Review



py816 trkb fl  (Boster Bio)


Bioz Verified Symbol Boster Bio is a verified supplier
Bioz Manufacturer Symbol Boster Bio manufactures this product  
  • Logo
  • About
  • News
  • Press Release
  • Team
  • Advisors
  • Partners
  • Contact
  • Bioz Stars
  • Bioz vStars
    • 93
      Buy from Supplier

    Structured Review

    Boster Bio py816 trkb fl
    A – D Kinetics of TrkB-FL downregulation. Primary cortical cultures were treated with 100 μM NMDA and its co-agonist 10 μM glycine (hereafter referred to as ‘NMDA’). Immunofluorescence ( A ) and immunoblotting ( B ) used a C-terminal (C-ter) isoform-specific antibody (TrkB-FL Ct) recognizing both the full-length protein (FL) and the intracellular fragment (f32). A Shows TrkB-FL (green) and nuclei (blue, DAPI stain). Arrowheads indicate varicosities in neuronal projections. Scale bar: 20 μm. Insets show cell body details for untreated cells and cells treated with NMDA for 120 min. B Compares the decrease in TrkB-FL and formation of f32 with PSD-95 downregulation, detected using a C-terminal antibody (PSD-95 Ct). Calpain activation was confirmed by the accumulation of characteristic spectrin breakdown products (BDPs; 150 and 145 kDa). Neuron-specific enolase (NSE) served as a loading control for protein normalization. C , D Quantification of normalized TrkB-FL and PSD-95 levels, shown relative to levels in the absence of NMDA (control). Data are represented as means ± SD. Statistical analysis: one-way analysis of variance (ANOVA) followed by Bonferroni post hoc test (** P < 0.01, *** P < 0.001, **** P < 0.0001; 0-90 min, n = 5; 120 min, n = 3). E , F Effect of dynasore preincubation (80 μM, 30 min) on TrkB-FL levels after 2 h NMDA treatment. Data are means ± SD ( n = 4); statistical analysis as above (* P < 0.05). G Sequences of the cell-penetrating neuroprotective peptide (MTFL 457 ) and control peptide (MTMyc). Both contain Tat amino acids (aa) 47–57 (italic), followed by rat TrkB-FL aa 457-471 (light blue) or c-Myc aa 408-421 (dark blue), respectively. H , I Effect of peptide preincubation (25 μM, 30 min) on TrkB-FL shedding and processing during NMDA treatment. Culture media were analyzed using an antibody against the TrkB-FL extracellular domain (panTrkB), which recognizes the ectodomains (ECDs) of all isoforms (TrkB-ECD), to assess receptor shedding by metalloproteinase (MP) activation. Total lysates were analyzed with the TrkB-FL Ct antibody to evaluate TrkB-FL calpain processing via f32 production. Relative TrkB-ECD levels are shown as means ± SD (0-4 h, n = 7; 6 h, n = 4). Statistical analysis: two-way ANOVA followed by Bonferroni post hoc test (** P < 0.01, **** P < 0.0001, comparing each peptide + NMDA vs. peptide alone; # P < 0.05, #### P < 0.0001, comparing MTMyc vs. MTFL 457 at each time point). J , K Effect of NMDA on total and cell-surface <t>pY816-TrkB-FL</t> levels. Cultures were preincubated with peptides as above, then treated briefly with NMDA (1 h) to minimize receptor degradation. Cell-surface proteins were biotin-labeled and precipitated, then compared to corresponding total lysates. Data are represented as means ± SD ( n = 4). Statistical analysis: two-way ANOVA followed by Bonferroni post hoc test ( n.s . = n ot significant; ** P < 0.01, comparing NMDA vs. no NMDA; ## P < 0.01, comparing MTMyc + NMDA vs. MTFL 457 + NMDA).
    Py816 Trkb Fl, supplied by Boster Bio, used in various techniques. Bioz Stars score: 93/100, based on 3 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/py816 trkb fl/product/Boster Bio
    Average 93 stars, based on 3 article reviews
    py816 trkb fl - by Bioz Stars, 2026-03
    93/100 stars

    Images

    1) Product Images from "Retrograde transport of neurotrophin receptor TrkB-FL induced by excitotoxicity regulates Golgi stability and is a target for stroke neuroprotection"

    Article Title: Retrograde transport of neurotrophin receptor TrkB-FL induced by excitotoxicity regulates Golgi stability and is a target for stroke neuroprotection

