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Elabscience anti s1pr3 edg3 extracellular antibody
S1P-induced pro-inflammatory cytokine release was <t>S1PR3</t> dependent. ( A ) Western blotting shows that healthy volunteers (H)-derived PBMCs expressed lower levels of S1PR3 compared to lung cancer (LK)-derived PBMCs. GAPDH was used as a loading control. The experiment was repeated three times. M refers to protein molecular weight marker. ( B ) S1PR3 expression analysis was performed by means of ImageJ software (NIH, USA) and expressed as a ratio between S1PR3 and GAPDH (loading control). S1PR3 inhibition with TY52156 (αS1PR3, 10 µM) reduced the release of TNF-α ( C ) and IL-6 ( D ) from LK-derived PBMCs after S1P (10 nM) addition. We used match-paired LK samples. n = 15 LK (Ctr-S1P) were tested for TNF-α ( C ) and n = 22 LK (Ctr-S1P) were tested for IL-6 ( D ). Data are represented as scatter dot plots indicating the median (confidence interval = 95%). Statistical differences were assessed by means of two-tailed Wilcoxon matched-pairs signed rank test.
Anti S1pr3 Edg3 Extracellular Antibody, supplied by Elabscience, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/result/anti s1pr3 edg3 extracellular antibody/product/Elabscience
Average 90 stars, based on 1 article reviews
Price from $9.99 to $1999.99
anti s1pr3 edg3 extracellular antibody - by Bioz Stars, 2022-10
90/100 stars

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1) Product Images from "S1P-Induced TNF-α and IL-6 Release from PBMCs Exacerbates Lung Cancer-Associated Inflammation"

Article Title: S1P-Induced TNF-α and IL-6 Release from PBMCs Exacerbates Lung Cancer-Associated Inflammation

Journal: Cells

doi: 10.3390/cells11162524

S1P-induced pro-inflammatory cytokine release was S1PR3 dependent. ( A ) Western blotting shows that healthy volunteers (H)-derived PBMCs expressed lower levels of S1PR3 compared to lung cancer (LK)-derived PBMCs. GAPDH was used as a loading control. The experiment was repeated three times. M refers to protein molecular weight marker. ( B ) S1PR3 expression analysis was performed by means of ImageJ software (NIH, USA) and expressed as a ratio between S1PR3 and GAPDH (loading control). S1PR3 inhibition with TY52156 (αS1PR3, 10 µM) reduced the release of TNF-α ( C ) and IL-6 ( D ) from LK-derived PBMCs after S1P (10 nM) addition. We used match-paired LK samples. n = 15 LK (Ctr-S1P) were tested for TNF-α ( C ) and n = 22 LK (Ctr-S1P) were tested for IL-6 ( D ). Data are represented as scatter dot plots indicating the median (confidence interval = 95%). Statistical differences were assessed by means of two-tailed Wilcoxon matched-pairs signed rank test.
Figure Legend Snippet: S1P-induced pro-inflammatory cytokine release was S1PR3 dependent. ( A ) Western blotting shows that healthy volunteers (H)-derived PBMCs expressed lower levels of S1PR3 compared to lung cancer (LK)-derived PBMCs. GAPDH was used as a loading control. The experiment was repeated three times. M refers to protein molecular weight marker. ( B ) S1PR3 expression analysis was performed by means of ImageJ software (NIH, USA) and expressed as a ratio between S1PR3 and GAPDH (loading control). S1PR3 inhibition with TY52156 (αS1PR3, 10 µM) reduced the release of TNF-α ( C ) and IL-6 ( D ) from LK-derived PBMCs after S1P (10 nM) addition. We used match-paired LK samples. n = 15 LK (Ctr-S1P) were tested for TNF-α ( C ) and n = 22 LK (Ctr-S1P) were tested for IL-6 ( D ). Data are represented as scatter dot plots indicating the median (confidence interval = 95%). Statistical differences were assessed by means of two-tailed Wilcoxon matched-pairs signed rank test.

