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hsyn1 promoter  (Addgene inc)


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    Addgene inc hsyn1 promoter
    CNH in neurons exerts neuroprotection. (A) Experimental design to examine CNH function in astrocytes. Gene expression is controlled by the astrocyte-specific human GFAP ( hGFAP ) promoter. (B) Representative images showing GFAP + cells surrounding the cortical lesion. Scale bar: 50 µm. (C) Quantification of fluorescence intensity of GFAP (mean ± SEM; n = 5 mice per group; P = 0.1767). (D) Representative images showing AT8 surrounding the cortical lesion. Scale bar: 50 µm. (E) Quantification of AT8 fluorescence intensity (mean ± SEM; n = 5 mice per group; P = 0.7153). (F) Representative images of brain sections showing GFAP + glial scar (yellow outlined). Scale bar: 1 mm. (G) Quantification of GFAP + scar volumes (mean ± SEM; n = 5 mice per group; P = 0.7448). (H) Representative images of brain sections for lesion quantification (yellow outlined). Scale bar: 1 mm. (I) Quantification of cortical volumes post injury (mean ± SEM; n = 5 mice per group; P = 0.9039). (J) Experimental design to examine CNH function in neurons. Gene expression is controlled by the neuron-specific human SYN1 ( <t>hSYN1</t> ) promoter. (K) Representative images showing GFAP + cells surrounding the cortical lesion. Scale bar: 50 µm. (L) Quantification of fluorescence intensity of GFAP (mean ± SEM; n = 6 mice per group; P = 0.0007). (M) Representative images showing immunostaining of AT8 surrounding the cortical lesion. Scale bar: 50 µm. (N) Quantification of AT8 fluorescence intensity (mean ± SEM; n = 6 mice per group; P = 0.0152). (O) Representative images of brain sections showing GFAP + glial scar (yellow outlined). Scale bar: 1 mm. (P) Quantification of GFAP + scar volumes (mean ± SEM; n = 6 mice per group; P = 0.0042). (Q) Representative images of brain sections for lesion quantifications (yellow outlined). Scale bar: 1 mm. (R) Quantification of cortical volumes post injury (mean ± SEM; n = 6 mice per group; P = 0.0227). AAV: Adeno-associated virus; Br: bregma; CCI: controlled cortical impact; CNH: Citron homology domain; dpi: days post-injury; GFAP: glial acidic fibrillary acidic protein; IHC: immunohistochemistry.
    Hsyn1 Promoter, supplied by Addgene inc, used in various techniques. Bioz Stars score: 96/100, based on 158 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/hsyn1 promoter/product/Addgene inc
    Average 96 stars, based on 158 article reviews
    hsyn1 promoter - by Bioz Stars, 2026-03
    96/100 stars

    Images

    1) Product Images from "The Citron homology domain of MAP4Ks improves outcomes of traumatic brain injury"

    Article Title: The Citron homology domain of MAP4Ks improves outcomes of traumatic brain injury

