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rabbit anti tuj1 antibody  (Boster Bio)


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    Structured Review

    Boster Bio rabbit anti tuj1 antibody
    ADSC-CM promotes neurite outgrowth in OGD-injured neurons through the JAK1-STAT3 signaling pathway. (A) On day 5 of cultivation, neuronal neurites extended and formed an extensive neural network. Immunofluorescence staining showed that the neurons were positive for the neuronal-specific marker <t>Tuj1.</t> After OGD injury, neuronal neurites were damaged, partially interrupted, and disappeared. (B) Western blot bands of JAK1, pJAK1, STAT3, pSTAT3, and GAPDH for each group. (C) Comparison of the relative ratio of pJAK1 to JAK1 across experimental groups ( n = 4). (D) Comparison of the relative ratio of pSTAT3 to STAT3 across experimental groups ( n = 4). (E) Immunofluorescence images of neurons from each group, showing the effects of ADSC-CM and GLPG0634 on neurite outgrowth. Neurons were stained with the <t>Tuj1</t> antibody (red) to label the neuronal cytoskeleton, and nuclei were counterstained with DAPI (blue). (F) Diagram illustrating how to measure the length of the longest neurite and the number of primary neurites in neurons. The green line shows the trajectory of the longest neurite, and white arrows point to primary neurites. (G,H) Comparison of the length of the longest neurite and the number of primary neurites in neurons across experimental groups ( n = 4). Data are expressed as means ± SEM. The difference between the groups was assessed using a one-way ANOVA followed by Bonferroni post hoc tests. * p < 0.05, ** p < 0.01, *** p < 0.001. Scale bars: 100 μm (A) , 20 μm (E,F) .
    Rabbit Anti Tuj1 Antibody, supplied by Boster Bio, 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/rabbit anti tuj1 antibody/product/Boster Bio
    Average 94 stars, based on 1 article reviews
    rabbit anti tuj1 antibody - by Bioz Stars, 2026-06
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    Images

    1) Product Images from "Adipose-derived stem cell-conditioned medium mitigates ischemia-induced neuronal injury via the JAK1/STAT3 signaling pathway"

    Article Title: Adipose-derived stem cell-conditioned medium mitigates ischemia-induced neuronal injury via the JAK1/STAT3 signaling pathway

    Journal: Frontiers in Cellular Neuroscience

    doi: 10.3389/fncel.2026.1744887

    ADSC-CM promotes neurite outgrowth in OGD-injured neurons through the JAK1-STAT3 signaling pathway. (A) On day 5 of cultivation, neuronal neurites extended and formed an extensive neural network. Immunofluorescence staining showed that the neurons were positive for the neuronal-specific marker Tuj1. After OGD injury, neuronal neurites were damaged, partially interrupted, and disappeared. (B) Western blot bands of JAK1, pJAK1, STAT3, pSTAT3, and GAPDH for each group. (C) Comparison of the relative ratio of pJAK1 to JAK1 across experimental groups ( n = 4). (D) Comparison of the relative ratio of pSTAT3 to STAT3 across experimental groups ( n = 4). (E) Immunofluorescence images of neurons from each group, showing the effects of ADSC-CM and GLPG0634 on neurite outgrowth. Neurons were stained with the Tuj1 antibody (red) to label the neuronal cytoskeleton, and nuclei were counterstained with DAPI (blue). (F) Diagram illustrating how to measure the length of the longest neurite and the number of primary neurites in neurons. The green line shows the trajectory of the longest neurite, and white arrows point to primary neurites. (G,H) Comparison of the length of the longest neurite and the number of primary neurites in neurons across experimental groups ( n = 4). Data are expressed as means ± SEM. The difference between the groups was assessed using a one-way ANOVA followed by Bonferroni post hoc tests. * p < 0.05, ** p < 0.01, *** p < 0.001. Scale bars: 100 μm (A) , 20 μm (E,F) .
    Figure Legend Snippet: ADSC-CM promotes neurite outgrowth in OGD-injured neurons through the JAK1-STAT3 signaling pathway. (A) On day 5 of cultivation, neuronal neurites extended and formed an extensive neural network. Immunofluorescence staining showed that the neurons were positive for the neuronal-specific marker Tuj1. After OGD injury, neuronal neurites were damaged, partially interrupted, and disappeared. (B) Western blot bands of JAK1, pJAK1, STAT3, pSTAT3, and GAPDH for each group. (C) Comparison of the relative ratio of pJAK1 to JAK1 across experimental groups ( n = 4). (D) Comparison of the relative ratio of pSTAT3 to STAT3 across experimental groups ( n = 4). (E) Immunofluorescence images of neurons from each group, showing the effects of ADSC-CM and GLPG0634 on neurite outgrowth. Neurons were stained with the Tuj1 antibody (red) to label the neuronal cytoskeleton, and nuclei were counterstained with DAPI (blue). (F) Diagram illustrating how to measure the length of the longest neurite and the number of primary neurites in neurons. The green line shows the trajectory of the longest neurite, and white arrows point to primary neurites. (G,H) Comparison of the length of the longest neurite and the number of primary neurites in neurons across experimental groups ( n = 4). Data are expressed as means ± SEM. The difference between the groups was assessed using a one-way ANOVA followed by Bonferroni post hoc tests. * p < 0.05, ** p < 0.01, *** p < 0.001. Scale bars: 100 μm (A) , 20 μm (E,F) .