    Journal: Cell Death & Disease

    doi: 10.1038/s41419-025-07990-6

    A – D Kinetics of TrkB-FL downregulation. Primary cortical cultures were treated with 100 μM NMDA and its co-agonist 10 μM glycine (hereafter referred to as ‘NMDA’). Immunofluorescence ( A ) and immunoblotting ( B ) used a C-terminal (C-ter) isoform-specific antibody (TrkB-FL Ct) recognizing both the full-length protein (FL) and the intracellular fragment (f32). A Shows TrkB-FL (green) and nuclei (blue, DAPI stain). Arrowheads indicate varicosities in neuronal projections. Scale bar: 20 μm. Insets show cell body details for untreated cells and cells treated with NMDA for 120 min. B Compares the decrease in TrkB-FL and formation of f32 with PSD-95 downregulation, detected using a C-terminal antibody (PSD-95 Ct). Calpain activation was confirmed by the accumulation of characteristic spectrin breakdown products (BDPs; 150 and 145 kDa). Neuron-specific enolase (NSE) served as a loading control for protein normalization. C , D Quantification of normalized TrkB-FL and PSD-95 levels, shown relative to levels in the absence of NMDA (control). Data are represented as means ± SD. Statistical analysis: one-way analysis of variance (ANOVA) followed by Bonferroni post hoc test (** P < 0.01, *** P < 0.001, **** P < 0.0001; 0-90 min, n = 5; 120 min, n = 3). E , F Effect of dynasore preincubation (80 μM, 30 min) on TrkB-FL levels after 2 h NMDA treatment. Data are means ± SD ( n = 4); statistical analysis as above (* P < 0.05). G Sequences of the cell-penetrating neuroprotective peptide (MTFL 457 ) and control peptide (MTMyc). Both contain Tat amino acids (aa) 47–57 (italic), followed by rat TrkB-FL aa 457-471 (light blue) or c-Myc aa 408-421 (dark blue), respectively. H , I Effect of peptide preincubation (25 μM, 30 min) on TrkB-FL shedding and processing during NMDA treatment. Culture media were analyzed using an antibody against the TrkB-FL extracellular domain (panTrkB), which recognizes the ectodomains (ECDs) of all isoforms (TrkB-ECD), to assess receptor shedding by metalloproteinase (MP) activation. Total lysates were analyzed with the TrkB-FL Ct antibody to evaluate TrkB-FL calpain processing via f32 production. Relative TrkB-ECD levels are shown as means ± SD (0-4 h, n = 7; 6 h, n = 4). Statistical analysis: two-way ANOVA followed by Bonferroni post hoc test (** P < 0.01, **** P < 0.0001, comparing each peptide + NMDA vs. peptide alone; # P < 0.05, #### P < 0.0001, comparing MTMyc vs. MTFL 457 at each time point). J , K Effect of NMDA on total and cell-surface pY816-TrkB-FL levels. Cultures were preincubated with peptides as above, then treated briefly with NMDA (1 h) to minimize receptor degradation. Cell-surface proteins were biotin-labeled and precipitated, then compared to corresponding total lysates. Data are represented as means ± SD ( n = 4). Statistical analysis: two-way ANOVA followed by Bonferroni post hoc test ( n.s . = n ot significant; ** P < 0.01, comparing NMDA vs. no NMDA; ## P < 0.01, comparing MTMyc + NMDA vs. MTFL 457 + NMDA).
    Figure Legend Snippet: A – D Kinetics of TrkB-FL downregulation. Primary cortical cultures were treated with 100 μM NMDA and its co-agonist 10 μM glycine (hereafter referred to as ‘NMDA’). Immunofluorescence ( A ) and immunoblotting ( B ) used a C-terminal (C-ter) isoform-specific antibody (TrkB-FL Ct) recognizing both the full-length protein (FL) and the intracellular fragment (f32). A Shows TrkB-FL (green) and nuclei (blue, DAPI stain). Arrowheads indicate varicosities in neuronal projections. Scale bar: 20 μm. Insets show cell body details for untreated cells and cells treated with NMDA for 120 min. B Compares the decrease in TrkB-FL and formation of f32 with PSD-95 downregulation, detected using a C-terminal antibody (PSD-95 Ct). Calpain activation was confirmed by the accumulation of characteristic spectrin breakdown products (BDPs; 150 and 145 kDa). Neuron-specific enolase (NSE) served as a loading control for protein normalization. C , D Quantification of normalized TrkB-FL and PSD-95 levels, shown relative to levels in the absence of NMDA (control). Data are represented as means ± SD. Statistical analysis: one-way analysis of variance (ANOVA) followed by Bonferroni post hoc test (** P < 0.01, *** P < 0.001, **** P < 0.0001; 0-90 min, n = 5; 120 min, n = 3). E , F Effect of dynasore preincubation (80 μM, 30 min) on TrkB-FL levels after 2 h NMDA treatment. Data are means ± SD ( n = 4); statistical analysis as above (* P < 0.05). G Sequences of the cell-penetrating neuroprotective peptide (MTFL 457 ) and control peptide (MTMyc). Both contain Tat amino acids (aa) 47–57 (italic), followed by rat TrkB-FL aa 457-471 (light blue) or c-Myc aa 408-421 (dark blue), respectively. H , I Effect of peptide preincubation (25 μM, 30 min) on TrkB-FL shedding and processing during NMDA treatment. Culture media were analyzed using an antibody against the TrkB-FL extracellular domain (panTrkB), which recognizes the ectodomains (ECDs) of all isoforms (TrkB-ECD), to assess receptor shedding by metalloproteinase (MP) activation. Total lysates were analyzed with the TrkB-FL Ct antibody to evaluate TrkB-FL calpain processing via f32 production. Relative TrkB-ECD levels are shown as means ± SD (0-4 h, n = 7; 6 h, n = 4). Statistical analysis: two-way ANOVA followed by Bonferroni post hoc test (** P < 0.01, **** P < 0.0001, comparing each peptide + NMDA vs. peptide alone; # P < 0.05, #### P < 0.0001, comparing MTMyc vs. MTFL 457 at each time point). J , K Effect of NMDA on total and cell-surface pY816-TrkB-FL levels. Cultures were preincubated with peptides as above, then treated briefly with NMDA (1 h) to minimize receptor degradation. Cell-surface proteins were biotin-labeled and precipitated, then compared to corresponding total lysates. Data are represented as means ± SD ( n = 4). Statistical analysis: two-way ANOVA followed by Bonferroni post hoc test ( n.s . = n ot significant; ** P < 0.01, comparing NMDA vs. no NMDA; ## P < 0.01, comparing MTMyc + NMDA vs. MTFL 457 + NMDA).

