rabbit anti s1pr1  (Alomone Labs)


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    Alomone Labs rabbit anti s1pr1
    Modulation of <t>S1PR1</t> expression by the CNTF/Stat3 pathway in optic nerve-injured retinae. (a, b) S1PR1 expression changes were monitored 3 d after ONC in retinae infected with ShH10.CNTF or ShH10.Empty, a control vector that was deprived of cDNA sequence. ShH10 viruses preferentially infected Müller glia in the retina [ 16 ]. P-Stat3 and S1PR1 were markedly increased by ShH10.CNTF in RGC somata identified using β 3-tubulin as a specific marker. (c) Five days after ONC, qRT-PCR measurements showed that the infection of RGCs with AAV2.Stat3 significantly increased the mRNA level of S1pr1 compared with control AAV2.GFP vector. ShH10 and AAV2 viruses were intravitreally injected 4 weeks before ONC. Three mice were analyzed/grouped. Statistics: one-way ANOVA; ∗ p
    Rabbit Anti S1pr1, 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/rabbit anti s1pr1/product/Alomone Labs
    Average 94 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    rabbit anti s1pr1 - by Bioz Stars, 2022-01
    94/100 stars

    Images

    1) Product Images from "Sphingosine 1-Phosphate Receptor 1 Modulates CNTF-Induced Axonal Growth and Neuroprotection in the Mouse Visual System"

    Article Title: Sphingosine 1-Phosphate Receptor 1 Modulates CNTF-Induced Axonal Growth and Neuroprotection in the Mouse Visual System

    Journal: Neural Plasticity

    doi: 10.1155/2017/6818970

    Modulation of S1PR1 expression by the CNTF/Stat3 pathway in optic nerve-injured retinae. (a, b) S1PR1 expression changes were monitored 3 d after ONC in retinae infected with ShH10.CNTF or ShH10.Empty, a control vector that was deprived of cDNA sequence. ShH10 viruses preferentially infected Müller glia in the retina [ 16 ]. P-Stat3 and S1PR1 were markedly increased by ShH10.CNTF in RGC somata identified using β 3-tubulin as a specific marker. (c) Five days after ONC, qRT-PCR measurements showed that the infection of RGCs with AAV2.Stat3 significantly increased the mRNA level of S1pr1 compared with control AAV2.GFP vector. ShH10 and AAV2 viruses were intravitreally injected 4 weeks before ONC. Three mice were analyzed/grouped. Statistics: one-way ANOVA; ∗ p
    Figure Legend Snippet: Modulation of S1PR1 expression by the CNTF/Stat3 pathway in optic nerve-injured retinae. (a, b) S1PR1 expression changes were monitored 3 d after ONC in retinae infected with ShH10.CNTF or ShH10.Empty, a control vector that was deprived of cDNA sequence. ShH10 viruses preferentially infected Müller glia in the retina [ 16 ]. P-Stat3 and S1PR1 were markedly increased by ShH10.CNTF in RGC somata identified using β 3-tubulin as a specific marker. (c) Five days after ONC, qRT-PCR measurements showed that the infection of RGCs with AAV2.Stat3 significantly increased the mRNA level of S1pr1 compared with control AAV2.GFP vector. ShH10 and AAV2 viruses were intravitreally injected 4 weeks before ONC. Three mice were analyzed/grouped. Statistics: one-way ANOVA; ∗ p

    Techniques Used: Expressing, Infection, Plasmid Preparation, Sequencing, Marker, Quantitative RT-PCR, Injection, Mouse Assay

    S1PR1 knockdown alters CNTF-induced RGC survival after ONC. (a) Two weeks after ONC, surviving RGCs were observed in retinal flat-mounts after immunofluorescent staining for β 3-tubulin. Less RGCs were visible in retinae infected with AAV2.shRNA-S1PR1 and ShH10.CNTF ( n = 5 mice) than in mice injected with ShH10.CNTF/AAV2.GFP ( n = 7 mice) or ShH10.CNTF/AAV2.shRNA-S1PR1 ( n = 5 mice). (b) Quantitatively, the average number of surviving RGCs was statistically lower in whole retinae transduced with ShH10.CNTF/AAV2.shRNA-S1PR1 than in the two other groups of animals (ANOVA, ∗∗∗ p
    Figure Legend Snippet: S1PR1 knockdown alters CNTF-induced RGC survival after ONC. (a) Two weeks after ONC, surviving RGCs were observed in retinal flat-mounts after immunofluorescent staining for β 3-tubulin. Less RGCs were visible in retinae infected with AAV2.shRNA-S1PR1 and ShH10.CNTF ( n = 5 mice) than in mice injected with ShH10.CNTF/AAV2.GFP ( n = 7 mice) or ShH10.CNTF/AAV2.shRNA-S1PR1 ( n = 5 mice). (b) Quantitatively, the average number of surviving RGCs was statistically lower in whole retinae transduced with ShH10.CNTF/AAV2.shRNA-S1PR1 than in the two other groups of animals (ANOVA, ∗∗∗ p