Techniques Used: Western Blot, Derivative Assay, Molecular Weight, Marker, Expressing, Software, Inhibition, Two Tailed Test

S1P exacerbates the pro-inflammatory milieu by inducing pro-inflammatory cytokine release from lung cancer-derived PBMCs in a S1PR3-dependent manner. The activation of S1PR3 by the exogenous S1P enhances its own production and fosters the release of TNF-α in a SPHK I-dependent manner (black arrows), and of IL-6 via SPHK I/II (red arrows); S1P-induced IL-6, but not TNF-α, release from PBMCs of lung cancer patients is mTOR- and K-Ras-dependent (red arrows).
Figure Legend Snippet: S1P exacerbates the pro-inflammatory milieu by inducing pro-inflammatory cytokine release from lung cancer-derived PBMCs in a S1PR3-dependent manner. The activation of S1PR3 by the exogenous S1P enhances its own production and fosters the release of TNF-α in a SPHK I-dependent manner (black arrows), and of IL-6 via SPHK I/II (red arrows); S1P-induced IL-6, but not TNF-α, release from PBMCs of lung cancer patients is mTOR- and K-Ras-dependent (red arrows).

Techniques Used: Derivative Assay, Activation Assay

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    Elabscience anti s1pr3 edg3 extracellular antibody
    S1P-induced pro-inflammatory cytokine release was <t>S1PR3</t> dependent. ( A ) Western blotting shows that healthy volunteers (H)-derived PBMCs expressed lower levels of S1PR3 compared to lung cancer (LK)-derived PBMCs. GAPDH was used as a loading control. The experiment was repeated three times. M refers to protein molecular weight marker. ( B ) S1PR3 expression analysis was performed by means of ImageJ software (NIH, USA) and expressed as a ratio between S1PR3 and GAPDH (loading control). S1PR3 inhibition with TY52156 (αS1PR3, 10 µM) reduced the release of TNF-α ( C ) and IL-6 ( D ) from LK-derived PBMCs after S1P (10 nM) addition. We used match-paired LK samples. n = 15 LK (Ctr-S1P) were tested for TNF-α ( C ) and n = 22 LK (Ctr-S1P) were tested for IL-6 ( D ). Data are represented as scatter dot plots indicating the median (confidence interval = 95%). Statistical differences were assessed by means of two-tailed Wilcoxon matched-pairs signed rank test.
    Anti S1pr3 Edg3 Extracellular Antibody, supplied by Elabscience, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/anti s1pr3 edg3 extracellular antibody/product/Elabscience
    Average 90 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    anti s1pr3 edg3 extracellular antibody - by Bioz Stars, 2022-10
    90/100 stars
      Buy from Supplier

    88
    Alomone Labs unconjugated anti s1pr3 antibody
    Local FTY720 release recruits biased progenitors of wound healing macrophages to inflamed tissue. Circulating non-classical <t>S1PR3</t> hi monocytes are recruited by local delivery of FTY720 from a material implanted within an injury site. Upon entrance into inflamed tissue, non-classical monocytes give rise to alternatively activated, wound healing macrophages. Conversely, classical monocytes differentiate into both inflammatory and wound healing macrophages.
    Unconjugated Anti S1pr3 Antibody, supplied by Alomone Labs, used in various techniques. Bioz Stars score: 88/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/unconjugated anti s1pr3 antibody/product/Alomone Labs
    Average 88 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    unconjugated anti s1pr3 antibody - by Bioz Stars, 2022-10
    88/100 stars
      Buy from Supplier

    91
    Alomone Labs anti s1pr3 edg3 extracellular antibody
    Local FTY720 release recruits biased progenitors of wound healing macrophages to inflamed tissue. Circulating non-classical <t>S1PR3</t> hi monocytes are recruited by local delivery of FTY720 from a material implanted within an injury site. Upon entrance into inflamed tissue, non-classical monocytes give rise to alternatively activated, wound healing macrophages. Conversely, classical monocytes differentiate into both inflammatory and wound healing macrophages.
    Anti S1pr3 Edg3 Extracellular Antibody, supplied by Alomone Labs, used in various techniques. Bioz Stars score: 91/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/anti s1pr3 edg3 extracellular antibody/product/Alomone Labs
    Average 91 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    anti s1pr3 edg3 extracellular antibody - by Bioz Stars, 2022-10
    91/100 stars
      Buy from Supplier

    Image Search Results


    S1P-induced pro-inflammatory cytokine release was S1PR3 dependent. ( A ) Western blotting shows that healthy volunteers (H)-derived PBMCs expressed lower levels of S1PR3 compared to lung cancer (LK)-derived PBMCs. GAPDH was used as a loading control. The experiment was repeated three times. M refers to protein molecular weight marker. ( B ) S1PR3 expression analysis was performed by means of ImageJ software (NIH, USA) and expressed as a ratio between S1PR3 and GAPDH (loading control). S1PR3 inhibition with TY52156 (αS1PR3, 10 µM) reduced the release of TNF-α ( C ) and IL-6 ( D ) from LK-derived PBMCs after S1P (10 nM) addition. We used match-paired LK samples. n = 15 LK (Ctr-S1P) were tested for TNF-α ( C ) and n = 22 LK (Ctr-S1P) were tested for IL-6 ( D ). Data are represented as scatter dot plots indicating the median (confidence interval = 95%). Statistical differences were assessed by means of two-tailed Wilcoxon matched-pairs signed rank test.