    Techniques Used: Immunofluorescence, Staining, Marker, Western Blot, Comparison



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    ADSC-CM promotes neurite outgrowth in OGD-injured neurons through the JAK1-STAT3 signaling pathway. (A) On day 5 of cultivation, neuronal neurites extended and formed an extensive neural network. Immunofluorescence staining showed that the neurons were positive for the neuronal-specific marker <t>Tuj1.</t> After OGD injury, neuronal neurites were damaged, partially interrupted, and disappeared. (B) Western blot bands of JAK1, pJAK1, STAT3, pSTAT3, and GAPDH for each group. (C) Comparison of the relative ratio of pJAK1 to JAK1 across experimental groups ( n = 4). (D) Comparison of the relative ratio of pSTAT3 to STAT3 across experimental groups ( n = 4). (E) Immunofluorescence images of neurons from each group, showing the effects of ADSC-CM and GLPG0634 on neurite outgrowth. Neurons were stained with the <t>Tuj1</t> antibody (red) to label the neuronal cytoskeleton, and nuclei were counterstained with DAPI (blue). (F) Diagram illustrating how to measure the length of the longest neurite and the number of primary neurites in neurons. The green line shows the trajectory of the longest neurite, and white arrows point to primary neurites. (G,H) Comparison of the length of the longest neurite and the number of primary neurites in neurons across experimental groups ( n = 4). Data are expressed as means ± SEM. The difference between the groups was assessed using a one-way ANOVA followed by Bonferroni post hoc tests. * p < 0.05, ** p < 0.01, *** p < 0.001. Scale bars: 100 μm (A) , 20 μm (E,F) .
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    ADSC-CM promotes neurite outgrowth in OGD-injured neurons through the JAK1-STAT3 signaling pathway. (A) On day 5 of cultivation, neuronal neurites extended and formed an extensive neural network. Immunofluorescence staining showed that the neurons were positive for the neuronal-specific marker <t>Tuj1.</t> After OGD injury, neuronal neurites were damaged, partially interrupted, and disappeared. (B) Western blot bands of JAK1, pJAK1, STAT3, pSTAT3, and GAPDH for each group. (C) Comparison of the relative ratio of pJAK1 to JAK1 across experimental groups ( n = 4). (D) Comparison of the relative ratio of pSTAT3 to STAT3 across experimental groups ( n = 4). (E) Immunofluorescence images of neurons from each group, showing the effects of ADSC-CM and GLPG0634 on neurite outgrowth. Neurons were stained with the <t>Tuj1</t> antibody (red) to label the neuronal cytoskeleton, and nuclei were counterstained with DAPI (blue). (F) Diagram illustrating how to measure the length of the longest neurite and the number of primary neurites in neurons. The green line shows the trajectory of the longest neurite, and white arrows point to primary neurites. (G,H) Comparison of the length of the longest neurite and the number of primary neurites in neurons across experimental groups ( n = 4). Data are expressed as means ± SEM. The difference between the groups was assessed using a one-way ANOVA followed by Bonferroni post hoc tests. * p < 0.05, ** p < 0.01, *** p < 0.001. Scale bars: 100 μm (A) , 20 μm (E,F) .
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    ADSC-CM promotes neurite outgrowth in OGD-injured neurons through the JAK1-STAT3 signaling pathway. (A) On day 5 of cultivation, neuronal neurites extended and formed an extensive neural network. Immunofluorescence staining showed that the neurons were positive for the neuronal-specific marker <t>Tuj1.</t> After OGD injury, neuronal neurites were damaged, partially interrupted, and disappeared. (B) Western blot bands of JAK1, pJAK1, STAT3, pSTAT3, and GAPDH for each group. (C) Comparison of the relative ratio of pJAK1 to JAK1 across experimental groups ( n = 4). (D) Comparison of the relative ratio of pSTAT3 to STAT3 across experimental groups ( n = 4). (E) Immunofluorescence images of neurons from each group, showing the effects of ADSC-CM and GLPG0634 on neurite outgrowth. Neurons were stained with the <t>Tuj1</t> antibody (red) to label the neuronal cytoskeleton, and nuclei were counterstained with DAPI (blue). (F) Diagram illustrating how to measure the length of the longest neurite and the number of primary neurites in neurons. The green line shows the trajectory of the longest neurite, and white arrows point to primary neurites. (G,H) Comparison of the length of the longest neurite and the number of primary neurites in neurons across experimental groups ( n = 4). Data are expressed as means ± SEM. The difference between the groups was assessed using a one-way ANOVA followed by Bonferroni post hoc tests. * p < 0.05, ** p < 0.01, *** p < 0.001. Scale bars: 100 μm (A) , 20 μm (E,F) .
