA. The Anti group was bilaterally infused with anti-proBDNF antibody into the CA1 region throughout the whole PD4w, whereas the Con group received the same volume of ACSF. Eight-week-old rats were selected for detecting hippocampal synaptic function in the Schaffer collateral-CA1 pathway immediately following TBOA (Anti+TBOA and TBOA groups), Ro25 (Ro25 group), or ACSF (Con and Anti groups) injection. (A) Input–output curves of fEPSP slopes. (B) PPF, a form of short-term plasticity, was measured and expressed as the ratio of fEPSPs2 to fEPSPs1. (* p

    Journal: Frontiers in Cell and Developmental Biology

    Article Title: Requirements of Postnatal proBDNF in the Hippocampus for Spatial Memory Consolidation and Neural Function

    doi: 10.3389/fcell.2021.678182

    Figure Lengend Snippet: GluN2B-dependent neural function is enhanced by TBOA. The Anti group was bilaterally infused with anti-proBDNF antibody into the CA1 region throughout the whole PD4w, whereas the Con group received the same volume of ACSF. Eight-week-old rats were selected for detecting hippocampal synaptic function in the Schaffer collateral-CA1 pathway immediately following TBOA (Anti+TBOA and TBOA groups), Ro25 (Ro25 group), or ACSF (Con and Anti groups) injection. (A) Input–output curves of fEPSP slopes. (B) PPF, a form of short-term plasticity, was measured and expressed as the ratio of fEPSPs2 to fEPSPs1. (* p

    Article Snippet: Anti-proBDNF antibody was purchased from Alomone Labs, Ltd. (Jerusalem, Israel; Cat. No. ANT-006).

    Techniques: Injection

    proBDNF Is Induced in Astrocytes After TBI. Adult mice were subjected to CCI and perfused 3 days after injury. Representative sections through the injury site 3 days after CCI show increased proBDNF labeling (red), some of which colocalizes with GFAP (green) adjacent to the area of tissue damage. In contrast, sections through the contralateral side 3 days after the injury show little expression of proBDNF. (A) Arrows indicate colocalization of proBDNF and GFAP-positive cells. (B) Arrowheads indicate GFAP-positive cells that do not express proBDNF. Scale bar = 50 µm. GFAP = glial fibrillary acidic protein; proBDNF = pro-brain-derived neurotrophic factor.

    Journal: ASN NEURO

    Article Title: Proneurotrophins Induce Apoptotic Neuronal Death After Controlled Cortical Impact Injury in Adult Mice

    doi: 10.1177/1759091420930865

    Figure Lengend Snippet: proBDNF Is Induced in Astrocytes After TBI. Adult mice were subjected to CCI and perfused 3 days after injury. Representative sections through the injury site 3 days after CCI show increased proBDNF labeling (red), some of which colocalizes with GFAP (green) adjacent to the area of tissue damage. In contrast, sections through the contralateral side 3 days after the injury show little expression of proBDNF. (A) Arrows indicate colocalization of proBDNF and GFAP-positive cells. (B) Arrowheads indicate GFAP-positive cells that do not express proBDNF. Scale bar = 50 µm. GFAP = glial fibrillary acidic protein; proBDNF = pro-brain-derived neurotrophic factor.

    Article Snippet: The following were the primary antibodies used: anti-NeuN (1:500; Cell Signaling Technology, Danvers, MA, USA, Cat# 12943, RRID:AB_2630395 ), anti-proBDNF (1:500; Alomone Labs, Jerusalem, Israel, Cat# ANT-006, RRID:AB_2039758 ), anti-glial fibrillary acidic protein (GFAP; 1:500; R & D Systems, Minneapolis, MN, USA, Cat# AF2594, RRID:AB_2109656 ), and anti-p75NTR (1:500; R & D Systems, Cat# AF1157, RRID:AB_2298561).

