anti probdnf  (Alomone Labs)


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    Alomone Labs anti probdnf
    Effect of deletion of Sort1 −/− gene on BDNF system. Western blot analyses and their corresponding histogram quantification of the expression of proteins involved in the BDNF system in brain extracts from WT and Sort1 −/− mice. (A) BDNF, (B) <t>proBDNF,</t> and (C) phospho-TrkB. ∗∗ p
    Anti Probdnf, supplied by Alomone Labs, used in various techniques. Bioz Stars score: 94/100, based on 8 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/anti probdnf/product/Alomone Labs
    Average 94 stars, based on 8 article reviews
    Price from $9.99 to $1999.99
    anti probdnf - by Bioz Stars, 2022-08
    94/100 stars

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    1) Product Images from "Altered Trek-1 Function in Sortilin Deficient Mice Results in Decreased Depressive-Like Behavior"

    Article Title: Altered Trek-1 Function in Sortilin Deficient Mice Results in Decreased Depressive-Like Behavior

    Journal: Frontiers in Pharmacology

    doi: 10.3389/fphar.2018.00863

    Effect of deletion of Sort1 −/− gene on BDNF system. Western blot analyses and their corresponding histogram quantification of the expression of proteins involved in the BDNF system in brain extracts from WT and Sort1 −/− mice. (A) BDNF, (B) proBDNF, and (C) phospho-TrkB. ∗∗ p
    Figure Legend Snippet: Effect of deletion of Sort1 −/− gene on BDNF system. Western blot analyses and their corresponding histogram quantification of the expression of proteins involved in the BDNF system in brain extracts from WT and Sort1 −/− mice. (A) BDNF, (B) proBDNF, and (C) phospho-TrkB. ∗∗ p

    Techniques Used: Western Blot, Expressing, Mouse Assay

    2) Product Images from "Altered Trek-1 Function in Sortilin Deficient Mice Results in Decreased Depressive-Like Behavior"

    Article Title: Altered Trek-1 Function in Sortilin Deficient Mice Results in Decreased Depressive-Like Behavior

    Journal: Frontiers in Pharmacology

    doi: 10.3389/fphar.2018.00863

    Effect of deletion of Sort1 −/− gene on BDNF system. Western blot analyses and their corresponding histogram quantification of the expression of proteins involved in the BDNF system in brain extracts from WT and Sort1 −/− mice. (A) BDNF, (B) proBDNF, and (C) phospho-TrkB. ∗∗ p
    Figure Legend Snippet: Effect of deletion of Sort1 −/− gene on BDNF system. Western blot analyses and their corresponding histogram quantification of the expression of proteins involved in the BDNF system in brain extracts from WT and Sort1 −/− mice. (A) BDNF, (B) proBDNF, and (C) phospho-TrkB. ∗∗ p

    Techniques Used: Western Blot, Expressing, Mouse Assay

    3) Product Images from "Dexmedetomidine Attenuates Neurotoxicity in Developing Rats Induced by Sevoflurane through Upregulating BDNF-TrkB-CREB and Downregulating ProBDNF-P75NRT-RhoA Signaling Pathway"

    Article Title: Dexmedetomidine Attenuates Neurotoxicity in Developing Rats Induced by Sevoflurane through Upregulating BDNF-TrkB-CREB and Downregulating ProBDNF-P75NRT-RhoA Signaling Pathway

    Journal: Mediators of Inflammation

    doi: 10.1155/2020/5458061

    Dexmedetomidine could decrease the level of proBDNF and restore the ratio of proBDNF/mBDNF and alleviates activation of the proBDNF-P75NRT-RHOA pathway after sevoflurane. (a) Western blot band. (b) ProBDNF/mBDNF. (c–e) Bar graph of Western blot. (f) Immunofluorescence of proBDNF (scale bar = 50 μ m). ∗ Compare with the control group, P
    Figure Legend Snippet: Dexmedetomidine could decrease the level of proBDNF and restore the ratio of proBDNF/mBDNF and alleviates activation of the proBDNF-P75NRT-RHOA pathway after sevoflurane. (a) Western blot band. (b) ProBDNF/mBDNF. (c–e) Bar graph of Western blot. (f) Immunofluorescence of proBDNF (scale bar = 50 μ m). ∗ Compare with the control group, P

    Techniques Used: Activation Assay, Western Blot, Immunofluorescence

    4) Product Images from "Altered Trek-1 Function in Sortilin Deficient Mice Results in Decreased Depressive-Like Behavior"

    Article Title: Altered Trek-1 Function in Sortilin Deficient Mice Results in Decreased Depressive-Like Behavior

    Journal: Frontiers in Pharmacology

    doi: 10.3389/fphar.2018.00863

    Effect of deletion of Sort1 −/− gene on BDNF system. Western blot analyses and their corresponding histogram quantification of the expression of proteins involved in the BDNF system in brain extracts from WT and Sort1 −/− mice. (A) BDNF, (B) proBDNF, and (C) phospho-TrkB. ∗∗ p
    Figure Legend Snippet: Effect of deletion of Sort1 −/− gene on BDNF system. Western blot analyses and their corresponding histogram quantification of the expression of proteins involved in the BDNF system in brain extracts from WT and Sort1 −/− mice. (A) BDNF, (B) proBDNF, and (C) phospho-TrkB. ∗∗ p