    Journal: Neural Regeneration Research

    doi: 10.4103/NRR.NRR-D-24-00113

    CNH in neurons exerts neuroprotection. (A) Experimental design to examine CNH function in astrocytes. Gene expression is controlled by the astrocyte-specific human GFAP ( hGFAP ) promoter. (B) Representative images showing GFAP + cells surrounding the cortical lesion. Scale bar: 50 µm. (C) Quantification of fluorescence intensity of GFAP (mean ± SEM; n = 5 mice per group; P = 0.1767). (D) Representative images showing AT8 surrounding the cortical lesion. Scale bar: 50 µm. (E) Quantification of AT8 fluorescence intensity (mean ± SEM; n = 5 mice per group; P = 0.7153). (F) Representative images of brain sections showing GFAP + glial scar (yellow outlined). Scale bar: 1 mm. (G) Quantification of GFAP + scar volumes (mean ± SEM; n = 5 mice per group; P = 0.7448). (H) Representative images of brain sections for lesion quantification (yellow outlined). Scale bar: 1 mm. (I) Quantification of cortical volumes post injury (mean ± SEM; n = 5 mice per group; P = 0.9039). (J) Experimental design to examine CNH function in neurons. Gene expression is controlled by the neuron-specific human SYN1 ( hSYN1 ) promoter. (K) Representative images showing GFAP + cells surrounding the cortical lesion. Scale bar: 50 µm. (L) Quantification of fluorescence intensity of GFAP (mean ± SEM; n = 6 mice per group; P = 0.0007). (M) Representative images showing immunostaining of AT8 surrounding the cortical lesion. Scale bar: 50 µm. (N) Quantification of AT8 fluorescence intensity (mean ± SEM; n = 6 mice per group; P = 0.0152). (O) Representative images of brain sections showing GFAP + glial scar (yellow outlined). Scale bar: 1 mm. (P) Quantification of GFAP + scar volumes (mean ± SEM; n = 6 mice per group; P = 0.0042). (Q) Representative images of brain sections for lesion quantifications (yellow outlined). Scale bar: 1 mm. (R) Quantification of cortical volumes post injury (mean ± SEM; n = 6 mice per group; P = 0.0227). AAV: Adeno-associated virus; Br: bregma; CCI: controlled cortical impact; CNH: Citron homology domain; dpi: days post-injury; GFAP: glial acidic fibrillary acidic protein; IHC: immunohistochemistry.
    Figure Legend Snippet: CNH in neurons exerts neuroprotection. (A) Experimental design to examine CNH function in astrocytes. Gene expression is controlled by the astrocyte-specific human GFAP ( hGFAP ) promoter. (B) Representative images showing GFAP + cells surrounding the cortical lesion. Scale bar: 50 µm. (C) Quantification of fluorescence intensity of GFAP (mean ± SEM; n = 5 mice per group; P = 0.1767). (D) Representative images showing AT8 surrounding the cortical lesion. Scale bar: 50 µm. (E) Quantification of AT8 fluorescence intensity (mean ± SEM; n = 5 mice per group; P = 0.7153). (F) Representative images of brain sections showing GFAP + glial scar (yellow outlined). Scale bar: 1 mm. (G) Quantification of GFAP + scar volumes (mean ± SEM; n = 5 mice per group; P = 0.7448). (H) Representative images of brain sections for lesion quantification (yellow outlined). Scale bar: 1 mm. (I) Quantification of cortical volumes post injury (mean ± SEM; n = 5 mice per group; P = 0.9039). (J) Experimental design to examine CNH function in neurons. Gene expression is controlled by the neuron-specific human SYN1 ( hSYN1 ) promoter. (K) Representative images showing GFAP + cells surrounding the cortical lesion. Scale bar: 50 µm. (L) Quantification of fluorescence intensity of GFAP (mean ± SEM; n = 6 mice per group; P = 0.0007). (M) Representative images showing immunostaining of AT8 surrounding the cortical lesion. Scale bar: 50 µm. (N) Quantification of AT8 fluorescence intensity (mean ± SEM; n = 6 mice per group; P = 0.0152). (O) Representative images of brain sections showing GFAP + glial scar (yellow outlined). Scale bar: 1 mm. (P) Quantification of GFAP + scar volumes (mean ± SEM; n = 6 mice per group; P = 0.0042). (Q) Representative images of brain sections for lesion quantifications (yellow outlined). Scale bar: 1 mm. (R) Quantification of cortical volumes post injury (mean ± SEM; n = 6 mice per group; P = 0.0227). AAV: Adeno-associated virus; Br: bregma; CCI: controlled cortical impact; CNH: Citron homology domain; dpi: days post-injury; GFAP: glial acidic fibrillary acidic protein; IHC: immunohistochemistry.

    Techniques Used: Gene Expression, Fluorescence, Immunostaining, Virus, Immunohistochemistry



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    Survival analysis of fALS iMN and effects of therapeutic compounds. (A) Workflow of survival tracking in iMN. Cultures were transfected with <t>Synapsin-GFP</t> on Day <t>8</t> <t>(D8)</t> and imaged from Day 12 (D12) to Day 46 (D46). iMN detection and tracking were performed with a finetuned ML model (YOLOv8) to monitor individual cells. (B) Representative images of iMN cultures with tracked cells (identified by orange labels) over time, from D12 to D46. (C) Kaplan-Meier fitted survival from control and fALS iMN under baseline conditions, showing reduced survival in certain fALS lines (p-values are in the legend). (D-H) Cox proportional hazards model hazard ratios of iMN survival for control and fALS mutants under different drug treatments, relative to vehicle (log(HR)=0). Squares represent the log(HR), error bars the 95% confidence interval. n=100-3500 cells for each group (sampled from 7 control, 3 SOD1 A4V 3 C9orf72, 4 TDP-43 N352S , 4 FUS R521G , 3 CHCHD10 R15L lines, and 1-9 technical replicates from 3 batches of differentiations).
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    Image Search Results