    Techniques Used: Staining, Infection, shRNA, Mouse Assay, Injection, Transduction

    The expression of P-Stat3 is not changed by S1PR1 silencing after CNTF stimulation. The expression of P-Stat3 was assessed by western blotting in protein lysates (20 μ g) from retinae treated with ShH10 and AAV2 viruses. P-Stat3 and Stat3 blots were quantified by densitometry using the ImageJ software (NIH). The level of P-Stat3/Stat3 was not significantly different between mice treated with ShH10.CNTF/AAV2.shRNA-S1PR1 and ShH10.CNTF/AAV2.GFP. Three mice were analyzed for each group.
    Figure Legend Snippet: The expression of P-Stat3 is not changed by S1PR1 silencing after CNTF stimulation. The expression of P-Stat3 was assessed by western blotting in protein lysates (20 μ g) from retinae treated with ShH10 and AAV2 viruses. P-Stat3 and Stat3 blots were quantified by densitometry using the ImageJ software (NIH). The level of P-Stat3/Stat3 was not significantly different between mice treated with ShH10.CNTF/AAV2.shRNA-S1PR1 and ShH10.CNTF/AAV2.GFP. Three mice were analyzed for each group.

    Techniques Used: Expressing, Western Blot, Software, Mouse Assay, shRNA

    Hypothetical mechanism by which CNTF/Stat3 and S1P/S1PR1 interaction may orchestrate neuronal survival and axonal growth. CNTF binds and activates a heterotrimeric receptor complex, composed of CNTFR α , leukemia inhibitory factor receptor (LIFR), and gp130, leading to Stat3 phosphorylation (P-Stat3) and activation. (a) P-Stat3-driven transcription may increase the expression of S1PR1 and its translocation to the plasma membrane. The activation of S1PR1 by S1P may trigger downstream growth mechanisms resulting in (b) neuronal survival and (c) axonal growth.
    Figure Legend Snippet: Hypothetical mechanism by which CNTF/Stat3 and S1P/S1PR1 interaction may orchestrate neuronal survival and axonal growth. CNTF binds and activates a heterotrimeric receptor complex, composed of CNTFR α , leukemia inhibitory factor receptor (LIFR), and gp130, leading to Stat3 phosphorylation (P-Stat3) and activation. (a) P-Stat3-driven transcription may increase the expression of S1PR1 and its translocation to the plasma membrane. The activation of S1PR1 by S1P may trigger downstream growth mechanisms resulting in (b) neuronal survival and (c) axonal growth.

    Techniques Used: Activation Assay, Expressing, Translocation Assay

    S1PR1 knockdown potentiates CNTF-induced axonal regeneration. (a) Axonal regeneration was visualized on longitudinal sections of optic nerves two weeks after crush injury and 4 weeks after coinfection with ShH10.CNTF and AAV2 vectors. Axons were traced with cholera toxin β subunit (CTb) conjugated to Alexa 594 the day before tissue fixation. (b) The infection of retinal cells with ShH10.CNTF and AAV2.shRNA-S1PR1 promoted lengthy axonal regeneration in the optic nerve compared with the ShH10.CNTF/AAV2.GFP combination. (c) Quantitatively, axonal fibers were significantly more numerous between 1300 and 1800 μ m past the lesion site with ShH10.CNTF/AAV2.shRNA-S1PR1 ( n = 6 mice) than with ShH10.CNTF/AAV2.GFP ( n = 5 mice) treatments (ANOVA, ∗ p
    Figure Legend Snippet: S1PR1 knockdown potentiates CNTF-induced axonal regeneration. (a) Axonal regeneration was visualized on longitudinal sections of optic nerves two weeks after crush injury and 4 weeks after coinfection with ShH10.CNTF and AAV2 vectors. Axons were traced with cholera toxin β subunit (CTb) conjugated to Alexa 594 the day before tissue fixation. (b) The infection of retinal cells with ShH10.CNTF and AAV2.shRNA-S1PR1 promoted lengthy axonal regeneration in the optic nerve compared with the ShH10.CNTF/AAV2.GFP combination. (c) Quantitatively, axonal fibers were significantly more numerous between 1300 and 1800 μ m past the lesion site with ShH10.CNTF/AAV2.shRNA-S1PR1 ( n = 6 mice) than with ShH10.CNTF/AAV2.GFP ( n = 5 mice) treatments (ANOVA, ∗ p

