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rabbit polyclonal abs against tlr2  (Santa Cruz Biotechnology)


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    Structured Review

    Santa Cruz Biotechnology rabbit polyclonal abs against tlr2
    PA14 CRISPR-Cas regulates innate immunity through TLR4/NF-κB signaling. (A) MH-S cells were infected with PA14 WT and ΔTCR mutant at an MOI of 20:1 for 2 h. qPCR primer assay of immune response-related factors in ΔTCR mutant-infected MH-S cells versus PA14 WT-infected controls. Red dots indicate increased genes and green dots indicate decreased genes (over 10-fold change and P ≤ 0.05, n = 2 biological replicates). (B) Expression of <t>TLR2,</t> TLR4 and indicated signaling factors in PA14 WT-, ΔTCR mutant- and complemented strain-infected MH-S cells (30 min). (C) MH-S cells were infected with PA14 WT, ΔTCR mutant and complemented strain at an MOI of 20:1 for 0, 15, 30 and 60 min. CSLM results show the translocation of p-NF-κB (p-p65) in MH-S cells using immune staining. DAPI was used for staining the nucleus (arrows showing the nuclear translocation). (D) CSLM results show the production of TLR4 in MH-S cells. (E) TLR4 expression was determined in C57BL/6J WT and TLR4 KO mice by immunoblotting. (F) Secretion of TNF-α, IL-1β and IL-6 in BALF from C57BL/6J WT and TLR4 KO mice after WT PA14, ΔTCR mutant and complemented strain infection. (G) Phagocytosis of indicated MH-S cells was measured by CFU count assay. MH-S cells were infected with an MOI of 20:1, 25:1, 30:1, 35:1 and 40:1 PA14 WT. The MOI of 20:1 ΔTCR mutant infection was a control. (H) Expression of TLR4 and production of TNF-α, IL-1β and IL-6 in PA14 WT-infected and ΔTCR mutant-infected MH-S cells were detected by immunoblotting. Data are representative of three experiments expressed as means SEM (n = 3, one-way ANOVA with Tukey's post hoc; *P ≤ 0.05; **P ≤ 0.005).
    Rabbit Polyclonal Abs Against Tlr2, supplied by Santa Cruz Biotechnology, used in various techniques. Bioz Stars score: 96/100, based on 4689 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    1) Product Images from "Type I CRISPR-Cas targets endogenous genes and regulates virulence to evade mammalian host immunity"

    Article Title: Type I CRISPR-Cas targets endogenous genes and regulates virulence to evade mammalian host immunity

    Journal: Cell Research

    doi: 10.1038/cr.2016.135

    PA14 CRISPR-Cas regulates innate immunity through TLR4/NF-κB signaling. (A) MH-S cells were infected with PA14 WT and ΔTCR mutant at an MOI of 20:1 for 2 h. qPCR primer assay of immune response-related factors in ΔTCR mutant-infected MH-S cells versus PA14 WT-infected controls. Red dots indicate increased genes and green dots indicate decreased genes (over 10-fold change and P ≤ 0.05, n = 2 biological replicates). (B) Expression of TLR2, TLR4 and indicated signaling factors in PA14 WT-, ΔTCR mutant- and complemented strain-infected MH-S cells (30 min). (C) MH-S cells were infected with PA14 WT, ΔTCR mutant and complemented strain at an MOI of 20:1 for 0, 15, 30 and 60 min. CSLM results show the translocation of p-NF-κB (p-p65) in MH-S cells using immune staining. DAPI was used for staining the nucleus (arrows showing the nuclear translocation). (D) CSLM results show the production of TLR4 in MH-S cells. (E) TLR4 expression was determined in C57BL/6J WT and TLR4 KO mice by immunoblotting. (F) Secretion of TNF-α, IL-1β and IL-6 in BALF from C57BL/6J WT and TLR4 KO mice after WT PA14, ΔTCR mutant and complemented strain infection. (G) Phagocytosis of indicated MH-S cells was measured by CFU count assay. MH-S cells were infected with an MOI of 20:1, 25:1, 30:1, 35:1 and 40:1 PA14 WT. The MOI of 20:1 ΔTCR mutant infection was a control. (H) Expression of TLR4 and production of TNF-α, IL-1β and IL-6 in PA14 WT-infected and ΔTCR mutant-infected MH-S cells were detected by immunoblotting. Data are representative of three experiments expressed as means SEM (n = 3, one-way ANOVA with Tukey's post hoc; *P ≤ 0.05; **P ≤ 0.005).
    Figure Legend Snippet: PA14 CRISPR-Cas regulates innate immunity through TLR4/NF-κB signaling. (A) MH-S cells were infected with PA14 WT and ΔTCR mutant at an MOI of 20:1 for 2 h. qPCR primer assay of immune response-related factors in ΔTCR mutant-infected MH-S cells versus PA14 WT-infected controls. Red dots indicate increased genes and green dots indicate decreased genes (over 10-fold change and P ≤ 0.05, n = 2 biological replicates). (B) Expression of TLR2, TLR4 and indicated signaling factors in PA14 WT-, ΔTCR mutant- and complemented strain-infected MH-S cells (30 min). (C) MH-S cells were infected with PA14 WT, ΔTCR mutant and complemented strain at an MOI of 20:1 for 0, 15, 30 and 60 min. CSLM results show the translocation of p-NF-κB (p-p65) in MH-S cells using immune staining. DAPI was used for staining the nucleus (arrows showing the nuclear translocation). (D) CSLM results show the production of TLR4 in MH-S cells. (E) TLR4 expression was determined in C57BL/6J WT and TLR4 KO mice by immunoblotting. (F) Secretion of TNF-α, IL-1β and IL-6 in BALF from C57BL/6J WT and TLR4 KO mice after WT PA14, ΔTCR mutant and complemented strain infection. (G) Phagocytosis of indicated MH-S cells was measured by CFU count assay. MH-S cells were infected with an MOI of 20:1, 25:1, 30:1, 35:1 and 40:1 PA14 WT. The MOI of 20:1 ΔTCR mutant infection was a control. (H) Expression of TLR4 and production of TNF-α, IL-1β and IL-6 in PA14 WT-infected and ΔTCR mutant-infected MH-S cells were detected by immunoblotting. Data are representative of three experiments expressed as means SEM (n = 3, one-way ANOVA with Tukey's post hoc; *P ≤ 0.05; **P ≤ 0.005).