    CNH in neurons exerts neuroprotection. (A) Experimental design to examine CNH function in astrocytes. Gene expression is controlled by the astrocyte-specific human GFAP ( hGFAP ) promoter. (B) Representative images showing GFAP + cells surrounding the cortical lesion. Scale bar: 50 µm. (C) Quantification of fluorescence intensity of GFAP (mean ± SEM; n = 5 mice per group; P = 0.1767). (D) Representative images showing AT8 surrounding the cortical lesion. Scale bar: 50 µm. (E) Quantification of AT8 fluorescence intensity (mean ± SEM; n = 5 mice per group; P = 0.7153). (F) Representative images of brain sections showing GFAP + glial scar (yellow outlined). Scale bar: 1 mm. (G) Quantification of GFAP + scar volumes (mean ± SEM; n = 5 mice per group; P = 0.7448). (H) Representative images of brain sections for lesion quantification (yellow outlined). Scale bar: 1 mm. (I) Quantification of cortical volumes post injury (mean ± SEM; n = 5 mice per group; P = 0.9039). (J) Experimental design to examine CNH function in neurons. Gene expression is controlled by the neuron-specific human SYN1 ( hSYN1 ) promoter. (K) Representative images showing GFAP + cells surrounding the cortical lesion. Scale bar: 50 µm. (L) Quantification of fluorescence intensity of GFAP (mean ± SEM; n = 6 mice per group; P = 0.0007). (M) Representative images showing immunostaining of AT8 surrounding the cortical lesion. Scale bar: 50 µm. (N) Quantification of AT8 fluorescence intensity (mean ± SEM; n = 6 mice per group; P = 0.0152). (O) Representative images of brain sections showing GFAP + glial scar (yellow outlined). Scale bar: 1 mm. (P) Quantification of GFAP + scar volumes (mean ± SEM; n = 6 mice per group; P = 0.0042). (Q) Representative images of brain sections for lesion quantifications (yellow outlined). Scale bar: 1 mm. (R) Quantification of cortical volumes post injury (mean ± SEM; n = 6 mice per group; P = 0.0227). AAV: Adeno-associated virus; Br: bregma; CCI: controlled cortical impact; CNH: Citron homology domain; dpi: days post-injury; GFAP: glial acidic fibrillary acidic protein; IHC: immunohistochemistry.

    Journal: Neural Regeneration Research

    Article Title: The Citron homology domain of MAP4Ks improves outcomes of traumatic brain injury

    doi: 10.4103/NRR.NRR-D-24-00113

    Figure Lengend Snippet: CNH in neurons exerts neuroprotection. (A) Experimental design to examine CNH function in astrocytes. Gene expression is controlled by the astrocyte-specific human GFAP ( hGFAP ) promoter. (B) Representative images showing GFAP + cells surrounding the cortical lesion. Scale bar: 50 µm. (C) Quantification of fluorescence intensity of GFAP (mean ± SEM; n = 5 mice per group; P = 0.1767). (D) Representative images showing AT8 surrounding the cortical lesion. Scale bar: 50 µm. (E) Quantification of AT8 fluorescence intensity (mean ± SEM; n = 5 mice per group; P = 0.7153). (F) Representative images of brain sections showing GFAP + glial scar (yellow outlined). Scale bar: 1 mm. (G) Quantification of GFAP + scar volumes (mean ± SEM; n = 5 mice per group; P = 0.7448). (H) Representative images of brain sections for lesion quantification (yellow outlined). Scale bar: 1 mm. (I) Quantification of cortical volumes post injury (mean ± SEM; n = 5 mice per group; P = 0.9039). (J) Experimental design to examine CNH function in neurons. Gene expression is controlled by the neuron-specific human SYN1 ( hSYN1 ) promoter. (K) Representative images showing GFAP + cells surrounding the cortical lesion. Scale bar: 50 µm. (L) Quantification of fluorescence intensity of GFAP (mean ± SEM; n = 6 mice per group; P = 0.0007). (M) Representative images showing immunostaining of AT8 surrounding the cortical lesion. Scale bar: 50 µm. (N) Quantification of AT8 fluorescence intensity (mean ± SEM; n = 6 mice per group; P = 0.0152). (O) Representative images of brain sections showing GFAP + glial scar (yellow outlined). Scale bar: 1 mm. (P) Quantification of GFAP + scar volumes (mean ± SEM; n = 6 mice per group; P = 0.0042). (Q) Representative images of brain sections for lesion quantifications (yellow outlined). Scale bar: 1 mm. (R) Quantification of cortical volumes post injury (mean ± SEM; n = 6 mice per group; P = 0.0227). AAV: Adeno-associated virus; Br: bregma; CCI: controlled cortical impact; CNH: Citron homology domain; dpi: days post-injury; GFAP: glial acidic fibrillary acidic protein; IHC: immunohistochemistry.

