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tlr7  (MedChemExpress)


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    Structured Review

    MedChemExpress tlr7
    Tlr7, supplied by MedChemExpress, used in various techniques. Bioz Stars score: 94/100, based on 8 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/tlr7/product/MedChemExpress
    Average 94 stars, based on 8 article reviews
    tlr7 - by Bioz Stars, 2026-03
    94/100 stars

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    Characterization of the sonodynamic and drug release properties of nanostimulants. (a) Zeta potential measurements of SPN NR , SPN N H, and SPN NR H in aqueous solutions. b) Morphology characterization of SPN NR , SPN N H, and SPN NR H using TEM. (c) DLS size of SPN NR , SPN N H, and SPN NR H. (d) Absorbance spectra of SPN NR , SPN N H, and SPN NR H. (e) Fluorescence emission spectra of SPN NR , SPN N H, and SPN NR H. (f) The 1 O 2 generation efficacies of SPN NR , SPN N H, and SPN NR H (n = 3). (g) Release profiles of <t>R848</t> inhibitors from SPN NR H after US irradiation at different time points (n = 3). (h) Release percentages of NLG919 from SPN NR H after US irradiation at various time points (n = 3). Data are expressed as mean ± SD.
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    Characterization of the sonodynamic and drug release properties of nanostimulants. (a) Zeta potential measurements of SPN NR , SPN N H, and SPN NR H in aqueous solutions. b) Morphology characterization of SPN NR , SPN N H, and SPN NR H using TEM. (c) DLS size of SPN NR , SPN N H, and SPN NR H. (d) Absorbance spectra of SPN NR , SPN N H, and SPN NR H. (e) Fluorescence emission spectra of SPN NR , SPN N H, and SPN NR H. (f) The 1 O 2 generation efficacies of SPN NR , SPN N H, and SPN NR H (n = 3). (g) Release profiles of <t>R848</t> inhibitors from SPN NR H after US irradiation at different time points (n = 3). (h) Release percentages of NLG919 from SPN NR H after US irradiation at various time points (n = 3). Data are expressed as mean ± SD.
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    Characterization of the sonodynamic and drug release properties of nanostimulants. (a) Zeta potential measurements of SPN NR , SPN N H, and SPN NR H in aqueous solutions. b) Morphology characterization of SPN NR , SPN N H, and SPN NR H using TEM. (c) DLS size of SPN NR , SPN N H, and SPN NR H. (d) Absorbance spectra of SPN NR , SPN N H, and SPN NR H. (e) Fluorescence emission spectra of SPN NR , SPN N H, and SPN NR H. (f) The 1 O 2 generation efficacies of SPN NR , SPN N H, and SPN NR H (n = 3). (g) Release profiles of <t>R848</t> inhibitors from SPN NR H after US irradiation at different time points (n = 3). (h) Release percentages of NLG919 from SPN NR H after US irradiation at various time points (n = 3). Data are expressed as mean ± SD.
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    Characterization of the sonodynamic and drug release properties of nanostimulants. (a) Zeta potential measurements of SPN NR , SPN N H, and SPN NR H in aqueous solutions. b) Morphology characterization of SPN NR , SPN N H, and SPN NR H using TEM. (c) DLS size of SPN NR , SPN N H, and SPN NR H. (d) Absorbance spectra of SPN NR , SPN N H, and SPN NR H. (e) Fluorescence emission spectra of SPN NR , SPN N H, and SPN NR H. (f) The 1 O 2 generation efficacies of SPN NR , SPN N H, and SPN NR H (n = 3). (g) Release profiles of <t>R848</t> inhibitors from SPN NR H after US irradiation at different time points (n = 3). (h) Release percentages of NLG919 from SPN NR H after US irradiation at various time points (n = 3). Data are expressed as mean ± SD.
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    Characterization of the sonodynamic and drug release properties of nanostimulants. (a) Zeta potential measurements of SPN NR , SPN N H, and SPN NR H in aqueous solutions. b) Morphology characterization of SPN NR , SPN N H, and SPN NR H using TEM. (c) DLS size of SPN NR , SPN N H, and SPN NR H. (d) Absorbance spectra of SPN NR , SPN N H, and SPN NR H. (e) Fluorescence emission spectra of SPN NR , SPN N H, and SPN NR H. (f) The 1 O 2 generation efficacies of SPN NR , SPN N H, and SPN NR H (n = 3). (g) Release profiles of <t>R848</t> inhibitors from SPN NR H after US irradiation at different time points (n = 3). (h) Release percentages of NLG919 from SPN NR H after US irradiation at various time points (n = 3). Data are expressed as mean ± SD.
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    Infection with RABV strains exhibiting varying levels of virulence activating <t>TLR7</t> in mouse brain tissue: ( A ) illustrative representations of IHC analysis of TLR7 in sections of mouse brains infected with the RABV strains SC16, HN10 and CVS-11; ( B ) integrated optical density of TLR7 in mouse brain tissue. Statistical evaluations were conducted utilizing ANOVA (* p < 0.05, ** p < 0.01).
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    Infection with RABV strains exhibiting varying levels of virulence activating <t>TLR7</t> in mouse brain tissue: ( A ) illustrative representations of IHC analysis of TLR7 in sections of mouse brains infected with the RABV strains SC16, HN10 and CVS-11; ( B ) integrated optical density of TLR7 in mouse brain tissue. Statistical evaluations were conducted utilizing ANOVA (* p < 0.05, ** p < 0.01).
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    Characterization of the sonodynamic and drug release properties of nanostimulants. (a) Zeta potential measurements of SPN NR , SPN N H, and SPN NR H in aqueous solutions. b) Morphology characterization of SPN NR , SPN N H, and SPN NR H using TEM. (c) DLS size of SPN NR , SPN N H, and SPN NR H. (d) Absorbance spectra of SPN NR , SPN N H, and SPN NR H. (e) Fluorescence emission spectra of SPN NR , SPN N H, and SPN NR H. (f) The 1 O 2 generation efficacies of SPN NR , SPN N H, and SPN NR H (n = 3). (g) Release profiles of R848 inhibitors from SPN NR H after US irradiation at different time points (n = 3). (h) Release percentages of NLG919 from SPN NR H after US irradiation at various time points (n = 3). Data are expressed as mean ± SD.