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    ADSC-CM promotes neurite outgrowth in OGD-injured neurons through the JAK1-STAT3 signaling pathway. (A) On day 5 of cultivation, neuronal neurites extended and formed an extensive neural network. Immunofluorescence staining showed that the neurons were positive for the neuronal-specific marker <t>Tuj1.</t> After OGD injury, neuronal neurites were damaged, partially interrupted, and disappeared. (B) Western blot bands of JAK1, pJAK1, STAT3, pSTAT3, and GAPDH for each group. (C) Comparison of the relative ratio of pJAK1 to JAK1 across experimental groups ( n = 4). (D) Comparison of the relative ratio of pSTAT3 to STAT3 across experimental groups ( n = 4). (E) Immunofluorescence images of neurons from each group, showing the effects of ADSC-CM and GLPG0634 on neurite outgrowth. Neurons were stained with the <t>Tuj1</t> antibody (red) to label the neuronal cytoskeleton, and nuclei were counterstained with DAPI (blue). (F) Diagram illustrating how to measure the length of the longest neurite and the number of primary neurites in neurons. The green line shows the trajectory of the longest neurite, and white arrows point to primary neurites. (G,H) Comparison of the length of the longest neurite and the number of primary neurites in neurons across experimental groups ( n = 4). Data are expressed as means ± SEM. The difference between the groups was assessed using a one-way ANOVA followed by Bonferroni post hoc tests. * p < 0.05, ** p < 0.01, *** p < 0.001. Scale bars: 100 μm (A) , 20 μm (E,F) .
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    Neuroprotective effects of miR-937-3p-I in Aβ-induced cell death. The protein expression of neuronal markers (NeuN, NFH, <t>Tuj1,</t> and SYP) was investigated by western blot analysis ( A ) and calculated the levels ( B ) ( n = 6 per group). The level of genes, which are neuronal markers, was investigated via qPCR ( C – F ) ( n = 5 per group). The expression of neuronal markers increased with the miR-937-3p-I treatment in Aβ-induced cells compared with that in the Aβ-treated group. ( G ) ICC showed MAP2 (green) expression treated with miR-937-3p-I after Aβ exposure ( n = 5 per group). ( H ) MAP2-positive cells were quantified as relative to total nuclei (DAPI, blue). ( I ) Neurite length calculated and remained unchanged following Aβ or miR-937-3p-I treatment. All experiments were independently repeated, and technical replicates were also performed to ensure the reliability of the results. Results represent means ± SEMs. Statistical significance is indicated as follows: * p < 0.05, ** p < 0.01, and *** p < 0.001 compared with the control; # p < 0.05, ## p < 0.01, and ### p < 0.001 compared with the Aβ.
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    Neuroprotective effects of miR-937-3p-I in Aβ-induced cell death. The protein expression of neuronal markers (NeuN, NFH, <t>Tuj1,</t> and SYP) was investigated by western blot analysis ( A ) and calculated the levels ( B ) ( n = 6 per group). The level of genes, which are neuronal markers, was investigated via qPCR ( C – F ) ( n = 5 per group). The expression of neuronal markers increased with the miR-937-3p-I treatment in Aβ-induced cells compared with that in the Aβ-treated group. ( G ) ICC showed MAP2 (green) expression treated with miR-937-3p-I after Aβ exposure ( n = 5 per group). ( H ) MAP2-positive cells were quantified as relative to total nuclei (DAPI, blue). ( I ) Neurite length calculated and remained unchanged following Aβ or miR-937-3p-I treatment. All experiments were independently repeated, and technical replicates were also performed to ensure the reliability of the results. Results represent means ± SEMs. Statistical significance is indicated as follows: * p < 0.05, ** p < 0.01, and *** p < 0.001 compared with the control; # p < 0.05, ## p < 0.01, and ### p < 0.001 compared with the Aβ.
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    Neuroprotective effects of miR-937-3p-I in Aβ-induced cell death. The protein expression of neuronal markers (NeuN, NFH, <t>Tuj1,</t> and SYP) was investigated by western blot analysis ( A ) and calculated the levels ( B ) ( n = 6 per group). The level of genes, which are neuronal markers, was investigated via qPCR ( C – F ) ( n = 5 per group). The expression of neuronal markers increased with the miR-937-3p-I treatment in Aβ-induced cells compared with that in the Aβ-treated group. ( G ) ICC showed MAP2 (green) expression treated with miR-937-3p-I after Aβ exposure ( n = 5 per group). ( H ) MAP2-positive cells were quantified as relative to total nuclei (DAPI, blue). ( I ) Neurite length calculated and remained unchanged following Aβ or miR-937-3p-I treatment. All experiments were independently repeated, and technical replicates were also performed to ensure the reliability of the results. Results represent means ± SEMs. Statistical significance is indicated as follows: * p < 0.05, ** p < 0.01, and *** p < 0.001 compared with the control; # p < 0.05, ## p < 0.01, and ### p < 0.001 compared with the Aβ.
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    Image Search Results