    Article Snippet: The following plasmids were obtained from Addgene (Watertown, MA, USA): pAd-deltaF6 (#112867), pUCmini-iCAP-PHP.eB (#103005), pAAV2/5 (#104964), pAAV2/9 (#112865), and pAAV-CAG-GFP (#37825). pAAV-hGFAP-GFP was previously described (Wang et al., 2021). pAAV-hSYN1-GFP was made by replacing the hGFAP promoter with the hSYN1 promoter (from Addgene #50457). pAAV-CAG-GFP-CNH , pAAV-CAG-BioID2-CNH , pAAV-hGFAP-CNH , and pAAV-hSYN1-CNH were then constructed through PCR-based subcloning into pAAV-CAG-GFP , pAAV-hGFAP-GFP and pAAV-hSYN1-GFP , respectively.

    Techniques: Gene Expression, Fluorescence, Immunostaining, Virus, Immunohistochemistry

    Survival analysis of fALS iMN and effects of therapeutic compounds. (A) Workflow of survival tracking in iMN. Cultures were transfected with Synapsin-GFP on Day 8 (D8) and imaged from Day 12 (D12) to Day 46 (D46). iMN detection and tracking were performed with a finetuned ML model (YOLOv8) to monitor individual cells. (B) Representative images of iMN cultures with tracked cells (identified by orange labels) over time, from D12 to D46. (C) Kaplan-Meier fitted survival from control and fALS iMN under baseline conditions, showing reduced survival in certain fALS lines (p-values are in the legend). (D-H) Cox proportional hazards model hazard ratios of iMN survival for control and fALS mutants under different drug treatments, relative to vehicle (log(HR)=0). Squares represent the log(HR), error bars the 95% confidence interval. n=100-3500 cells for each group (sampled from 7 control, 3 SOD1 A4V 3 C9orf72, 4 TDP-43 N352S , 4 FUS R521G , 3 CHCHD10 R15L lines, and 1-9 technical replicates from 3 batches of differentiations).

    Journal: bioRxiv

    Article Title: Investigation of mitochondrial phenotypes in motor neurons derived by direct conversion of fibroblasts from familial ALS subjects

    doi: 10.1101/2025.02.13.637962

    Figure Lengend Snippet: Survival analysis of fALS iMN and effects of therapeutic compounds. (A) Workflow of survival tracking in iMN. Cultures were transfected with Synapsin-GFP on Day 8 (D8) and imaged from Day 12 (D12) to Day 46 (D46). iMN detection and tracking were performed with a finetuned ML model (YOLOv8) to monitor individual cells. (B) Representative images of iMN cultures with tracked cells (identified by orange labels) over time, from D12 to D46. (C) Kaplan-Meier fitted survival from control and fALS iMN under baseline conditions, showing reduced survival in certain fALS lines (p-values are in the legend). (D-H) Cox proportional hazards model hazard ratios of iMN survival for control and fALS mutants under different drug treatments, relative to vehicle (log(HR)=0). Squares represent the log(HR), error bars the 95% confidence interval. n=100-3500 cells for each group (sampled from 7 control, 3 SOD1 A4V 3 C9orf72, 4 TDP-43 N352S , 4 FUS R521G , 3 CHCHD10 R15L lines, and 1-9 technical replicates from 3 batches of differentiations).

    Article Snippet: On D8 cells were transduced with an eGFP expressing lentiviral vector under the synapsin promoter, pHR-hSyn-EGFP (Addgene #114215), at 0.5×10^6 TU total / well without polybrene or spinfection.

    Techniques: Transfection, Control