    Journal: Cells

    Article Title: S1P-Induced TNF-α and IL-6 Release from PBMCs Exacerbates Lung Cancer-Associated Inflammation

    doi: 10.3390/cells11162524

    Figure Lengend Snippet: S1P-induced pro-inflammatory cytokine release was S1PR3 dependent. ( A ) Western blotting shows that healthy volunteers (H)-derived PBMCs expressed lower levels of S1PR3 compared to lung cancer (LK)-derived PBMCs. GAPDH was used as a loading control. The experiment was repeated three times. M refers to protein molecular weight marker. ( B ) S1PR3 expression analysis was performed by means of ImageJ software (NIH, USA) and expressed as a ratio between S1PR3 and GAPDH (loading control). S1PR3 inhibition with TY52156 (αS1PR3, 10 µM) reduced the release of TNF-α ( C ) and IL-6 ( D ) from LK-derived PBMCs after S1P (10 nM) addition. We used match-paired LK samples. n = 15 LK (Ctr-S1P) were tested for TNF-α ( C ) and n = 22 LK (Ctr-S1P) were tested for IL-6 ( D ). Data are represented as scatter dot plots indicating the median (confidence interval = 95%). Statistical differences were assessed by means of two-tailed Wilcoxon matched-pairs signed rank test.

    Article Snippet: The expression of S1PR3 (55–70 kDa; diluted 1:500 in a PBS 1× solution containing 5%BSA; #ASR-013; Alomone labs; Jerusalem, Israel) and of ceramidase active form (40 kDa; N-acylsphingosine amidohydrolase 1, ASAH1; diluted 1:750 in a PBS 1× solution containing 2% BSA; #E-AB-10959; Elabscience, Houston, TX, USA) were evaluated in healthy volunteers (H)- and lung cancer (LK)-derived PBMCs.

    Techniques: Western Blot, Derivative Assay, Molecular Weight, Marker, Expressing, Software, Inhibition, Two Tailed Test

    S1P exacerbates the pro-inflammatory milieu by inducing pro-inflammatory cytokine release from lung cancer-derived PBMCs in a S1PR3-dependent manner. The activation of S1PR3 by the exogenous S1P enhances its own production and fosters the release of TNF-α in a SPHK I-dependent manner (black arrows), and of IL-6 via SPHK I/II (red arrows); S1P-induced IL-6, but not TNF-α, release from PBMCs of lung cancer patients is mTOR- and K-Ras-dependent (red arrows).

    Journal: Cells

    Article Title: S1P-Induced TNF-α and IL-6 Release from PBMCs Exacerbates Lung Cancer-Associated Inflammation

    doi: 10.3390/cells11162524

    Figure Lengend Snippet: S1P exacerbates the pro-inflammatory milieu by inducing pro-inflammatory cytokine release from lung cancer-derived PBMCs in a S1PR3-dependent manner. The activation of S1PR3 by the exogenous S1P enhances its own production and fosters the release of TNF-α in a SPHK I-dependent manner (black arrows), and of IL-6 via SPHK I/II (red arrows); S1P-induced IL-6, but not TNF-α, release from PBMCs of lung cancer patients is mTOR- and K-Ras-dependent (red arrows).

    Article Snippet: The expression of S1PR3 (55–70 kDa; diluted 1:500 in a PBS 1× solution containing 5%BSA; #ASR-013; Alomone labs; Jerusalem, Israel) and of ceramidase active form (40 kDa; N-acylsphingosine amidohydrolase 1, ASAH1; diluted 1:750 in a PBS 1× solution containing 2% BSA; #E-AB-10959; Elabscience, Houston, TX, USA) were evaluated in healthy volunteers (H)- and lung cancer (LK)-derived PBMCs.

    Techniques: Derivative Assay, Activation Assay

    Local FTY720 release recruits biased progenitors of wound healing macrophages to inflamed tissue. Circulating non-classical S1PR3 hi monocytes are recruited by local delivery of FTY720 from a material implanted within an injury site. Upon entrance into inflamed tissue, non-classical monocytes give rise to alternatively activated, wound healing macrophages. Conversely, classical monocytes differentiate into both inflammatory and wound healing macrophages.

