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antibody neun d3s3i rabbit mab primary anti neun antibody  (Cell Signaling Technology Inc)


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    Cell Signaling Technology Inc antibody neun d3s3i rabbit mab primary anti neun antibody
    Antibody Neun D3s3i Rabbit Mab Primary Anti Neun Antibody, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 96/100, based on 304 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/primary+antibodies+rabbit+anti+neun/bio_rxiv__2025__09__10__675281-233-5-13?v=Cell+Signaling+Technology+Inc
    Average 96 stars, based on 304 article reviews
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    Fig. 2 Knockdown of SIRPα enhances efferocytosis by microglia and mitigates neuroinflammation following SAH in vivo. A. Western blot assay for the expression of SIRPα and CD47 in the temporal lobe after SAH. B. Quantification of SIRPα and CD47 protein levels (n = 6 each group). C. RT-qPCR for SIRPα in the temporal lobe after SAH (n = 6 each group). D. Representative immunofluorescence images and three-dimensional imaging showing the extent of efferocytosis following SAH for 24 h. White arrowheads indicate dead/dying neurons that were engulfed by <t>microglia</t> <t>(Neun(red)+Iba1(green)+).</t> Scale bar, 50 μm. E. Quantification of efferocytosis levels (Neun(red)+Iba1(green)+ microglia) following SAH for 24 h (n = 6 each group). F. Western blot assay for the expression of IL-1β, IL-18, IL-10, TGF-β1, Bax, Bcl-2 and Cleaved caspase-3 in all groups in the temporal lobe following SAH after knockdown of SIRPα in microglia. G. Quantification of IL-1β, IL-18, IL-10, TGF-β1, Bax, Bcl-2 and Cleaved caspase-3 protein levels (n = 6 each group). H. Skeletonized analysis: Representative images of microglia. Scale bar, 50 μm. I. Quantification of soma area, branch numbers, and total branch length (n = 6 each group). J-K. Rep resentative swimming tracks of the mice in all groups of the MWM tests and quantitative analyses of latency and distance. L. Representative fluorescent images and quantification of TUNEL + neurons following SAH for 24 h. Nuclei were counterstained with DAPI (blue), (n = 6 each group). Scale bar, 100 μm. M. Representative Nissl staining images of the temporal lobe in all groups (n = 6 each group). Scale bar, 50 μm. All values are means ± SEM, *P < 0.05, **P < 0.01, ***P < 0.001, ****P < 0.0001, ns, no significant changes
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    Fig. 2 Knockdown of SIRPα enhances efferocytosis by microglia and mitigates neuroinflammation following SAH in vivo. A. Western blot assay for the expression of SIRPα and CD47 in the temporal lobe after SAH. B. Quantification of SIRPα and CD47 protein levels (n = 6 each group). C. RT-qPCR for SIRPα in the temporal lobe after SAH (n = 6 each group). D. Representative immunofluorescence images and three-dimensional imaging showing the extent of efferocytosis following SAH for 24 h. White arrowheads indicate dead/dying neurons that were engulfed by <t>microglia</t> <t>(Neun(red)+Iba1(green)+).</t> Scale bar, 50 μm. E. Quantification of efferocytosis levels (Neun(red)+Iba1(green)+ microglia) following SAH for 24 h (n = 6 each group). F. Western blot assay for the expression of IL-1β, IL-18, IL-10, TGF-β1, Bax, Bcl-2 and Cleaved caspase-3 in all groups in the temporal lobe following SAH after knockdown of SIRPα in microglia. G. Quantification of IL-1β, IL-18, IL-10, TGF-β1, Bax, Bcl-2 and Cleaved caspase-3 protein levels (n = 6 each group). H. Skeletonized analysis: Representative images of microglia. Scale bar, 50 μm. I. Quantification of soma area, branch numbers, and total branch length (n = 6 each group). J-K. Rep resentative swimming tracks of the mice in all groups of the MWM tests and quantitative analyses of latency and distance. L. Representative fluorescent images and quantification of TUNEL + neurons following SAH for 24 h. Nuclei were counterstained with DAPI (blue), (n = 6 each group). Scale bar, 100 μm. M. Representative Nissl staining images of the temporal lobe in all groups (n = 6 each group). Scale bar, 50 μm. All values are means ± SEM, *P < 0.05, **P < 0.01, ***P < 0.001, ****P < 0.0001, ns, no significant changes
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    TRIM14 knockdown promotes neuronal survival, spinal tissue repair, and functional recovery after spinal cord injury in rats. (A) Representative immunofluorescence images showing NF (green, neurofilament) and GFAP (red, glial fibrillary acidic protein) distribution in spinal cord lesions of rats from different groups at 28 days post-injury (dpi). Scale bars: 500 μm (low magnification), 50 μm (high magnification); n = 3. Quantitative analysis of mean fluorescence density for NF and GFAP at the injury epicenter is shown ( n = 3). (B) Protein levels of NF in spinal cord tissues analyzed by western blot ( n = 3). (C) Representative IHC images of <t>NeuN</t> + neurons in injured spinal cords (28 dpi; scale bar: 100 μm; n = 3). Bar graph indicates the mean number of surviving NeuN + neurons per field. (D) Nissl staining of injured spinal cords (28 dpi; scale bar: 100 μm; n = 3). Arrows denote Nissl-positive cells. Bar graph displays the mean number of Nissl + cells per field. In (C, D), three stained sections were randomly selected from each experimental rats to evaluate the average number of surviving neurons in the anterior horns of spinal cord. (E) HE staining of spinal cord lesion cavities. Bar graph quantifies lesion cavity areas across groups ( n = 3). (F) Hindlimb motor function evaluated by Basso–Beattie–Bresnahan (BBB) locomotor rating scale ( n = 3). Interrater reliability was confirmed by an intraclass correlation coefficient (ICC > 0.85). Data represent mean ± SD. ⁣ ∗ p < 0.05, ⁣ ∗∗ p < 0.01, and ⁣ ∗∗∗ p < 0.001. NC, negative control. sgTRIM14, sgRNA targeting TRIM14.
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    Image Search Results