    Techniques Used: Western Blot, Expressing, Mouse Assay

    5) Product Images from "Altered Trek-1 Function in Sortilin Deficient Mice Results in Decreased Depressive-Like Behavior"

    Article Title: Altered Trek-1 Function in Sortilin Deficient Mice Results in Decreased Depressive-Like Behavior

    Journal: Frontiers in Pharmacology

    doi: 10.3389/fphar.2018.00863

    Effect of deletion of Sort1 −/− gene on BDNF system. Western blot analyses and their corresponding histogram quantification of the expression of proteins involved in the BDNF system in brain extracts from WT and Sort1 −/− mice. (A) BDNF, (B) proBDNF, and (C) phospho-TrkB. ∗∗ p
    Figure Legend Snippet: Effect of deletion of Sort1 −/− gene on BDNF system. Western blot analyses and their corresponding histogram quantification of the expression of proteins involved in the BDNF system in brain extracts from WT and Sort1 −/− mice. (A) BDNF, (B) proBDNF, and (C) phospho-TrkB. ∗∗ p

    Techniques Used: Western Blot, Expressing, Mouse Assay

    6) Product Images from "Extracellular Vesicles Derived from Lactobacillus plantarum Increase BDNF Expression in Cultured Hippocampal Neurons and Produce Antidepressant-like Effects in Mice"

    Article Title: Extracellular Vesicles Derived from Lactobacillus plantarum Increase BDNF Expression in Cultured Hippocampal Neurons and Produce Antidepressant-like Effects in Mice