    ADSC-CM promotes neurite outgrowth in OGD-injured neurons through the JAK1-STAT3 signaling pathway. (A) On day 5 of cultivation, neuronal neurites extended and formed an extensive neural network. Immunofluorescence staining showed that the neurons were positive for the neuronal-specific marker Tuj1. After OGD injury, neuronal neurites were damaged, partially interrupted, and disappeared. (B) Western blot bands of JAK1, pJAK1, STAT3, pSTAT3, and GAPDH for each group. (C) Comparison of the relative ratio of pJAK1 to JAK1 across experimental groups ( n = 4). (D) Comparison of the relative ratio of pSTAT3 to STAT3 across experimental groups ( n = 4). (E) Immunofluorescence images of neurons from each group, showing the effects of ADSC-CM and GLPG0634 on neurite outgrowth. Neurons were stained with the Tuj1 antibody (red) to label the neuronal cytoskeleton, and nuclei were counterstained with DAPI (blue). (F) Diagram illustrating how to measure the length of the longest neurite and the number of primary neurites in neurons. The green line shows the trajectory of the longest neurite, and white arrows point to primary neurites. (G,H) Comparison of the length of the longest neurite and the number of primary neurites in neurons across experimental groups ( n = 4). Data are expressed as means ± SEM. The difference between the groups was assessed using a one-way ANOVA followed by Bonferroni post hoc tests. * p < 0.05, ** p < 0.01, *** p < 0.001. Scale bars: 100 μm (A) , 20 μm (E,F) .