    Techniques Used: CtB Assay, Infection, shRNA, Mouse Assay

    2) Product Images from "Differential sphingosine-1-phosphate receptor-1 (S1PR1) protein expressions in the dorsolateral prefrontal cortex between schizophrenia Type 1 and Type 2"

    Article Title: Differential sphingosine-1-phosphate receptor-1 (S1PR1) protein expressions in the dorsolateral prefrontal cortex between schizophrenia Type 1 and Type 2

    Journal: bioRxiv

    doi: 10.1101/2021.05.15.444302

    Autoradiograph analysis of S1PR1 using S1PR1 specific [ 3 H]CS1P1 in control and schizophrenia DLPFC. A) Comparison among control, schizophrenia Type 1 and schizophrenia Type 2 (* represents p
    Figure Legend Snippet: Autoradiograph analysis of S1PR1 using S1PR1 specific [ 3 H]CS1P1 in control and schizophrenia DLPFC. A) Comparison among control, schizophrenia Type 1 and schizophrenia Type 2 (* represents p

    Techniques Used: Autoradiography

    Representative images of autoradiograph analysis of S1PR1 using S1PR1 specific [ 3 H]CS1P1 in control and schizophrenia DLPFC.
    Figure Legend Snippet: Representative images of autoradiograph analysis of S1PR1 using S1PR1 specific [ 3 H]CS1P1 in control and schizophrenia DLPFC.

    Techniques Used: Autoradiography

    Immunohistochemistry of S1PR1 in control and schizophrenia DLPFC.
    Figure Legend Snippet: Immunohistochemistry of S1PR1 in control and schizophrenia DLPFC.

    Techniques Used: Immunohistochemistry

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    Alomone Labs rabbit anti s1pr1
    Modulation of <t>S1PR1</t> expression by the CNTF/Stat3 pathway in optic nerve-injured retinae. (a, b) S1PR1 expression changes were monitored 3 d after ONC in retinae infected with ShH10.CNTF or ShH10.Empty, a control vector that was deprived of cDNA sequence. ShH10 viruses preferentially infected Müller glia in the retina [ 16 ]. P-Stat3 and S1PR1 were markedly increased by ShH10.CNTF in RGC somata identified using β 3-tubulin as a specific marker. (c) Five days after ONC, qRT-PCR measurements showed that the infection of RGCs with AAV2.Stat3 significantly increased the mRNA level of S1pr1 compared with control AAV2.GFP vector. ShH10 and AAV2 viruses were intravitreally injected 4 weeks before ONC. Three mice were analyzed/grouped. Statistics: one-way ANOVA; ∗ p
    Rabbit Anti S1pr1, 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/rabbit anti s1pr1/product/Alomone Labs
    Average 94 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    rabbit anti s1pr1 - by Bioz Stars, 2022-01
    94/100 stars
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    Modulation of S1PR1 expression by the CNTF/Stat3 pathway in optic nerve-injured retinae. (a, b) S1PR1 expression changes were monitored 3 d after ONC in retinae infected with ShH10.CNTF or ShH10.Empty, a control vector that was deprived of cDNA sequence. ShH10 viruses preferentially infected Müller glia in the retina [ 16 ]. P-Stat3 and S1PR1 were markedly increased by ShH10.CNTF in RGC somata identified using β 3-tubulin as a specific marker. (c) Five days after ONC, qRT-PCR measurements showed that the infection of RGCs with AAV2.Stat3 significantly increased the mRNA level of S1pr1 compared with control AAV2.GFP vector. ShH10 and AAV2 viruses were intravitreally injected 4 weeks before ONC. Three mice were analyzed/grouped. Statistics: one-way ANOVA; ∗ p