    Techniques Used: CRISPR, Infection, Mutagenesis, Expressing, Translocation Assay, Staining, Western Blot, Control



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    Santa Cruz Biotechnology rabbit polyclonal abs against tlr2
    PA14 CRISPR-Cas regulates innate immunity through TLR4/NF-κB signaling. (A) MH-S cells were infected with PA14 WT and ΔTCR mutant at an MOI of 20:1 for 2 h. qPCR primer assay of immune response-related factors in ΔTCR mutant-infected MH-S cells versus PA14 WT-infected controls. Red dots indicate increased genes and green dots indicate decreased genes (over 10-fold change and P ≤ 0.05, n = 2 biological replicates). (B) Expression of <t>TLR2,</t> TLR4 and indicated signaling factors in PA14 WT-, ΔTCR mutant- and complemented strain-infected MH-S cells (30 min). (C) MH-S cells were infected with PA14 WT, ΔTCR mutant and complemented strain at an MOI of 20:1 for 0, 15, 30 and 60 min. CSLM results show the translocation of p-NF-κB (p-p65) in MH-S cells using immune staining. DAPI was used for staining the nucleus (arrows showing the nuclear translocation). (D) CSLM results show the production of TLR4 in MH-S cells. (E) TLR4 expression was determined in C57BL/6J WT and TLR4 KO mice by immunoblotting. (F) Secretion of TNF-α, IL-1β and IL-6 in BALF from C57BL/6J WT and TLR4 KO mice after WT PA14, ΔTCR mutant and complemented strain infection. (G) Phagocytosis of indicated MH-S cells was measured by CFU count assay. MH-S cells were infected with an MOI of 20:1, 25:1, 30:1, 35:1 and 40:1 PA14 WT. The MOI of 20:1 ΔTCR mutant infection was a control. (H) Expression of TLR4 and production of TNF-α, IL-1β and IL-6 in PA14 WT-infected and ΔTCR mutant-infected MH-S cells were detected by immunoblotting. Data are representative of three experiments expressed as means SEM (n = 3, one-way ANOVA with Tukey's post hoc; *P ≤ 0.05; **P ≤ 0.005).
    Rabbit Polyclonal Abs Against Tlr2, supplied by Santa Cruz Biotechnology, used in various techniques. Bioz Stars score: 96/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Santa Cruz Biotechnology polyclonal rabbit abs against tlr2
    PA14 CRISPR-Cas regulates innate immunity through TLR4/NF-κB signaling. (A) MH-S cells were infected with PA14 WT and ΔTCR mutant at an MOI of 20:1 for 2 h. qPCR primer assay of immune response-related factors in ΔTCR mutant-infected MH-S cells versus PA14 WT-infected controls. Red dots indicate increased genes and green dots indicate decreased genes (over 10-fold change and P ≤ 0.05, n = 2 biological replicates). (B) Expression of <t>TLR2,</t> TLR4 and indicated signaling factors in PA14 WT-, ΔTCR mutant- and complemented strain-infected MH-S cells (30 min). (C) MH-S cells were infected with PA14 WT, ΔTCR mutant and complemented strain at an MOI of 20:1 for 0, 15, 30 and 60 min. CSLM results show the translocation of p-NF-κB (p-p65) in MH-S cells using immune staining. DAPI was used for staining the nucleus (arrows showing the nuclear translocation). (D) CSLM results show the production of TLR4 in MH-S cells. (E) TLR4 expression was determined in C57BL/6J WT and TLR4 KO mice by immunoblotting. (F) Secretion of TNF-α, IL-1β and IL-6 in BALF from C57BL/6J WT and TLR4 KO mice after WT PA14, ΔTCR mutant and complemented strain infection. (G) Phagocytosis of indicated MH-S cells was measured by CFU count assay. MH-S cells were infected with an MOI of 20:1, 25:1, 30:1, 35:1 and 40:1 PA14 WT. The MOI of 20:1 ΔTCR mutant infection was a control. (H) Expression of TLR4 and production of TNF-α, IL-1β and IL-6 in PA14 WT-infected and ΔTCR mutant-infected MH-S cells were detected by immunoblotting. Data are representative of three experiments expressed as means SEM (n = 3, one-way ANOVA with Tukey's post hoc; *P ≤ 0.05; **P ≤ 0.005).