    Fig. 2 Knockdown of SIRPα enhances efferocytosis by microglia and mitigates neuroinflammation following SAH in vivo. A. Western blot assay for the expression of SIRPα and CD47 in the temporal lobe after SAH. B. Quantification of SIRPα and CD47 protein levels (n = 6 each group). C. RT-qPCR for SIRPα in the temporal lobe after SAH (n = 6 each group). D. Representative immunofluorescence images and three-dimensional imaging showing the extent of efferocytosis following SAH for 24 h. White arrowheads indicate dead/dying neurons that were engulfed by microglia (Neun(red)+Iba1(green)+). Scale bar, 50 μm. E. Quantification of efferocytosis levels (Neun(red)+Iba1(green)+ microglia) following SAH for 24 h (n = 6 each group). F. Western blot assay for the expression of IL-1β, IL-18, IL-10, TGF-β1, Bax, Bcl-2 and Cleaved caspase-3 in all groups in the temporal lobe following SAH after knockdown of SIRPα in microglia. G. Quantification of IL-1β, IL-18, IL-10, TGF-β1, Bax, Bcl-2 and Cleaved caspase-3 protein levels (n = 6 each group). H. Skeletonized analysis: Representative images of microglia. Scale bar, 50 μm. I. Quantification of soma area, branch numbers, and total branch length (n = 6 each group). J-K. Rep resentative swimming tracks of the mice in all groups of the MWM tests and quantitative analyses of latency and distance. L. Representative fluorescent images and quantification of TUNEL + neurons following SAH for 24 h. Nuclei were counterstained with DAPI (blue), (n = 6 each group). Scale bar, 100 μm. M. Representative Nissl staining images of the temporal lobe in all groups (n = 6 each group). Scale bar, 50 μm. All values are means ± SEM, *P < 0.05, **P < 0.01, ***P < 0.001, ****P < 0.0001, ns, no significant changes

    Journal: Journal of neuroinflammation

    Article Title: SIRPα modulates microglial efferocytosis and neuroinflammation following experimental subarachnoid hemorrhage via the SHP1/STAT6 axis.

    doi: 10.1186/s12974-025-03414-6

    Figure Lengend Snippet: Fig. 2 Knockdown of SIRPα enhances efferocytosis by microglia and mitigates neuroinflammation following SAH in vivo. A. Western blot assay for the expression of SIRPα and CD47 in the temporal lobe after SAH. B. Quantification of SIRPα and CD47 protein levels (n = 6 each group). C. RT-qPCR for SIRPα in the temporal lobe after SAH (n = 6 each group). D. Representative immunofluorescence images and three-dimensional imaging showing the extent of efferocytosis following SAH for 24 h. White arrowheads indicate dead/dying neurons that were engulfed by microglia (Neun(red)+Iba1(green)+). Scale bar, 50 μm. E. Quantification of efferocytosis levels (Neun(red)+Iba1(green)+ microglia) following SAH for 24 h (n = 6 each group). F. Western blot assay for the expression of IL-1β, IL-18, IL-10, TGF-β1, Bax, Bcl-2 and Cleaved caspase-3 in all groups in the temporal lobe following SAH after knockdown of SIRPα in microglia. G. Quantification of IL-1β, IL-18, IL-10, TGF-β1, Bax, Bcl-2 and Cleaved caspase-3 protein levels (n = 6 each group). H. Skeletonized analysis: Representative images of microglia. Scale bar, 50 μm. I. Quantification of soma area, branch numbers, and total branch length (n = 6 each group). J-K. Rep resentative swimming tracks of the mice in all groups of the MWM tests and quantitative analyses of latency and distance. L. Representative fluorescent images and quantification of TUNEL + neurons following SAH for 24 h. Nuclei were counterstained with DAPI (blue), (n = 6 each group). Scale bar, 100 μm. M. Representative Nissl staining images of the temporal lobe in all groups (n = 6 each group). Scale bar, 50 μm. All values are means ± SEM, *P < 0.05, **P < 0.01, ***P < 0.001, ****P < 0.0001, ns, no significant changes

    Article Snippet: These samples were incubated with specific primary antibodies for Neun (1:400, Cell Signaling Technology, 24307), Iba1(1:100, Abcam, ab283319), MAP2 (1:200, ABclonal, A22206) in Universal Antibody Diluent (New Cell & Molecular, Suzhou, China) at 4 °C overnight.