    Journal: Neural Plasticity

    Article Title: Sphingosine 1-Phosphate Receptor 1 Modulates CNTF-Induced Axonal Growth and Neuroprotection in the Mouse Visual System

    doi: 10.1155/2017/6818970

    Figure Lengend Snippet: Modulation of S1PR1 expression by the CNTF/Stat3 pathway in optic nerve-injured retinae. (a, b) S1PR1 expression changes were monitored 3 d after ONC in retinae infected with ShH10.CNTF or ShH10.Empty, a control vector that was deprived of cDNA sequence. ShH10 viruses preferentially infected Müller glia in the retina [ 16 ]. P-Stat3 and S1PR1 were markedly increased by ShH10.CNTF in RGC somata identified using β 3-tubulin as a specific marker. (c) Five days after ONC, qRT-PCR measurements showed that the infection of RGCs with AAV2.Stat3 significantly increased the mRNA level of S1pr1 compared with control AAV2.GFP vector. ShH10 and AAV2 viruses were intravitreally injected 4 weeks before ONC. Three mice were analyzed/grouped. Statistics: one-way ANOVA; ∗ p

    Article Snippet: Primary antibodies were rabbit anti-β 3-tubulin (1 : 1000; ab18207, Abcam), mouse anti-β 3-tubulin (1 : 1000; G712A, Promega, Madison, WI, USA), rabbit anti-S1PR1 (1 : 50; ASR-011; Alomone Labs, Jerusalem, Israel), rabbit anti-S1PR1 (1 : 200; PA1-1040, Life Technologies), and rabbit anti-phospho-Stat3 (1 : 100; 9131, Cell Signaling, Whitby, ON, Canada).

    Techniques: Expressing, Infection, Plasmid Preparation, Sequencing, Marker, Quantitative RT-PCR, Injection, Mouse Assay

    S1PR1 knockdown alters CNTF-induced RGC survival after ONC. (a) Two weeks after ONC, surviving RGCs were observed in retinal flat-mounts after immunofluorescent staining for β 3-tubulin. Less RGCs were visible in retinae infected with AAV2.shRNA-S1PR1 and ShH10.CNTF ( n = 5 mice) than in mice injected with ShH10.CNTF/AAV2.GFP ( n = 7 mice) or ShH10.CNTF/AAV2.shRNA-S1PR1 ( n = 5 mice). (b) Quantitatively, the average number of surviving RGCs was statistically lower in whole retinae transduced with ShH10.CNTF/AAV2.shRNA-S1PR1 than in the two other groups of animals (ANOVA, ∗∗∗ p

    Journal: Neural Plasticity

    Article Title: Sphingosine 1-Phosphate Receptor 1 Modulates CNTF-Induced Axonal Growth and Neuroprotection in the Mouse Visual System

    doi: 10.1155/2017/6818970

    Figure Lengend Snippet: S1PR1 knockdown alters CNTF-induced RGC survival after ONC. (a) Two weeks after ONC, surviving RGCs were observed in retinal flat-mounts after immunofluorescent staining for β 3-tubulin. Less RGCs were visible in retinae infected with AAV2.shRNA-S1PR1 and ShH10.CNTF ( n = 5 mice) than in mice injected with ShH10.CNTF/AAV2.GFP ( n = 7 mice) or ShH10.CNTF/AAV2.shRNA-S1PR1 ( n = 5 mice). (b) Quantitatively, the average number of surviving RGCs was statistically lower in whole retinae transduced with ShH10.CNTF/AAV2.shRNA-S1PR1 than in the two other groups of animals (ANOVA, ∗∗∗ p

    Article Snippet: Primary antibodies were rabbit anti-β 3-tubulin (1 : 1000; ab18207, Abcam), mouse anti-β 3-tubulin (1 : 1000; G712A, Promega, Madison, WI, USA), rabbit anti-S1PR1 (1 : 50; ASR-011; Alomone Labs, Jerusalem, Israel), rabbit anti-S1PR1 (1 : 200; PA1-1040, Life Technologies), and rabbit anti-phospho-Stat3 (1 : 100; 9131, Cell Signaling, Whitby, ON, Canada).

    Techniques: Staining, Infection, shRNA, Mouse Assay, Injection, Transduction

    The expression of P-Stat3 is not changed by S1PR1 silencing after CNTF stimulation. The expression of P-Stat3 was assessed by western blotting in protein lysates (20 μ g) from retinae treated with ShH10 and AAV2 viruses. P-Stat3 and Stat3 blots were quantified by densitometry using the ImageJ software (NIH). The level of P-Stat3/Stat3 was not significantly different between mice treated with ShH10.CNTF/AAV2.shRNA-S1PR1 and ShH10.CNTF/AAV2.GFP. Three mice were analyzed for each group.