    Techniques Used: Immunofluorescence, Western Blot, Staining, Activation Assay, Control, Labeling



    Similar Products

    py816 trkb fl  (Boster Bio)
    93
    Boster Bio py816 trkb fl
    A – D Kinetics of TrkB-FL downregulation. Primary cortical cultures were treated with 100 μM NMDA and its co-agonist 10 μM glycine (hereafter referred to as ‘NMDA’). Immunofluorescence ( A ) and immunoblotting ( B ) used a C-terminal (C-ter) isoform-specific antibody (TrkB-FL Ct) recognizing both the full-length protein (FL) and the intracellular fragment (f32). A Shows TrkB-FL (green) and nuclei (blue, DAPI stain). Arrowheads indicate varicosities in neuronal projections. Scale bar: 20 μm. Insets show cell body details for untreated cells and cells treated with NMDA for 120 min. B Compares the decrease in TrkB-FL and formation of f32 with PSD-95 downregulation, detected using a C-terminal antibody (PSD-95 Ct). Calpain activation was confirmed by the accumulation of characteristic spectrin breakdown products (BDPs; 150 and 145 kDa). Neuron-specific enolase (NSE) served as a loading control for protein normalization. C , D Quantification of normalized TrkB-FL and PSD-95 levels, shown relative to levels in the absence of NMDA (control). Data are represented as means ± SD. Statistical analysis: one-way analysis of variance (ANOVA) followed by Bonferroni post hoc test (** P < 0.01, *** P < 0.001, **** P < 0.0001; 0-90 min, n = 5; 120 min, n = 3). E , F Effect of dynasore preincubation (80 μM, 30 min) on TrkB-FL levels after 2 h NMDA treatment. Data are means ± SD ( n = 4); statistical analysis as above (* P < 0.05). G Sequences of the cell-penetrating neuroprotective peptide (MTFL 457 ) and control peptide (MTMyc). Both contain Tat amino acids (aa) 47–57 (italic), followed by rat TrkB-FL aa 457-471 (light blue) or c-Myc aa 408-421 (dark blue), respectively. H , I Effect of peptide preincubation (25 μM, 30 min) on TrkB-FL shedding and processing during NMDA treatment. Culture media were analyzed using an antibody against the TrkB-FL extracellular domain (panTrkB), which recognizes the ectodomains (ECDs) of all isoforms (TrkB-ECD), to assess receptor shedding by metalloproteinase (MP) activation. Total lysates were analyzed with the TrkB-FL Ct antibody to evaluate TrkB-FL calpain processing via f32 production. Relative TrkB-ECD levels are shown as means ± SD (0-4 h, n = 7; 6 h, n = 4). Statistical analysis: two-way ANOVA followed by Bonferroni post hoc test (** P < 0.01, **** P < 0.0001, comparing each peptide + NMDA vs. peptide alone; # P < 0.05, #### P < 0.0001, comparing MTMyc vs. MTFL 457 at each time point). J , K Effect of NMDA on total and cell-surface <t>pY816-TrkB-FL</t> levels. Cultures were preincubated with peptides as above, then treated briefly with NMDA (1 h) to minimize receptor degradation. Cell-surface proteins were biotin-labeled and precipitated, then compared to corresponding total lysates. Data are represented as means ± SD ( n = 4). Statistical analysis: two-way ANOVA followed by Bonferroni post hoc test ( n.s . = n ot significant; ** P < 0.01, comparing NMDA vs. no NMDA; ## P < 0.01, comparing MTMyc + NMDA vs. MTFL 457 + NMDA).
    Py816 Trkb Fl, supplied by Boster Bio, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/py816 trkb fl/product/Boster Bio
    Average 93 stars, based on 1 article reviews
    py816 trkb fl - by Bioz Stars, 2026-03
    93/100 stars
    		  Buy from Supplier