    Journal: Scientific Reports

    Article Title: Non-classical monocytes are biased progenitors of wound healing macrophages during soft tissue injury

    doi: 10.1038/s41598-017-00477-1

    Figure Lengend Snippet: Local FTY720 release recruits biased progenitors of wound healing macrophages to inflamed tissue. Circulating non-classical S1PR3 hi monocytes are recruited by local delivery of FTY720 from a material implanted within an injury site. Upon entrance into inflamed tissue, non-classical monocytes give rise to alternatively activated, wound healing macrophages. Conversely, classical monocytes differentiate into both inflammatory and wound healing macrophages.

    Article Snippet: S1PR3 flow cytometry was performed by first performing Fc block (Biolegend), followed by staining cells with primary unconjugated anti-S1PR3 antibody (Alomone Labs) and secondary staining with DyLight 650 anti-rabbit IgG (Abcam).

    Techniques:

    On-site delivery of FTY720 recruits blood-derived non-classical monocytes and increases the frequency of alternatively activated macrophages. PLGA films loaded with FTY720 were implanted immediately after DWC surgery. ( a ) Proportion of latex bead-positive (LX+) Ly6C lo monocytes that were derived from blood in tissue 3 days post-injury following labeling of Ly6C lo monocytes. ( b ) Overall frequency of CD206+ F4/80+CD11b+ macrophages in the presence of FTY720. ( c ) LX+ cells in tissue surrounding unloaded or FTY720-loaded PLGA implants. ( d ) Proportion of LX+ Ly6C hi monocytes that were derived from blood following labeling of Ly6C hi monocytes with Clod Lip. ( e ) Overall frequency of CD206+ F4/80+CD11b+ macrophages in the presence of FTY720 after Clod Lip administration. ( f ) LX+ cells in tissue surrounding unloaded or FTY720-loaded PLGA implants. ( g ) Ly6C expression in CX3CR1 hi monocytes and CX3CR1 lo monocytes obtained from the blood of CX3CR1 GFP/+ mice identify Ly6C lo monocytes and Ly6C hi monocytes, respectively. ( h,i ) Surface S1PR3 expression in blood CX3CR1 hi cells and CX3CR1 lo cells. To control for background staining, CX3CR1 GFP/+ cells were stained with secondary antibody (2° Ab) only, which is shown in the gray histogram. Scale bars, 500 µm. Data presented as mean ± S.E.M. Statistical analyses were performed using two-tailed t-tests. *p

    Journal: Scientific Reports

    Article Title: Non-classical monocytes are biased progenitors of wound healing macrophages during soft tissue injury

    doi: 10.1038/s41598-017-00477-1

    Figure Lengend Snippet: On-site delivery of FTY720 recruits blood-derived non-classical monocytes and increases the frequency of alternatively activated macrophages. PLGA films loaded with FTY720 were implanted immediately after DWC surgery. ( a ) Proportion of latex bead-positive (LX+) Ly6C lo monocytes that were derived from blood in tissue 3 days post-injury following labeling of Ly6C lo monocytes. ( b ) Overall frequency of CD206+ F4/80+CD11b+ macrophages in the presence of FTY720. ( c ) LX+ cells in tissue surrounding unloaded or FTY720-loaded PLGA implants. ( d ) Proportion of LX+ Ly6C hi monocytes that were derived from blood following labeling of Ly6C hi monocytes with Clod Lip. ( e ) Overall frequency of CD206+ F4/80+CD11b+ macrophages in the presence of FTY720 after Clod Lip administration. ( f ) LX+ cells in tissue surrounding unloaded or FTY720-loaded PLGA implants. ( g ) Ly6C expression in CX3CR1 hi monocytes and CX3CR1 lo monocytes obtained from the blood of CX3CR1 GFP/+ mice identify Ly6C lo monocytes and Ly6C hi monocytes, respectively. ( h,i ) Surface S1PR3 expression in blood CX3CR1 hi cells and CX3CR1 lo cells. To control for background staining, CX3CR1 GFP/+ cells were stained with secondary antibody (2° Ab) only, which is shown in the gray histogram. Scale bars, 500 µm. Data presented as mean ± S.E.M. Statistical analyses were performed using two-tailed t-tests. *p

    Article Snippet: S1PR3 flow cytometry was performed by first performing Fc block (Biolegend), followed by staining cells with primary unconjugated anti-S1PR3 antibody (Alomone Labs) and secondary staining with DyLight 650 anti-rabbit IgG (Abcam).

    Techniques: Derivative Assay, Labeling, Expressing, Mouse Assay, Staining, Two Tailed Test