    Journal: Neural Plasticity

    Article Title: Sphingosine 1-Phosphate Receptor 1 Modulates CNTF-Induced Axonal Growth and Neuroprotection in the Mouse Visual System

    doi: 10.1155/2017/6818970

    Figure Lengend Snippet: The expression of P-Stat3 is not changed by S1PR1 silencing after CNTF stimulation. The expression of P-Stat3 was assessed by western blotting in protein lysates (20 μ g) from retinae treated with ShH10 and AAV2 viruses. P-Stat3 and Stat3 blots were quantified by densitometry using the ImageJ software (NIH). The level of P-Stat3/Stat3 was not significantly different between mice treated with ShH10.CNTF/AAV2.shRNA-S1PR1 and ShH10.CNTF/AAV2.GFP. Three mice were analyzed for each group.

    Article Snippet: Primary antibodies were rabbit anti-β 3-tubulin (1 : 1000; ab18207, Abcam), mouse anti-β 3-tubulin (1 : 1000; G712A, Promega, Madison, WI, USA), rabbit anti-S1PR1 (1 : 50; ASR-011; Alomone Labs, Jerusalem, Israel), rabbit anti-S1PR1 (1 : 200; PA1-1040, Life Technologies), and rabbit anti-phospho-Stat3 (1 : 100; 9131, Cell Signaling, Whitby, ON, Canada).

    Techniques: Expressing, Western Blot, Software, Mouse Assay, shRNA

    Hypothetical mechanism by which CNTF/Stat3 and S1P/S1PR1 interaction may orchestrate neuronal survival and axonal growth. CNTF binds and activates a heterotrimeric receptor complex, composed of CNTFR α , leukemia inhibitory factor receptor (LIFR), and gp130, leading to Stat3 phosphorylation (P-Stat3) and activation. (a) P-Stat3-driven transcription may increase the expression of S1PR1 and its translocation to the plasma membrane. The activation of S1PR1 by S1P may trigger downstream growth mechanisms resulting in (b) neuronal survival and (c) axonal growth.

    Journal: Neural Plasticity

    Article Title: Sphingosine 1-Phosphate Receptor 1 Modulates CNTF-Induced Axonal Growth and Neuroprotection in the Mouse Visual System

    doi: 10.1155/2017/6818970

    Figure Lengend Snippet: Hypothetical mechanism by which CNTF/Stat3 and S1P/S1PR1 interaction may orchestrate neuronal survival and axonal growth. CNTF binds and activates a heterotrimeric receptor complex, composed of CNTFR α , leukemia inhibitory factor receptor (LIFR), and gp130, leading to Stat3 phosphorylation (P-Stat3) and activation. (a) P-Stat3-driven transcription may increase the expression of S1PR1 and its translocation to the plasma membrane. The activation of S1PR1 by S1P may trigger downstream growth mechanisms resulting in (b) neuronal survival and (c) axonal growth.

    Article Snippet: Primary antibodies were rabbit anti-β 3-tubulin (1 : 1000; ab18207, Abcam), mouse anti-β 3-tubulin (1 : 1000; G712A, Promega, Madison, WI, USA), rabbit anti-S1PR1 (1 : 50; ASR-011; Alomone Labs, Jerusalem, Israel), rabbit anti-S1PR1 (1 : 200; PA1-1040, Life Technologies), and rabbit anti-phospho-Stat3 (1 : 100; 9131, Cell Signaling, Whitby, ON, Canada).

    Techniques: Activation Assay, Expressing, Translocation Assay

    S1PR1 knockdown potentiates CNTF-induced axonal regeneration. (a) Axonal regeneration was visualized on longitudinal sections of optic nerves two weeks after crush injury and 4 weeks after coinfection with ShH10.CNTF and AAV2 vectors. Axons were traced with cholera toxin β subunit (CTb) conjugated to Alexa 594 the day before tissue fixation. (b) The infection of retinal cells with ShH10.CNTF and AAV2.shRNA-S1PR1 promoted lengthy axonal regeneration in the optic nerve compared with the ShH10.CNTF/AAV2.GFP combination. (c) Quantitatively, axonal fibers were significantly more numerous between 1300 and 1800 μ m past the lesion site with ShH10.CNTF/AAV2.shRNA-S1PR1 ( n = 6 mice) than with ShH10.CNTF/AAV2.GFP ( n = 5 mice) treatments (ANOVA, ∗ p