    Techniques: Knockdown, In Vivo, Western Blot, Expressing, Quantitative RT-PCR, Immunofluorescence, Imaging, TUNEL Assay, Staining

    TRIM14 knockdown promotes neuronal survival, spinal tissue repair, and functional recovery after spinal cord injury in rats. (A) Representative immunofluorescence images showing NF (green, neurofilament) and GFAP (red, glial fibrillary acidic protein) distribution in spinal cord lesions of rats from different groups at 28 days post-injury (dpi). Scale bars: 500 μm (low magnification), 50 μm (high magnification); n = 3. Quantitative analysis of mean fluorescence density for NF and GFAP at the injury epicenter is shown ( n = 3). (B) Protein levels of NF in spinal cord tissues analyzed by western blot ( n = 3). (C) Representative IHC images of NeuN + neurons in injured spinal cords (28 dpi; scale bar: 100 μm; n = 3). Bar graph indicates the mean number of surviving NeuN + neurons per field. (D) Nissl staining of injured spinal cords (28 dpi; scale bar: 100 μm; n = 3). Arrows denote Nissl-positive cells. Bar graph displays the mean number of Nissl + cells per field. In (C, D), three stained sections were randomly selected from each experimental rats to evaluate the average number of surviving neurons in the anterior horns of spinal cord. (E) HE staining of spinal cord lesion cavities. Bar graph quantifies lesion cavity areas across groups ( n = 3). (F) Hindlimb motor function evaluated by Basso–Beattie–Bresnahan (BBB) locomotor rating scale ( n = 3). Interrater reliability was confirmed by an intraclass correlation coefficient (ICC > 0.85). Data represent mean ± SD. ⁣ ∗ p < 0.05, ⁣ ∗∗ p < 0.01, and ⁣ ∗∗∗ p < 0.001. NC, negative control. sgTRIM14, sgRNA targeting TRIM14.

    Journal: Mediators of Inflammation

    Article Title: TRIM14 Inhibition Suppresses Microglial Polarization and Pyroptosis Through the NF-κB/NLRP3 Pathway to Enhance Spinal Cord Injury Repair

    doi: 10.1155/mi/5053685

    Figure Lengend Snippet: TRIM14 knockdown promotes neuronal survival, spinal tissue repair, and functional recovery after spinal cord injury in rats. (A) Representative immunofluorescence images showing NF (green, neurofilament) and GFAP (red, glial fibrillary acidic protein) distribution in spinal cord lesions of rats from different groups at 28 days post-injury (dpi). Scale bars: 500 μm (low magnification), 50 μm (high magnification); n = 3. Quantitative analysis of mean fluorescence density for NF and GFAP at the injury epicenter is shown ( n = 3). (B) Protein levels of NF in spinal cord tissues analyzed by western blot ( n = 3). (C) Representative IHC images of NeuN + neurons in injured spinal cords (28 dpi; scale bar: 100 μm; n = 3). Bar graph indicates the mean number of surviving NeuN + neurons per field. (D) Nissl staining of injured spinal cords (28 dpi; scale bar: 100 μm; n = 3). Arrows denote Nissl-positive cells. Bar graph displays the mean number of Nissl + cells per field. In (C, D), three stained sections were randomly selected from each experimental rats to evaluate the average number of surviving neurons in the anterior horns of spinal cord. (E) HE staining of spinal cord lesion cavities. Bar graph quantifies lesion cavity areas across groups ( n = 3). (F) Hindlimb motor function evaluated by Basso–Beattie–Bresnahan (BBB) locomotor rating scale ( n = 3). Interrater reliability was confirmed by an intraclass correlation coefficient (ICC > 0.85). Data represent mean ± SD. ⁣ ∗ p < 0.05, ⁣ ∗∗ p < 0.01, and ⁣ ∗∗∗ p < 0.001. NC, negative control. sgTRIM14, sgRNA targeting TRIM14.

    Article Snippet: Sections were blocked with 5% normal goat serum for 1 h at room temperature, then incubated with rabbit anti-neuronal nucle (NeuN) primary antibody (24307S, 1:200, CST) for 2 h at 37°C, followed by HRP-conjugated goat anti-rabbit IgG secondary antibody (A0208, 1:500, Beyotime) for 1 h at room temperature.

    Techniques: Knockdown, Functional Assay, Immunofluorescence, Fluorescence, Western Blot, Staining, Negative Control