    Techniques: Mouse Assay, Labeling, Expressing, Derivative Assay

    Behavioral Analysis of Mice Receiving Intranasal Neutralizing Antibodies to proNGF or proBDNF Following CCI. (A) Outline of the experimental paradigm of CCI injury and behavioral testing. Control IgG, anti-proNGF, or anti-proBDNF was infused intranasally to each nostril every 2 min for a total of 20 µl immediately after CCI. (B) The mNSS score showed behavioral sparing of mice that received either anti-proNGF or anti-proBDNF compared with mice that received control IgG following CCI. Data were collected across 5 to 8 animals per group. Asterisks indicate significant difference from IgG control by Kruskal–Wallis test followed by Dunn’s multiple comparison test for nonparametric values, with p = .0204 for IgG control versus proNGF-treated mice; p = .045 for IgG control versus proBDNF-treated mice. CCI = controlled cortical impact; mNSS = modified neurological severity scoring; IgG = immunoglobulin G; BDNF = brain-derived neurotrophic factor; NGF = nerve growth factor.

    Journal: ASN NEURO

    Article Title: Proneurotrophins Induce Apoptotic Neuronal Death After Controlled Cortical Impact Injury in Adult Mice

    doi: 10.1177/1759091420930865

    Figure Lengend Snippet: Behavioral Analysis of Mice Receiving Intranasal Neutralizing Antibodies to proNGF or proBDNF Following CCI. (A) Outline of the experimental paradigm of CCI injury and behavioral testing. Control IgG, anti-proNGF, or anti-proBDNF was infused intranasally to each nostril every 2 min for a total of 20 µl immediately after CCI. (B) The mNSS score showed behavioral sparing of mice that received either anti-proNGF or anti-proBDNF compared with mice that received control IgG following CCI. Data were collected across 5 to 8 animals per group. Asterisks indicate significant difference from IgG control by Kruskal–Wallis test followed by Dunn’s multiple comparison test for nonparametric values, with p = .0204 for IgG control versus proNGF-treated mice; p = .045 for IgG control versus proBDNF-treated mice. CCI = controlled cortical impact; mNSS = modified neurological severity scoring; IgG = immunoglobulin G; BDNF = brain-derived neurotrophic factor; NGF = nerve growth factor.

    Article Snippet: The following were the primary antibodies used: anti-NeuN (1:500; Cell Signaling Technology, Danvers, MA, USA, Cat# 12943, RRID:AB_2630395 ), anti-proBDNF (1:500; Alomone Labs, Jerusalem, Israel, Cat# ANT-006, RRID:AB_2039758 ), anti-glial fibrillary acidic protein (GFAP; 1:500; R & D Systems, Minneapolis, MN, USA, Cat# AF2594, RRID:AB_2109656 ), and anti-p75NTR (1:500; R & D Systems, Cat# AF1157, RRID:AB_2298561).

    Techniques: Mouse Assay, Modification, Derivative Assay

    Neutralizing Antibodies to proNGF and proBDNF Provide Neuroprotection. (A) Mice were infused intranasally with anti-proNGF, anti-proBDNF, or control IgG immediately after the CCI. At 3 days of recovery, sections were stained for NeuN and counterstained with DAPI to reveal the area of damage. (B) The area of total damage comprised of the area of tissue loss and the penumbra (dotted line), where the density of DAPI and NeuN staining was reduced. The percentage of the total area of damage (relative to the contralateral hemisphere) was significantly reduced by the antiproneurotrophin antibodies. Scale bar = 200 µm. (C) Representative images of TUNEL staining in the penumbra showed fewer apoptotic cells in the mice that received anti-proNGF or anti-proBDNF. Scale bar = 50 µm. Data were collected from 3 to 4 animals per group. Graphs depict the means ± SEM. Asterisks indicate significance by one-way analysis of variance followed by Tukey’s post hoc analysis with p