    Journal: Experimental Neurobiology

    doi: 10.5607/en.2019.28.2.158

    L -EV treatment during the stress-treatment period blocked the stress-induced decrease in the expression of neurotrophic factors in the hippocampus and inhibited stress-induced depressive-like behaviors. (A) Experimental design (Exp. 1). Mice were treated with restraint for 2-h daily for 14 days (2h×14 d RST). Saline or L -EV (0.1 µg/kg) were i.p. injected 30 min before restraint treatment each day. Behavioral tests were performed on post-stress days 1-3 ( p 1~ p 3) and mice were sacrificed on post-stress day 7 ( p 7). Control mice injected with saline (CON+veh), mice treated with L -EV (CON+ L -EV), mice treated with repeated restraint and injected with saline (CRST+veh), and mice treated with repeated restraint and injected with L -EV (CRST+ L -EV) were prepared. (B) Body weight (g) changes of CON+veh, CON+ L -EV, CRST+veh, and CRST+ L -EV (n=8~12 animals per group). (C) Expression levels of Ngf , t Bdnf , Bdnf1 , Bdnf4 , Nt3 , Nt4/5 , and Trkb in the hippocampus of CON+veh, CON+ L -EV, CRST+veh, and CRST+ L -EV (n=6 animals and 4~8 PCR repeats per group). Two-way ANOVA followed by Bonferroni post hoc test ( Ngf , F (1,28) =2.900 and p=0.0997 for CRST main effect, F (1,28) =0.6187 and p=0.4381 for L -EV main effect, and F (1,28) =1.024 and p=0.3202 for CRST× L -EV; t Bdnf , F (1,25) =0.2452 and p=0.6248 for CRST main effect, F (1,25) =15.43 and p=0.0006 for L -EV main effect, and F (1,25) =1.932 and p=0.1768 for CRST× L -EV; Bdnf1 , F (1,12) =9.542 and p=0.0094 for CRST main effect, F (1,12) =15.01 and p=0.0022 for L -EV main effect, and F (1,12) =2.324 and p=0.1533 for CRST× L -EV; Bdnf4 , F (1,12) =13.95 and p=0.0028 for CRST main effect, F (1,12) =9.418 and p=0.0097 for L -EV main effect, and F (1,12) =8.003 and p=0.0152 for CRST× L -EV; Nt3 , F (1,28) 0.9424 and p=0.3400 for CRST main effect, F (1,28) =0.1996 and p=0.6585 for L -EV main effect, and F (1,28) =1.974 and p=0.1710 for CRST× L -EV; Nt4/5 , F (1,24) =14.45 and p=0.0009 for CRST main effect, F (1,24) =1.654 and p=0.2106 for L -EV main effect, and F (1,24) =8.419 and p=0.0078 for CRST× L -EV; Trkb , F (1,14) =0.0650 and p=0.8025 for CRST main effect, F (1,14) =1.768 and p=0.2049 for L -EV main effect, and F (1,14) =2.969 and p=0.1069 for CRST× L -EV). (D) Western blot data showing the expression level of proBDNF in the hippocampus of CON+veh, CON+ L -EV, CRST+veh, and CRST+ L -EV (n=6 animals and 4 WB repeats per group). Two-way ANOVA followed by Bonferroni post hoc test (F (1,12) =12.29 and p=0.0043 for CRST main effect, F (1,12) =1.697 and p=0.2172 for L -EV main effect, and F (1,12) =8.952 and p=0.0112 for CRST× L -EV). (E) Expression levels of Sirt1 , Hdac2 , and Creb1 in the hippocampus of CON+veh, CON+ L -EV, CRST+veh, and CRST+ L -EV (n=6 animals and 6–10 PCR repeats per group). Two-way ANOVA followed by Bonferroni post hoc test ( Sirt1 , F (1,23) =6.483 and p=0.0181 for CRST main effect, F (1,23) =12.17 and p=0.0020 for L -EV main effect, and F (1,23) =2.365 and p=0.1377 for CRST× L -EV; Hdac2 , F (1,25) =10.31 and p=0.0036 for CRST main effect, F (1,25) =5.110 and p=0.0327 for L -EV main effect, and F (1,25) =1.340 and p=0.2280 for CRST× L -EV; Creb1 , F (1,22) =0.2456 and p=0.6251 for CRST main effect, F (1,22) =2.829 and p=0.1067 for L -EV main effect, and F (1,22) =1.358 and p=0.2564 for CRST× L -EV). (F, G) Immobility time in the tail suspension test (TST; F) and forced swim test (FST; G) of CON+veh, CON+ L -EV, CRST+veh, and CRST+ L -EV (n=7~12 animals per group). Two-way ANOVA followed by Bonferroni post hoc test (TST, F (1,33) =11.90 and p=0.0016 for CRST main effect, F (1,33) =6.235 and p=0.0177 for L -EV main effect, and F (1,33) =1.665 and p=0.2059 for CRST× L -EV; FST, F (1,36) =23.84 and p
    Figure Legend Snippet: L -EV treatment during the stress-treatment period blocked the stress-induced decrease in the expression of neurotrophic factors in the hippocampus and inhibited stress-induced depressive-like behaviors. (A) Experimental design (Exp. 1). Mice were treated with restraint for 2-h daily for 14 days (2h×14 d RST). Saline or L -EV (0.1 µg/kg) were i.p. injected 30 min before restraint treatment each day. Behavioral tests were performed on post-stress days 1-3 ( p 1~ p 3) and mice were sacrificed on post-stress day 7 ( p 7). Control mice injected with saline (CON+veh), mice treated with L -EV (CON+ L -EV), mice treated with repeated restraint and injected with saline (CRST+veh), and mice treated with repeated restraint and injected with L -EV (CRST+ L -EV) were prepared. (B) Body weight (g) changes of CON+veh, CON+ L -EV, CRST+veh, and CRST+ L -EV (n=8~12 animals per group). (C) Expression levels of Ngf , t Bdnf , Bdnf1 , Bdnf4 , Nt3 , Nt4/5 , and Trkb in the hippocampus of CON+veh, CON+ L -EV, CRST+veh, and CRST+ L -EV (n=6 animals and 4~8 PCR repeats per group). Two-way ANOVA followed by Bonferroni post hoc test ( Ngf , F (1,28) =2.900 and p=0.0997 for CRST main effect, F (1,28) =0.6187 and p=0.4381 for L -EV main effect, and F (1,28) =1.024 and p=0.3202 for CRST× L -EV; t Bdnf , F (1,25) =0.2452 and p=0.6248 for CRST main effect, F (1,25) =15.43 and p=0.0006 for L -EV main effect, and F (1,25) =1.932 and p=0.1768 for CRST× L -EV; Bdnf1 , F (1,12) =9.542 and p=0.0094 for CRST main effect, F (1,12) =15.01 and p=0.0022 for L -EV main effect, and F (1,12) =2.324 and p=0.1533 for CRST× L -EV; Bdnf4 , F (1,12) =13.95 and p=0.0028 for CRST main effect, F (1,12) =9.418 and p=0.0097 for L -EV main effect, and F (1,12) =8.003 and p=0.0152 for CRST× L -EV; Nt3 , F (1,28) 0.9424 and p=0.3400 for CRST main effect, F (1,28) =0.1996 and p=0.6585 for L -EV main effect, and F (1,28) =1.974 and p=0.1710 for CRST× L -EV; Nt4/5 , F (1,24) =14.45 and p=0.0009 for CRST main effect, F (1,24) =1.654 and p=0.2106 for L -EV main effect, and F (1,24) =8.419 and p=0.0078 for CRST× L -EV; Trkb , F (1,14) =0.0650 and p=0.8025 for CRST main effect, F (1,14) =1.768 and p=0.2049 for L -EV main effect, and F (1,14) =2.969 and p=0.1069 for CRST× L -EV). (D) Western blot data showing the expression level of proBDNF in the hippocampus of CON+veh, CON+ L -EV, CRST+veh, and CRST+ L -EV (n=6 animals and 4 WB repeats per group). Two-way ANOVA followed by Bonferroni post hoc test (F (1,12) =12.29 and p=0.0043 for CRST main effect, F (1,12) =1.697 and p=0.2172 for L -EV main effect, and F (1,12) =8.952 and p=0.0112 for CRST× L -EV). (E) Expression levels of Sirt1 , Hdac2 , and Creb1 in the hippocampus of CON+veh, CON+ L -EV, CRST+veh, and CRST+ L -EV (n=6 animals and 6–10 PCR repeats per group). Two-way ANOVA followed by Bonferroni post hoc test ( Sirt1 , F (1,23) =6.483 and p=0.0181 for CRST main effect, F (1,23) =12.17 and p=0.0020 for L -EV main effect, and F (1,23) =2.365 and p=0.1377 for CRST× L -EV; Hdac2 , F (1,25) =10.31 and p=0.0036 for CRST main effect, F (1,25) =5.110 and p=0.0327 for L -EV main effect, and F (1,25) =1.340 and p=0.2280 for CRST× L -EV; Creb1 , F (1,22) =0.2456 and p=0.6251 for CRST main effect, F (1,22) =2.829 and p=0.1067 for L -EV main effect, and F (1,22) =1.358 and p=0.2564 for CRST× L -EV). (F, G) Immobility time in the tail suspension test (TST; F) and forced swim test (FST; G) of CON+veh, CON+ L -EV, CRST+veh, and CRST+ L -EV (n=7~12 animals per group). Two-way ANOVA followed by Bonferroni post hoc test (TST, F (1,33) =11.90 and p=0.0016 for CRST main effect, F (1,33) =6.235 and p=0.0177 for L -EV main effect, and F (1,33) =1.665 and p=0.2059 for CRST× L -EV; FST, F (1,36) =23.84 and p