    Image Search Results


    A – D Kinetics of TrkB-FL downregulation. Primary cortical cultures were treated with 100 μM NMDA and its co-agonist 10 μM glycine (hereafter referred to as ‘NMDA’). Immunofluorescence ( A ) and immunoblotting ( B ) used a C-terminal (C-ter) isoform-specific antibody (TrkB-FL Ct) recognizing both the full-length protein (FL) and the intracellular fragment (f32). A Shows TrkB-FL (green) and nuclei (blue, DAPI stain). Arrowheads indicate varicosities in neuronal projections. Scale bar: 20 μm. Insets show cell body details for untreated cells and cells treated with NMDA for 120 min. B Compares the decrease in TrkB-FL and formation of f32 with PSD-95 downregulation, detected using a C-terminal antibody (PSD-95 Ct). Calpain activation was confirmed by the accumulation of characteristic spectrin breakdown products (BDPs; 150 and 145 kDa). Neuron-specific enolase (NSE) served as a loading control for protein normalization. C , D Quantification of normalized TrkB-FL and PSD-95 levels, shown relative to levels in the absence of NMDA (control). Data are represented as means ± SD. Statistical analysis: one-way analysis of variance (ANOVA) followed by Bonferroni post hoc test (** P < 0.01, *** P < 0.001, **** P < 0.0001; 0-90 min, n = 5; 120 min, n = 3). E , F Effect of dynasore preincubation (80 μM, 30 min) on TrkB-FL levels after 2 h NMDA treatment. Data are means ± SD ( n = 4); statistical analysis as above (* P < 0.05). G Sequences of the cell-penetrating neuroprotective peptide (MTFL 457 ) and control peptide (MTMyc). Both contain Tat amino acids (aa) 47–57 (italic), followed by rat TrkB-FL aa 457-471 (light blue) or c-Myc aa 408-421 (dark blue), respectively. H , I Effect of peptide preincubation (25 μM, 30 min) on TrkB-FL shedding and processing during NMDA treatment. Culture media were analyzed using an antibody against the TrkB-FL extracellular domain (panTrkB), which recognizes the ectodomains (ECDs) of all isoforms (TrkB-ECD), to assess receptor shedding by metalloproteinase (MP) activation. Total lysates were analyzed with the TrkB-FL Ct antibody to evaluate TrkB-FL calpain processing via f32 production. Relative TrkB-ECD levels are shown as means ± SD (0-4 h, n = 7; 6 h, n = 4). Statistical analysis: two-way ANOVA followed by Bonferroni post hoc test (** P < 0.01, **** P < 0.0001, comparing each peptide + NMDA vs. peptide alone; # P < 0.05, #### P < 0.0001, comparing MTMyc vs. MTFL 457 at each time point). J , K Effect of NMDA on total and cell-surface pY816-TrkB-FL levels. Cultures were preincubated with peptides as above, then treated briefly with NMDA (1 h) to minimize receptor degradation. Cell-surface proteins were biotin-labeled and precipitated, then compared to corresponding total lysates. Data are represented as means ± SD ( n = 4). Statistical analysis: two-way ANOVA followed by Bonferroni post hoc test ( n.s . = n ot significant; ** P < 0.01, comparing NMDA vs. no NMDA; ## P < 0.01, comparing MTMyc + NMDA vs. MTFL 457 + NMDA).