    Journal: ASN NEURO

    Article Title: Proneurotrophins Induce Apoptotic Neuronal Death After Controlled Cortical Impact Injury in Adult Mice

    doi: 10.1177/1759091420930865

    Figure Lengend Snippet: Neutralizing Antibodies to proNGF and proBDNF Provide Neuroprotection. (A) Mice were infused intranasally with anti-proNGF, anti-proBDNF, or control IgG immediately after the CCI. At 3 days of recovery, sections were stained for NeuN and counterstained with DAPI to reveal the area of damage. (B) The area of total damage comprised of the area of tissue loss and the penumbra (dotted line), where the density of DAPI and NeuN staining was reduced. The percentage of the total area of damage (relative to the contralateral hemisphere) was significantly reduced by the antiproneurotrophin antibodies. Scale bar = 200 µm. (C) Representative images of TUNEL staining in the penumbra showed fewer apoptotic cells in the mice that received anti-proNGF or anti-proBDNF. Scale bar = 50 µm. Data were collected from 3 to 4 animals per group. Graphs depict the means ± SEM. Asterisks indicate significance by one-way analysis of variance followed by Tukey’s post hoc analysis with p

    Article Snippet: The following were the primary antibodies used: anti-NeuN (1:500; Cell Signaling Technology, Danvers, MA, USA, Cat# 12943, RRID:AB_2630395 ), anti-proBDNF (1:500; Alomone Labs, Jerusalem, Israel, Cat# ANT-006, RRID:AB_2039758 ), anti-glial fibrillary acidic protein (GFAP; 1:500; R & D Systems, Minneapolis, MN, USA, Cat# AF2594, RRID:AB_2109656 ), and anti-p75NTR (1:500; R & D Systems, Cat# AF1157, RRID:AB_2298561).

    Techniques: Mouse Assay, Staining, TUNEL Assay

    The BDNF prodomain is secreted from cultured neurons. (a) Prodomain was detected in the media of day 6 in vitro rat hippocampal cultures. Cultures were treated with or without α-2 anti-plasmin and/or MMP inhibitor II (MMP1, 3, 7 and 9 inhibitor) in order to prevent extracellular cleavage of secreted proBDNF. Activity-dependent secretion was achieved by depolarization with KCl. (b) Quantification of (a). Bars represent mean ± s.e.m. of prodomain densitometry data. n=3 per group. (c) Treatment with N-glycanase reduced the molecular mass of the secreted prodomain. (d) Prodomain was detected in the media of day 6 in vitro hippocampal-cortical neurons from E18 pups obtained from Bdnf Met/+ × Bdnf Met/+ mice litters. Level of secreted prodomain differ between Bdnf Val/Val and Bdnf Met/Met cultures. (e) Quantification of (d). Bars represent mean ± s.e.m. of prodomain densitometry data. n=4 per group. Statistical comparisons were made by one way analysis of variance test. * p

    Journal: Nature communications

    Article Title: Val66Met Polymorphism of BDNF Alters Prodomain Structure to Induce Neuronal Growth Cone Retraction

    doi: 10.1038/ncomms3490

    Figure Lengend Snippet: The BDNF prodomain is secreted from cultured neurons. (a) Prodomain was detected in the media of day 6 in vitro rat hippocampal cultures. Cultures were treated with or without α-2 anti-plasmin and/or MMP inhibitor II (MMP1, 3, 7 and 9 inhibitor) in order to prevent extracellular cleavage of secreted proBDNF. Activity-dependent secretion was achieved by depolarization with KCl. (b) Quantification of (a). Bars represent mean ± s.e.m. of prodomain densitometry data. n=3 per group. (c) Treatment with N-glycanase reduced the molecular mass of the secreted prodomain. (d) Prodomain was detected in the media of day 6 in vitro hippocampal-cortical neurons from E18 pups obtained from Bdnf Met/+ × Bdnf Met/+ mice litters. Level of secreted prodomain differ between Bdnf Val/Val and Bdnf Met/Met cultures. (e) Quantification of (d). Bars represent mean ± s.e.m. of prodomain densitometry data. n=4 per group. Statistical comparisons were made by one way analysis of variance test. * p

    Article Snippet: Val66 proBDNF was collected from supernatants of HEK293FT cells (ATCC) transfected with a construct encoding human proBDNF (furin cleavage site mutated: RR128AA). proBDNF concentration was estimated by western blot (using BDNF antibody from Santa Cruz) comparing to known concentrations of recombinant BDNF (PeproTech, Rocky Hill, NJ, USA).

    Techniques: Cell Culture, In Vitro, Activity Assay, Mouse Assay