    Techniques Used: Expressing, Mouse Assay, Injection, Polymerase Chain Reaction, Western Blot

    7) Product Images from "Proneurotrophins Induce Apoptotic Neuronal Death After Controlled Cortical Impact Injury in Adult Mice"

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

    Journal: ASN NEURO

    doi: 10.1177/1759091420930865

    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.
    Figure Legend 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.

    Techniques Used: 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.
    Figure Legend 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.

    Techniques Used: 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
    Figure Legend 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

    Techniques Used: Mouse Assay, Staining, TUNEL Assay

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    Alomone Labs pro bdnf
    <t>α-BDNF,</t> α-Myc, and α–pro-BDNF antibodies all generate similar staining patterns. (A) A schematic representation of the BDNF precursor pro-BDNF and the two cleavage products pro-peptide and BDNF. (B) Low-power view of a WT hippocampal section stained with anti-BDNF antibodies. Note the intense staining in the hilus of the DG and in SL of CA3, each of which contains the axon terminals of mossy fibers. (C and D) Higher magnification view of the DG (C) and CA3 region (D) of the cbdnf ko hippocampus stained with anti-BDNF. Note the absence of immunoreactive signals in all cellular and neuropil layers. GCL, granule cell layer; H, hilus; IML, inner molecular layer; PCL, pyramidal cell layer. (E) Bdnf-Myc hippocampi stained with Myc antibodies show a similar staining pattern to that produced by BDNF antibodies. (F and G) Note the absence of staining in the corresponding DG (F) and CA3 regions (G) of WT sections treated with Myc antibodies. (H) <t>Polyclonal</t> pro-BDNF antibodies yield a similar pattern to that of anti-BDNF. (I and J) The same antibodies do not produce an immunoreactive signal in hippocampal sections from cbdnf ko animals. (B, E, and H) Arrows denote the end bulb of the mossy fiber projection, which delineates CA3 and CA1. Note the relative lack of staining in CA1 in WT and Bdnf-Myc sections. Bars: (B, E, and H) 500 µm; (C, F, and I) 100 µm; (D, G, and J) 50 µm.
    Pro Bdnf, 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
    https://www.bioz.com/result/pro bdnf/product/Alomone Labs
    Average 94 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    pro bdnf - by Bioz Stars, 2022-08
    94/100 stars
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    α-BDNF, α-Myc, and α–pro-BDNF antibodies all generate similar staining patterns. (A) A schematic representation of the BDNF precursor pro-BDNF and the two cleavage products pro-peptide and BDNF. (B) Low-power view of a WT hippocampal section stained with anti-BDNF antibodies. Note the intense staining in the hilus of the DG and in SL of CA3, each of which contains the axon terminals of mossy fibers. (C and D) Higher magnification view of the DG (C) and CA3 region (D) of the cbdnf ko hippocampus stained with anti-BDNF. Note the absence of immunoreactive signals in all cellular and neuropil layers. GCL, granule cell layer; H, hilus; IML, inner molecular layer; PCL, pyramidal cell layer. (E) Bdnf-Myc hippocampi stained with Myc antibodies show a similar staining pattern to that produced by BDNF antibodies. (F and G) Note the absence of staining in the corresponding DG (F) and CA3 regions (G) of WT sections treated with Myc antibodies. (H) Polyclonal pro-BDNF antibodies yield a similar pattern to that of anti-BDNF. (I and J) The same antibodies do not produce an immunoreactive signal in hippocampal sections from cbdnf ko animals. (B, E, and H) Arrows denote the end bulb of the mossy fiber projection, which delineates CA3 and CA1. Note the relative lack of staining in CA1 in WT and Bdnf-Myc sections. Bars: (B, E, and H) 500 µm; (C, F, and I) 100 µm; (D, G, and J) 50 µm.