    Journal: Materials Today Bio

    Article Title: Extracellular matrix-degradable polymer nanostimulants elicit potent immune responses in orthotopic pancreatic cancer via sono-activatable dual-drug synergism

    doi: 10.1016/j.mtbio.2025.101954

    Figure Lengend Snippet: Characterization of the sonodynamic and drug release properties of nanostimulants. (a) Zeta potential measurements of SPN NR , SPN N H, and SPN NR H in aqueous solutions. b) Morphology characterization of SPN NR , SPN N H, and SPN NR H using TEM. (c) DLS size of SPN NR , SPN N H, and SPN NR H. (d) Absorbance spectra of SPN NR , SPN N H, and SPN NR H. (e) Fluorescence emission spectra of SPN NR , SPN N H, and SPN NR H. (f) The 1 O 2 generation efficacies of SPN NR , SPN N H, and SPN NR H (n = 3). (g) Release profiles of R848 inhibitors from SPN NR H after US irradiation at different time points (n = 3). (h) Release percentages of NLG919 from SPN NR H after US irradiation at various time points (n = 3). Data are expressed as mean ± SD.

    Article Snippet: The TLR7/8 agonist R848 and IDO inhibitor NLG919 was procured from MedChemExpress (USA).

    Techniques: Zeta Potential Analyzer, Fluorescence, Irradiation

    Infection with RABV strains exhibiting varying levels of virulence activating TLR7 in mouse brain tissue: ( A ) illustrative representations of IHC analysis of TLR7 in sections of mouse brains infected with the RABV strains SC16, HN10 and CVS-11; ( B ) integrated optical density of TLR7 in mouse brain tissue. Statistical evaluations were conducted utilizing ANOVA (* p < 0.05, ** p < 0.01).

    Journal: International Journal of Molecular Sciences

    Article Title: Rabies Virus Regulates Inflammatory Response in BV-2 Cells through Activation of Myd88 and NF-κB Signaling Pathways via TLR7

    doi: 10.3390/ijms25179144

    Figure Lengend Snippet: Infection with RABV strains exhibiting varying levels of virulence activating TLR7 in mouse brain tissue: ( A ) illustrative representations of IHC analysis of TLR7 in sections of mouse brains infected with the RABV strains SC16, HN10 and CVS-11; ( B ) integrated optical density of TLR7 in mouse brain tissue. Statistical evaluations were conducted utilizing ANOVA (* p < 0.05, ** p < 0.01).

    Article Snippet: The TLR7 inhibitor (HY-124603, MCE, Princeton, NJ, USA), agonist (HY-117602, MCE, USA) and Myd88 inhibitor (HY-50937) were purchased from Med-Chem-Express.