    Journal: Neural Plasticity

    Article Title: Sphingosine 1-Phosphate Receptor 1 Modulates CNTF-Induced Axonal Growth and Neuroprotection in the Mouse Visual System

    doi: 10.1155/2017/6818970

    Figure Lengend Snippet: S1PR1 knockdown potentiates CNTF-induced axonal regeneration. (a) Axonal regeneration was visualized on longitudinal sections of optic nerves two weeks after crush injury and 4 weeks after coinfection with ShH10.CNTF and AAV2 vectors. Axons were traced with cholera toxin β subunit (CTb) conjugated to Alexa 594 the day before tissue fixation. (b) The infection of retinal cells with ShH10.CNTF and AAV2.shRNA-S1PR1 promoted lengthy axonal regeneration in the optic nerve compared with the ShH10.CNTF/AAV2.GFP combination. (c) Quantitatively, axonal fibers were significantly more numerous between 1300 and 1800 μ m past the lesion site with ShH10.CNTF/AAV2.shRNA-S1PR1 ( n = 6 mice) than with ShH10.CNTF/AAV2.GFP ( n = 5 mice) treatments (ANOVA, ∗ p

    Article Snippet: Primary antibodies were rabbit anti-β 3-tubulin (1 : 1000; ab18207, Abcam), mouse anti-β 3-tubulin (1 : 1000; G712A, Promega, Madison, WI, USA), rabbit anti-S1PR1 (1 : 50; ASR-011; Alomone Labs, Jerusalem, Israel), rabbit anti-S1PR1 (1 : 200; PA1-1040, Life Technologies), and rabbit anti-phospho-Stat3 (1 : 100; 9131, Cell Signaling, Whitby, ON, Canada).

    Techniques: CtB Assay, Infection, shRNA, Mouse Assay

    Autoradiograph analysis of S1PR1 using S1PR1 specific [ 3 H]CS1P1 in control and schizophrenia DLPFC. A) Comparison among control, schizophrenia Type 1 and schizophrenia Type 2 (* represents p

    Journal: bioRxiv

    Article Title: Differential sphingosine-1-phosphate receptor-1 (S1PR1) protein expressions in the dorsolateral prefrontal cortex between schizophrenia Type 1 and Type 2

    doi: 10.1101/2021.05.15.444302

    Figure Lengend Snippet: Autoradiograph analysis of S1PR1 using S1PR1 specific [ 3 H]CS1P1 in control and schizophrenia DLPFC. A) Comparison among control, schizophrenia Type 1 and schizophrenia Type 2 (* represents p

    Article Snippet: After that, all sections were stained with anti-S1PR1 antibody (Alomone, Jerusalem, Israel) overnight at 4°C, washed and followed by incubation with ImmPRESS HRP Horse anti-rabbit polymer for 1 hour at RT, and developed using ImmPACT DAB (Vector Laboratories, Burlingame, CA).

    Techniques: Autoradiography

    Representative images of autoradiograph analysis of S1PR1 using S1PR1 specific [ 3 H]CS1P1 in control and schizophrenia DLPFC.

    Journal: bioRxiv

    Article Title: Differential sphingosine-1-phosphate receptor-1 (S1PR1) protein expressions in the dorsolateral prefrontal cortex between schizophrenia Type 1 and Type 2

    doi: 10.1101/2021.05.15.444302

    Figure Lengend Snippet: Representative images of autoradiograph analysis of S1PR1 using S1PR1 specific [ 3 H]CS1P1 in control and schizophrenia DLPFC.

    Article Snippet: After that, all sections were stained with anti-S1PR1 antibody (Alomone, Jerusalem, Israel) overnight at 4°C, washed and followed by incubation with ImmPRESS HRP Horse anti-rabbit polymer for 1 hour at RT, and developed using ImmPACT DAB (Vector Laboratories, Burlingame, CA).

    Techniques: Autoradiography

    Immunohistochemistry of S1PR1 in control and schizophrenia DLPFC.

    Journal: bioRxiv

    Article Title: Differential sphingosine-1-phosphate receptor-1 (S1PR1) protein expressions in the dorsolateral prefrontal cortex between schizophrenia Type 1 and Type 2

    doi: 10.1101/2021.05.15.444302

    Figure Lengend Snippet: Immunohistochemistry of S1PR1 in control and schizophrenia DLPFC.

    Article Snippet: After that, all sections were stained with anti-S1PR1 antibody (Alomone, Jerusalem, Israel) overnight at 4°C, washed and followed by incubation with ImmPRESS HRP Horse anti-rabbit polymer for 1 hour at RT, and developed using ImmPACT DAB (Vector Laboratories, Burlingame, CA).

    Techniques: Immunohistochemistry