    Journal: The Journal of Cell Biology

    Article Title: BDNF and its pro-peptide are stored in presynaptic dense core vesicles in brain neurons

    doi: 10.1083/jcb.201201038

    Figure Lengend Snippet: α-BDNF, α-Myc, and α–pro-BDNF antibodies all generate similar staining patterns. (A) A schematic representation of the BDNF precursor pro-BDNF and the two cleavage products pro-peptide and BDNF. (B) Low-power view of a WT hippocampal section stained with anti-BDNF antibodies. Note the intense staining in the hilus of the DG and in SL of CA3, each of which contains the axon terminals of mossy fibers. (C and D) Higher magnification view of the DG (C) and CA3 region (D) of the cbdnf ko hippocampus stained with anti-BDNF. Note the absence of immunoreactive signals in all cellular and neuropil layers. GCL, granule cell layer; H, hilus; IML, inner molecular layer; PCL, pyramidal cell layer. (E) Bdnf-Myc hippocampi stained with Myc antibodies show a similar staining pattern to that produced by BDNF antibodies. (F and G) Note the absence of staining in the corresponding DG (F) and CA3 regions (G) of WT sections treated with Myc antibodies. (H) Polyclonal pro-BDNF antibodies yield a similar pattern to that of anti-BDNF. (I and J) The same antibodies do not produce an immunoreactive signal in hippocampal sections from cbdnf ko animals. (B, E, and H) Arrows denote the end bulb of the mossy fiber projection, which delineates CA3 and CA1. Note the relative lack of staining in CA1 in WT and Bdnf-Myc sections. Bars: (B, E, and H) 500 µm; (C, F, and I) 100 µm; (D, G, and J) 50 µm.

    Article Snippet: Pro-BDNF was detected with a rabbit polyclonal antibody (anti–pro-BDNF; #ANT-006, batch AN-03; Alomone Labs) raised against the prodomain of BDNF protein (see ).

    Techniques: Staining, Produced

    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: A total of 418 male offspring from an average of 84 litters were randomly assigned to one of six groups: ( ) anti-proBDNF (second week), ( ) anti-proBDNF (fourth week), and ( ) anti-proBDNF (eighth week) groups received bilateral infusion of rabbit polyclonal anti-proBDNF antibody ( ; ) in the CA1 region of the HPC throughout the entire second postnatal week (PD2w, from PD8 to PD14), fourth postnatal week (PD4w, from PD22 to PD28), and eighth postnatal week (PD8w, from PD50 to PD56), respectively; ( ) control group was treated with the same volume of the vehicle (artificial cerebrospinal fluid, ACSF) throughout the whole PD2w (Con@2w), PD4w (Con@4w), and PD8w (Con@8w); ( ) Anti+TBOA group, which received infusion of anti-proBDNF antibody during the postnatal weeks, was bilaterally infused with DL-threo-β-benzyloxyaspartate (DL-TBOA) 0.5 or 2.5 h before spatial training [Anti+TBOA0.5(a) or Anti+TBOA2.5(a)], immediately following behavioral training [Anti+TBOA(b)] or 0.5 h before probe test [Anti+TBOA(c)]; and ( ) control group, which received infusion of ACSF during the postnatal weeks, was bilaterally infused with DL-TBOA 0.5 h before spatial training [TBOA(a)], immediately following behavioral training [TBOA(b)] or 0.5 h before probe test [TBOA(c)]; ( ) naive group was reared as the control group without the treatment.

    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: A total of 418 male offspring from an average of 84 litters were randomly assigned to one of six groups: ( ) anti-proBDNF (second week), ( ) anti-proBDNF (fourth week), and ( ) anti-proBDNF (eighth week) groups received bilateral infusion of rabbit polyclonal anti-proBDNF antibody ( ; ) in the CA1 region of the HPC throughout the entire second postnatal week (PD2w, from PD8 to PD14), fourth postnatal week (PD4w, from PD22 to PD28), and eighth postnatal week (PD8w, from PD50 to PD56), respectively; ( ) control group was treated with the same volume of the vehicle (artificial cerebrospinal fluid, ACSF) throughout the whole PD2w (Con@2w), PD4w (Con@4w), and PD8w (Con@8w); ( ) Anti+TBOA group, which received infusion of anti-proBDNF antibody during the postnatal weeks, was bilaterally infused with DL-threo-β-benzyloxyaspartate (DL-TBOA) 0.5 or 2.5 h before spatial training [Anti+TBOA0.5(a) or Anti+TBOA2.5(a)], immediately following behavioral training [Anti+TBOA(b)] or 0.5 h before probe test [Anti+TBOA(c)]; and ( ) control group, which received infusion of ACSF during the postnatal weeks, was bilaterally infused with DL-TBOA 0.5 h before spatial training [TBOA(a)], immediately following behavioral training [TBOA(b)] or 0.5 h before probe test [TBOA(c)]; ( ) naive group was reared as the control group without the treatment.