    Techniques: Infection

    RABV inducing proinflammatory chemokines in vitro via TLR7. ( A ) N2a and BV-2 cells exposed to CVS-11, and subsequent Western blot analysis conducted to assess the expression of TLR7. ( B ) Quantitative assessment of the comparative signal intensities of TLR7. ( C ) Different RABV strains at an MOI of 0.1, 0.5, 1 and 10 of infected BV-2 cells. Cell culture supernatants were collected and the expression of CCL2 was measured. ( D ) The expression of CXCL10 of BV-2 cells infected with RABV at an MOI of 0.1, 0.5, 1 and 10. ( E ) The expression of IL-6 of BV-2 cells infected with RABV at an MOI of 0.1, 0.5, 1 and 10. ( F ) BV-2 cells incubated with or without the TLR7 inhibitor (HY-124603) before stimulation with CVS-11. The expression of CCL2 in the supernatant was measured via ELISA. ( G ) The expression of CXCL10 in the supernatant incubated with the TLR7 inhibitor (HY-124603) before stimulation with CVS-11. ( H ) The expression of IL-6 in the supernatant incubated with the TLR7 inhibitor (HY-124603) before stimulation with CVS-11. Statistical evaluations were conducted utilizing ANOVA (** p < 0.01).

    Journal: International Journal of Molecular Sciences

    Article Title: Rabies Virus Regulates Inflammatory Response in BV-2 Cells through Activation of Myd88 and NF-κB Signaling Pathways via TLR7

    doi: 10.3390/ijms25179144

    Figure Lengend Snippet: RABV inducing proinflammatory chemokines in vitro via TLR7. ( A ) N2a and BV-2 cells exposed to CVS-11, and subsequent Western blot analysis conducted to assess the expression of TLR7. ( B ) Quantitative assessment of the comparative signal intensities of TLR7. ( C ) Different RABV strains at an MOI of 0.1, 0.5, 1 and 10 of infected BV-2 cells. Cell culture supernatants were collected and the expression of CCL2 was measured. ( D ) The expression of CXCL10 of BV-2 cells infected with RABV at an MOI of 0.1, 0.5, 1 and 10. ( E ) The expression of IL-6 of BV-2 cells infected with RABV at an MOI of 0.1, 0.5, 1 and 10. ( F ) BV-2 cells incubated with or without the TLR7 inhibitor (HY-124603) before stimulation with CVS-11. The expression of CCL2 in the supernatant was measured via ELISA. ( G ) The expression of CXCL10 in the supernatant incubated with the TLR7 inhibitor (HY-124603) before stimulation with CVS-11. ( H ) The expression of IL-6 in the supernatant incubated with the TLR7 inhibitor (HY-124603) before stimulation with CVS-11. Statistical evaluations were conducted utilizing ANOVA (** p < 0.01).

    Article Snippet: The TLR7 inhibitor (HY-124603, MCE, Princeton, NJ, USA), agonist (HY-117602, MCE, USA) and Myd88 inhibitor (HY-50937) were purchased from Med-Chem-Express.

    Techniques: In Vitro, Western Blot, Expressing, Infection, Cell Culture, Incubation, Enzyme-linked Immunosorbent Assay

    RABV inducing the activation of the Myd88 pathway through TLR7. ( A ) The expression levels of TLR7, MyD88, IRAK4 and TRAF6 assessed via Western blotting. ( B ) BV-2 cells pre-treated for 2 h with the inhibitor (HY-124603) and agonist (HY-117602) of TLR7 before stimulation with CVS-11 for 6 h. TRL7, Myd88, IRAK4 and TRAF6 were analyzed via Western blotting. ( C ) Quantitative assessment of the relative expression levels of TLR7, Myd88, IRAK4 and TRAF6, normalized against β-actin. ( D ) Quantitative assessment of the relative expression levels of TLR7, Myd88, IRAK4 and TRAF6 following normalization against β-actin, in response to treatment with TLR7 inhibitors (HY-124603) and agonists (HY-117602). ( E ) The expression levels of viral P gene mRNA, quantified using qRT-PCR following treatment with the TLR7 inhibitor (HY-124603) and agonist (HY-117602). ( F ) BV-2 cells pre-treated for 2 h with the TLR7 inhibitor (HY-124603) and for 30 min with the Myd88 inhibitor (HY-50937). The supernatants were collected, and the concentration of CCL2 was quantified at 24 h. ( G ) The expression of CXCL10 was measured at 24 h. ( H ) The expression of IL-6 was measured at 24 h. Statistical evaluations were conducted utilizing ANOVA (* p < 0.05, ** p < 0.01).