    Journal: Frontiers in Cellular Neuroscience

    Article Title: Adipose-derived stem cell-conditioned medium mitigates ischemia-induced neuronal injury via the JAK1/STAT3 signaling pathway

    doi: 10.3389/fncel.2026.1744887

    Figure Lengend Snippet: ADSC-CM promotes neurite outgrowth in OGD-injured neurons through the JAK1-STAT3 signaling pathway. (A) On day 5 of cultivation, neuronal neurites extended and formed an extensive neural network. Immunofluorescence staining showed that the neurons were positive for the neuronal-specific marker Tuj1. After OGD injury, neuronal neurites were damaged, partially interrupted, and disappeared. (B) Western blot bands of JAK1, pJAK1, STAT3, pSTAT3, and GAPDH for each group. (C) Comparison of the relative ratio of pJAK1 to JAK1 across experimental groups ( n = 4). (D) Comparison of the relative ratio of pSTAT3 to STAT3 across experimental groups ( n = 4). (E) Immunofluorescence images of neurons from each group, showing the effects of ADSC-CM and GLPG0634 on neurite outgrowth. Neurons were stained with the Tuj1 antibody (red) to label the neuronal cytoskeleton, and nuclei were counterstained with DAPI (blue). (F) Diagram illustrating how to measure the length of the longest neurite and the number of primary neurites in neurons. The green line shows the trajectory of the longest neurite, and white arrows point to primary neurites. (G,H) Comparison of the length of the longest neurite and the number of primary neurites in neurons across experimental groups ( n = 4). Data are expressed as means ± SEM. The difference between the groups was assessed using a one-way ANOVA followed by Bonferroni post hoc tests. * p < 0.05, ** p < 0.01, *** p < 0.001. Scale bars: 100 μm (A) , 20 μm (E,F) .

    Article Snippet: After overnight incubation with rabbit anti-Tuj1 antibody (1:200, BM3881, Boster, Wuhan, China) at 4 °C, cells were washed and then incubated with Cy3-conjugated goat anti-rabbit IgG (1:400, AS007, ABclonal) for 1 h at room temperature in the dark.

    Techniques: Immunofluorescence, Staining, Marker, Western Blot, Comparison

    Neuroprotective effects of miR-937-3p-I in Aβ-induced cell death. The protein expression of neuronal markers (NeuN, NFH, Tuj1, and SYP) was investigated by western blot analysis ( A ) and calculated the levels ( B ) ( n = 6 per group). The level of genes, which are neuronal markers, was investigated via qPCR ( C – F ) ( n = 5 per group). The expression of neuronal markers increased with the miR-937-3p-I treatment in Aβ-induced cells compared with that in the Aβ-treated group. ( G ) ICC showed MAP2 (green) expression treated with miR-937-3p-I after Aβ exposure ( n = 5 per group). ( H ) MAP2-positive cells were quantified as relative to total nuclei (DAPI, blue). ( I ) Neurite length calculated and remained unchanged following Aβ or miR-937-3p-I treatment. All experiments were independently repeated, and technical replicates were also performed to ensure the reliability of the results. Results represent means ± SEMs. Statistical significance is indicated as follows: * p < 0.05, ** p < 0.01, and *** p < 0.001 compared with the control; # p < 0.05, ## p < 0.01, and ### p < 0.001 compared with the Aβ.

    Journal: Scientific Reports

    Article Title: Therapeutic effects of miR-937-3p by targeting NTN1 expression and regulating apoptosis in an Aβ-induced neuronal cell death

    doi: 10.1038/s41598-025-08015-0

    Figure Lengend Snippet: Neuroprotective effects of miR-937-3p-I in Aβ-induced cell death. The protein expression of neuronal markers (NeuN, NFH, Tuj1, and SYP) was investigated by western blot analysis ( A ) and calculated the levels ( B ) ( n = 6 per group). The level of genes, which are neuronal markers, was investigated via qPCR ( C – F ) ( n = 5 per group). The expression of neuronal markers increased with the miR-937-3p-I treatment in Aβ-induced cells compared with that in the Aβ-treated group. ( G ) ICC showed MAP2 (green) expression treated with miR-937-3p-I after Aβ exposure ( n = 5 per group). ( H ) MAP2-positive cells were quantified as relative to total nuclei (DAPI, blue). ( I ) Neurite length calculated and remained unchanged following Aβ or miR-937-3p-I treatment. All experiments were independently repeated, and technical replicates were also performed to ensure the reliability of the results. Results represent means ± SEMs. Statistical significance is indicated as follows: * p < 0.05, ** p < 0.01, and *** p < 0.001 compared with the control; # p < 0.05, ## p < 0.01, and ### p < 0.001 compared with the Aβ.

    Article Snippet: Tuj1 , Cell Signaling Technology , 5568 , 1:1000.

    Techniques: Expressing, Western Blot, Control