    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: A total of 418 male offspring from an average of 84 litters were randomly assigned to one of six groups: ( ) anti-proBDNF (second week), ( ) anti-proBDNF (fourth week), and ( ) anti-proBDNF (eighth week) groups received bilateral infusion of rabbit polyclonal anti-proBDNF antibody ( ; ) in the CA1 region of the HPC throughout the entire second postnatal week (PD2w, from PD8 to PD14), fourth postnatal week (PD4w, from PD22 to PD28), and eighth postnatal week (PD8w, from PD50 to PD56), respectively; ( ) control group was treated with the same volume of the vehicle (artificial cerebrospinal fluid, ACSF) throughout the whole PD2w (Con@2w), PD4w (Con@4w), and PD8w (Con@8w); ( ) Anti+TBOA group, which received infusion of anti-proBDNF antibody during the postnatal weeks, was bilaterally infused with DL-threo-β-benzyloxyaspartate (DL-TBOA) 0.5 or 2.5 h before spatial training [Anti+TBOA0.5(a) or Anti+TBOA2.5(a)], immediately following behavioral training [Anti+TBOA(b)] or 0.5 h before probe test [Anti+TBOA(c)]; and ( ) control group, which received infusion of ACSF during the postnatal weeks, was bilaterally infused with DL-TBOA 0.5 h before spatial training [TBOA(a)], immediately following behavioral training [TBOA(b)] or 0.5 h before probe test [TBOA(c)]; ( ) naive group was reared as the control group without the treatment.

    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: A total of 418 male offspring from an average of 84 litters were randomly assigned to one of six groups: ( ) anti-proBDNF (second week), ( ) anti-proBDNF (fourth week), and ( ) anti-proBDNF (eighth week) groups received bilateral infusion of rabbit polyclonal anti-proBDNF antibody ( ; ) in the CA1 region of the HPC throughout the entire second postnatal week (PD2w, from PD8 to PD14), fourth postnatal week (PD4w, from PD22 to PD28), and eighth postnatal week (PD8w, from PD50 to PD56), respectively; ( ) control group was treated with the same volume of the vehicle (artificial cerebrospinal fluid, ACSF) throughout the whole PD2w (Con@2w), PD4w (Con@4w), and PD8w (Con@8w); ( ) Anti+TBOA group, which received infusion of anti-proBDNF antibody during the postnatal weeks, was bilaterally infused with DL-threo-β-benzyloxyaspartate (DL-TBOA) 0.5 or 2.5 h before spatial training [Anti+TBOA0.5(a) or Anti+TBOA2.5(a)], immediately following behavioral training [Anti+TBOA(b)] or 0.5 h before probe test [Anti+TBOA(c)]; and ( ) control group, which received infusion of ACSF during the postnatal weeks, was bilaterally infused with DL-TBOA 0.5 h before spatial training [TBOA(a)], immediately following behavioral training [TBOA(b)] or 0.5 h before probe test [TBOA(c)]; ( ) naive group was reared as the control group without the treatment.

    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: A total of 418 male offspring from an average of 84 litters were randomly assigned to one of six groups: ( ) anti-proBDNF (second week), ( ) anti-proBDNF (fourth week), and ( ) anti-proBDNF (eighth week) groups received bilateral infusion of rabbit polyclonal anti-proBDNF antibody ( ; ) in the CA1 region of the HPC throughout the entire second postnatal week (PD2w, from PD8 to PD14), fourth postnatal week (PD4w, from PD22 to PD28), and eighth postnatal week (PD8w, from PD50 to PD56), respectively; ( ) control group was treated with the same volume of the vehicle (artificial cerebrospinal fluid, ACSF) throughout the whole PD2w (Con@2w), PD4w (Con@4w), and PD8w (Con@8w); ( ) Anti+TBOA group, which received infusion of anti-proBDNF antibody during the postnatal weeks, was bilaterally infused with DL-threo-β-benzyloxyaspartate (DL-TBOA) 0.5 or 2.5 h before spatial training [Anti+TBOA0.5(a) or Anti+TBOA2.5(a)], immediately following behavioral training [Anti+TBOA(b)] or 0.5 h before probe test [Anti+TBOA(c)]; and ( ) control group, which received infusion of ACSF during the postnatal weeks, was bilaterally infused with DL-TBOA 0.5 h before spatial training [TBOA(a)], immediately following behavioral training [TBOA(b)] or 0.5 h before probe test [TBOA(c)]; ( ) naive group was reared as the control group without the treatment.