    Journal: Cell Death & Disease

    Article Title: Retrograde transport of neurotrophin receptor TrkB-FL induced by excitotoxicity regulates Golgi stability and is a target for stroke neuroprotection

    doi: 10.1038/s41419-025-07990-6

    Figure Lengend Snippet: A – D Kinetics of TrkB-FL downregulation. Primary cortical cultures were treated with 100 μM NMDA and its co-agonist 10 μM glycine (hereafter referred to as ‘NMDA’). Immunofluorescence ( A ) and immunoblotting ( B ) used a C-terminal (C-ter) isoform-specific antibody (TrkB-FL Ct) recognizing both the full-length protein (FL) and the intracellular fragment (f32). A Shows TrkB-FL (green) and nuclei (blue, DAPI stain). Arrowheads indicate varicosities in neuronal projections. Scale bar: 20 μm. Insets show cell body details for untreated cells and cells treated with NMDA for 120 min. B Compares the decrease in TrkB-FL and formation of f32 with PSD-95 downregulation, detected using a C-terminal antibody (PSD-95 Ct). Calpain activation was confirmed by the accumulation of characteristic spectrin breakdown products (BDPs; 150 and 145 kDa). Neuron-specific enolase (NSE) served as a loading control for protein normalization. C , D Quantification of normalized TrkB-FL and PSD-95 levels, shown relative to levels in the absence of NMDA (control). Data are represented as means ± SD. Statistical analysis: one-way analysis of variance (ANOVA) followed by Bonferroni post hoc test (** P < 0.01, *** P < 0.001, **** P < 0.0001; 0-90 min, n = 5; 120 min, n = 3). E , F Effect of dynasore preincubation (80 μM, 30 min) on TrkB-FL levels after 2 h NMDA treatment. Data are means ± SD ( n = 4); statistical analysis as above (* P < 0.05). G Sequences of the cell-penetrating neuroprotective peptide (MTFL 457 ) and control peptide (MTMyc). Both contain Tat amino acids (aa) 47–57 (italic), followed by rat TrkB-FL aa 457-471 (light blue) or c-Myc aa 408-421 (dark blue), respectively. H , I Effect of peptide preincubation (25 μM, 30 min) on TrkB-FL shedding and processing during NMDA treatment. Culture media were analyzed using an antibody against the TrkB-FL extracellular domain (panTrkB), which recognizes the ectodomains (ECDs) of all isoforms (TrkB-ECD), to assess receptor shedding by metalloproteinase (MP) activation. Total lysates were analyzed with the TrkB-FL Ct antibody to evaluate TrkB-FL calpain processing via f32 production. Relative TrkB-ECD levels are shown as means ± SD (0-4 h, n = 7; 6 h, n = 4). Statistical analysis: two-way ANOVA followed by Bonferroni post hoc test (** P < 0.01, **** P < 0.0001, comparing each peptide + NMDA vs. peptide alone; # P < 0.05, #### P < 0.0001, comparing MTMyc vs. MTFL 457 at each time point). J , K Effect of NMDA on total and cell-surface pY816-TrkB-FL levels. Cultures were preincubated with peptides as above, then treated briefly with NMDA (1 h) to minimize receptor degradation. Cell-surface proteins were biotin-labeled and precipitated, then compared to corresponding total lysates. Data are represented as means ± SD ( n = 4). Statistical analysis: two-way ANOVA followed by Bonferroni post hoc test ( n.s . = n ot significant; ** P < 0.01, comparing NMDA vs. no NMDA; ## P < 0.01, comparing MTMyc + NMDA vs. MTFL 457 + NMDA).

    Article Snippet: Primary antibodies against the following proteins were used: Hrs (Santa Cruz Biotechnology; Cat#sc-271455, RRID:AB_10648901), NSE (Millipore; Cat#AB951, RRID:AB_92390), spectrin alpha chain (Millipore; Cat#MAB1622, RRID:AB_94295), TrkB-FL C-ter (Santa Cruz Biotechnology; sc-11, RRID:AB_632554), TrkB extracellular sequences or panTrkB (Santa Cruz Biotechnology; sc-136990, RRID:AB_2155262), PSD-95 C-ter (Transduction Laboratories; Cat#610496, RRID:AB_2315218), pY816-TrkB-FL (Boster; Cat# P01388 ).

    Techniques: Immunofluorescence, Western Blot, Staining, Activation Assay, Control, Labeling