    Journal: International Journal of Molecular Sciences

    Article Title: Rabies Virus Regulates Inflammatory Response in BV-2 Cells through Activation of Myd88 and NF-κB Signaling Pathways via TLR7

    doi: 10.3390/ijms25179144

    Figure Lengend Snippet: RABV inducing the activation of the Myd88 pathway through TLR7. ( A ) The expression levels of TLR7, MyD88, IRAK4 and TRAF6 assessed via Western blotting. ( B ) BV-2 cells pre-treated for 2 h with the inhibitor (HY-124603) and agonist (HY-117602) of TLR7 before stimulation with CVS-11 for 6 h. TRL7, Myd88, IRAK4 and TRAF6 were analyzed via Western blotting. ( C ) Quantitative assessment of the relative expression levels of TLR7, Myd88, IRAK4 and TRAF6, normalized against β-actin. ( D ) Quantitative assessment of the relative expression levels of TLR7, Myd88, IRAK4 and TRAF6 following normalization against β-actin, in response to treatment with TLR7 inhibitors (HY-124603) and agonists (HY-117602). ( E ) The expression levels of viral P gene mRNA, quantified using qRT-PCR following treatment with the TLR7 inhibitor (HY-124603) and agonist (HY-117602). ( F ) BV-2 cells pre-treated for 2 h with the TLR7 inhibitor (HY-124603) and for 30 min with the Myd88 inhibitor (HY-50937). The supernatants were collected, and the concentration of CCL2 was quantified at 24 h. ( G ) The expression of CXCL10 was measured at 24 h. ( H ) The expression of IL-6 was measured at 24 h. Statistical evaluations were conducted utilizing ANOVA (* p < 0.05, ** p < 0.01).

    Article Snippet: The TLR7 inhibitor (HY-124603, MCE, Princeton, NJ, USA), agonist (HY-117602, MCE, USA) and Myd88 inhibitor (HY-50937) were purchased from Med-Chem-Express.

    Techniques: Activation Assay, Expressing, Western Blot, Quantitative RT-PCR, Concentration Assay

    RABV inducing the phosphorylation and nuclear translocation of NF-κB. ( A ) BV-2 cells pre-treated for 2 h with the inhibitor (HY-124603) and agonist (HY-117602) of TLR7 before stimulation with CVS-11 for 30 min. NF-κB p-p65, NF-κB p65 and IκBα analyzed via Western blotting. ( B ) Analysis of the nuclear translocation of NF-κB in BV-2 cells incubated with or without the TLR7 inhibitor (HY-124603) with RABV infection for 30 min, carried out using Image Stream. ( C ) BV-2 cells under 2 h pre-treatment with the TLR7 inhibitor (HY-124603) and 1 h exposure to the NF-κB inhibitor (BAY11-7082). Afterward, the supernatants were collected, and CCL2 levels were quantified at 24 h. ( D ) The expression of CXCL10, measured at 24 h. ( E ) The expression of IL-6, measured at 24 h. Statistical evaluations were conducted utilizing ANOVA (** p < 0.01).

    Journal: International Journal of Molecular Sciences

    Article Title: Rabies Virus Regulates Inflammatory Response in BV-2 Cells through Activation of Myd88 and NF-κB Signaling Pathways via TLR7

    doi: 10.3390/ijms25179144

    Figure Lengend Snippet: RABV inducing the phosphorylation and nuclear translocation of NF-κB. ( A ) BV-2 cells pre-treated for 2 h with the inhibitor (HY-124603) and agonist (HY-117602) of TLR7 before stimulation with CVS-11 for 30 min. NF-κB p-p65, NF-κB p65 and IκBα analyzed via Western blotting. ( B ) Analysis of the nuclear translocation of NF-κB in BV-2 cells incubated with or without the TLR7 inhibitor (HY-124603) with RABV infection for 30 min, carried out using Image Stream. ( C ) BV-2 cells under 2 h pre-treatment with the TLR7 inhibitor (HY-124603) and 1 h exposure to the NF-κB inhibitor (BAY11-7082). Afterward, the supernatants were collected, and CCL2 levels were quantified at 24 h. ( D ) The expression of CXCL10, measured at 24 h. ( E ) The expression of IL-6, measured at 24 h. Statistical evaluations were conducted utilizing ANOVA (** p < 0.01).

    Article Snippet: The TLR7 inhibitor (HY-124603, MCE, Princeton, NJ, USA), agonist (HY-117602, MCE, USA) and Myd88 inhibitor (HY-50937) were purchased from Med-Chem-Express.

    Techniques: Translocation Assay, Western Blot, Incubation, Infection, Expressing