    Techniques: Injection

    Effect of deletion of Sort1 −/− gene on BDNF system. Western blot analyses and their corresponding histogram quantification of the expression of proteins involved in the BDNF system in brain extracts from WT and Sort1 −/− mice. (A) BDNF, (B) proBDNF, and (C) phospho-TrkB. ∗∗ p

    Journal: Frontiers in Pharmacology

    Article Title: Altered Trek-1 Function in Sortilin Deficient Mice Results in Decreased Depressive-Like Behavior

    doi: 10.3389/fphar.2018.00863

    Figure Lengend Snippet: Effect of deletion of Sort1 −/− gene on BDNF system. Western blot analyses and their corresponding histogram quantification of the expression of proteins involved in the BDNF system in brain extracts from WT and Sort1 −/− mice. (A) BDNF, (B) proBDNF, and (C) phospho-TrkB. ∗∗ p

    Article Snippet: Rabbit polyclonal antibodies anti-TREK-1 and anti-proBDNF were from Alomone Labs (Israel).

    Techniques: Western Blot, Expressing, Mouse Assay

    Expression of BDNF and its receptors in human CRC cell lines. (A): RT-PCR of BDNF, its high (TrkB) and low (p75 NTR ) affinity receptors, TrkA, and TrkC from cells cultured in basal (10% FCS medium), WiDr (lane: 1), SW480 (lane: 2), SW620 (lane: 3), COLO 205 (lane: 4). GAPDH mRNA levels was used as an internal control. Positive control (lane 5) was the neuroblastoma cell line (IMR32) for BDNF, TrkB and p75 NTR ; and the erythromyeloblastoid leukemia cells (K562) for TrkA and C. A representative result of at least three to five independent experiments. (B) Comparison of TrkB95 and p75 NTR on total RNA extracted from WiDr cells cultured in 10% FCS or after 24 to 72 h serum deprivation (0% FCS). TrkB95 and p75 NTR mRNA/GAPDH mRNA quantification of band intensities evaluated by densitometry are shown above lanes and expressed in arbitrary units (mean of three independent experiments). (C) Same experiment: RT-PCR of TrkA and TrkC on total RNA extracted from WiDr cells cultured under basal culture conditions (10% FCS) and after 24–72 h of serum starvation in comparison to positive control (K562) (D) Expression of pro-BDNF and BDNF, full length TrkB 145 and truncated TrkB 95 and p75 NTR proteins in CRC cell lines cultured in 10% FCS. TrkA and TrkC were not detected. Actin was used as loading protein control. WiDr (lane: 1), SW480 (lane: 2), SW620 (lane: 3), COLO 205 (lane: 4). Positive control (lane: 5) were IMR32 cells for BDNF, pro-BDNF, TrkB and p75 NTR and K562 cells or TrkA and TrkC. A representative result of at least three independent experiments.

    Journal: PLoS ONE

    Article Title: Fine-Tuning Roles of Endogenous Brain-Derived Neurotrophic Factor, TrkB and Sortilin in Colorectal Cancer Cell Survival

    doi: 10.1371/journal.pone.0025097

    Figure Lengend Snippet: Expression of BDNF and its receptors in human CRC cell lines. (A): RT-PCR of BDNF, its high (TrkB) and low (p75 NTR ) affinity receptors, TrkA, and TrkC from cells cultured in basal (10% FCS medium), WiDr (lane: 1), SW480 (lane: 2), SW620 (lane: 3), COLO 205 (lane: 4). GAPDH mRNA levels was used as an internal control. Positive control (lane 5) was the neuroblastoma cell line (IMR32) for BDNF, TrkB and p75 NTR ; and the erythromyeloblastoid leukemia cells (K562) for TrkA and C. A representative result of at least three to five independent experiments. (B) Comparison of TrkB95 and p75 NTR on total RNA extracted from WiDr cells cultured in 10% FCS or after 24 to 72 h serum deprivation (0% FCS). TrkB95 and p75 NTR mRNA/GAPDH mRNA quantification of band intensities evaluated by densitometry are shown above lanes and expressed in arbitrary units (mean of three independent experiments). (C) Same experiment: RT-PCR of TrkA and TrkC on total RNA extracted from WiDr cells cultured under basal culture conditions (10% FCS) and after 24–72 h of serum starvation in comparison to positive control (K562) (D) Expression of pro-BDNF and BDNF, full length TrkB 145 and truncated TrkB 95 and p75 NTR proteins in CRC cell lines cultured in 10% FCS. TrkA and TrkC were not detected. Actin was used as loading protein control. WiDr (lane: 1), SW480 (lane: 2), SW620 (lane: 3), COLO 205 (lane: 4). Positive control (lane: 5) were IMR32 cells for BDNF, pro-BDNF, TrkB and p75 NTR and K562 cells or TrkA and TrkC. A representative result of at least three independent experiments.

    Article Snippet: The following Abs were used: rabbit anti-BDNF Ab (1 µg/ml; Santa Cruz Biotechnology), rabbit anti-pro-BDNF Ab (8 µg/ml; Alomone Labs), mouse anti-TrkB Ab (2.5 µg/ml; R & D Systems), rabbit anti-p75NTR (2 µg/ml; Santa Cruz Biotechnology) and goat anti-sortilin Ab (1 µg/ml; Santa Cruz Biotechnology).

    Techniques: Expressing, Reverse Transcription Polymerase Chain Reaction, Cell Culture, Positive Control

    Membranous and cytoplasmic expression of BDNF and TrkB depending on culture conditions. Confocal microscopy of WiDr (A, B) and COLO 205 (C, D) cells, stained with an anti-BDNF Ab (red), anti-TrkB mAb (green) or both (overlay) cultured with 10% FCS (A, C) or after 24-h serum deprivation (B, D). Under basal culture conditions (10% FCS), TrkB and BDNF were sequestered in the cytoplasm (arrows) in WiDr (A) and COLO 205 (C) cells. The same staining patterns were obtained with the two other cell lines (data not shown). After serum starvation relocation to the cell membrane and colocalization of TrkB and BDNF (yellow in merged, arrows) were detected in WiDr (B) and COLO 205 (D). Images were representative for at least three to five independent experiments.

    Journal: PLoS ONE

    Article Title: Fine-Tuning Roles of Endogenous Brain-Derived Neurotrophic Factor, TrkB and Sortilin in Colorectal Cancer Cell Survival

    doi: 10.1371/journal.pone.0025097

    Figure Lengend Snippet: Membranous and cytoplasmic expression of BDNF and TrkB depending on culture conditions. Confocal microscopy of WiDr (A, B) and COLO 205 (C, D) cells, stained with an anti-BDNF Ab (red), anti-TrkB mAb (green) or both (overlay) cultured with 10% FCS (A, C) or after 24-h serum deprivation (B, D). Under basal culture conditions (10% FCS), TrkB and BDNF were sequestered in the cytoplasm (arrows) in WiDr (A) and COLO 205 (C) cells. The same staining patterns were obtained with the two other cell lines (data not shown). After serum starvation relocation to the cell membrane and colocalization of TrkB and BDNF (yellow in merged, arrows) were detected in WiDr (B) and COLO 205 (D). Images were representative for at least three to five independent experiments.

    Article Snippet: The following Abs were used: rabbit anti-BDNF Ab (1 µg/ml; Santa Cruz Biotechnology), rabbit anti-pro-BDNF Ab (8 µg/ml; Alomone Labs), mouse anti-TrkB Ab (2.5 µg/ml; R & D Systems), rabbit anti-p75NTR (2 µg/ml; Santa Cruz Biotechnology) and goat anti-sortilin Ab (1 µg/ml; Santa Cruz Biotechnology).

    Techniques: Expressing, Confocal Microscopy, Staining, Cell Culture

    BDNF-TrkB promotes the cell survival of CRC cell lines. (A) Role of endogenous BDNF and its receptor TrkB on CRC cell proliferation: effects of exogenous BDNF and suppressing endogenous TrkB receptor on cell proliferation. The four cell lines were cultured for 24 h in FCS-free medium (FCS 10%, −) in the presence of exogenous BDNF (+), K252a (+) alone or in combination. Cell proliferation was determined by flow cytometry analysis using EdU Alexa Fluor 488. The data are presented as histograms of proliferating cells in relative units ± SEM of five independent experiments. *, p

    Journal: PLoS ONE

    Article Title: Fine-Tuning Roles of Endogenous Brain-Derived Neurotrophic Factor, TrkB and Sortilin in Colorectal Cancer Cell Survival

    doi: 10.1371/journal.pone.0025097

    Figure Lengend Snippet: BDNF-TrkB promotes the cell survival of CRC cell lines. (A) Role of endogenous BDNF and its receptor TrkB on CRC cell proliferation: effects of exogenous BDNF and suppressing endogenous TrkB receptor on cell proliferation. The four cell lines were cultured for 24 h in FCS-free medium (FCS 10%, −) in the presence of exogenous BDNF (+), K252a (+) alone or in combination. Cell proliferation was determined by flow cytometry analysis using EdU Alexa Fluor 488. The data are presented as histograms of proliferating cells in relative units ± SEM of five independent experiments. *, p

    Article Snippet: The following Abs were used: rabbit anti-BDNF Ab (1 µg/ml; Santa Cruz Biotechnology), rabbit anti-pro-BDNF Ab (8 µg/ml; Alomone Labs), mouse anti-TrkB Ab (2.5 µg/ml; R & D Systems), rabbit anti-p75NTR (2 µg/ml; Santa Cruz Biotechnology) and goat anti-sortilin Ab (1 µg/ml; Santa Cruz Biotechnology).

    Techniques: Cell Culture, Flow Cytometry, Cytometry