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    PA14 CRISPR-Cas regulates innate immunity through TLR4/NF-κB signaling. (A) MH-S cells were infected with PA14 WT and ΔTCR mutant at an MOI of 20:1 for 2 h. qPCR primer assay of immune response-related factors in ΔTCR mutant-infected MH-S cells versus PA14 WT-infected controls. Red dots indicate increased genes and green dots indicate decreased genes (over 10-fold change and P ≤ 0.05, n = 2 biological replicates). (B) Expression of <t>TLR2,</t> TLR4 and indicated signaling factors in PA14 WT-, ΔTCR mutant- and complemented strain-infected MH-S cells (30 min). (C) MH-S cells were infected with PA14 WT, ΔTCR mutant and complemented strain at an MOI of 20:1 for 0, 15, 30 and 60 min. CSLM results show the translocation of p-NF-κB (p-p65) in MH-S cells using immune staining. DAPI was used for staining the nucleus (arrows showing the nuclear translocation). (D) CSLM results show the production of TLR4 in MH-S cells. (E) TLR4 expression was determined in C57BL/6J WT and TLR4 KO mice by immunoblotting. (F) Secretion of TNF-α, IL-1β and IL-6 in BALF from C57BL/6J WT and TLR4 KO mice after WT PA14, ΔTCR mutant and complemented strain infection. (G) Phagocytosis of indicated MH-S cells was measured by CFU count assay. MH-S cells were infected with an MOI of 20:1, 25:1, 30:1, 35:1 and 40:1 PA14 WT. The MOI of 20:1 ΔTCR mutant infection was a control. (H) Expression of TLR4 and production of TNF-α, IL-1β and IL-6 in PA14 WT-infected and ΔTCR mutant-infected MH-S cells were detected by immunoblotting. Data are representative of three experiments expressed as means SEM (n = 3, one-way ANOVA with Tukey's post hoc; *P ≤ 0.05; **P ≤ 0.005).
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    PA14 CRISPR-Cas regulates innate immunity through TLR4/NF-κB signaling. (A) MH-S cells were infected with PA14 WT and ΔTCR mutant at an MOI of 20:1 for 2 h. qPCR primer assay of immune response-related factors in ΔTCR mutant-infected MH-S cells versus PA14 WT-infected controls. Red dots indicate increased genes and green dots indicate decreased genes (over 10-fold change and P ≤ 0.05, n = 2 biological replicates). (B) Expression of TLR2, TLR4 and indicated signaling factors in PA14 WT-, ΔTCR mutant- and complemented strain-infected MH-S cells (30 min). (C) MH-S cells were infected with PA14 WT, ΔTCR mutant and complemented strain at an MOI of 20:1 for 0, 15, 30 and 60 min. CSLM results show the translocation of p-NF-κB (p-p65) in MH-S cells using immune staining. DAPI was used for staining the nucleus (arrows showing the nuclear translocation). (D) CSLM results show the production of TLR4 in MH-S cells. (E) TLR4 expression was determined in C57BL/6J WT and TLR4 KO mice by immunoblotting. (F) Secretion of TNF-α, IL-1β and IL-6 in BALF from C57BL/6J WT and TLR4 KO mice after WT PA14, ΔTCR mutant and complemented strain infection. (G) Phagocytosis of indicated MH-S cells was measured by CFU count assay. MH-S cells were infected with an MOI of 20:1, 25:1, 30:1, 35:1 and 40:1 PA14 WT. The MOI of 20:1 ΔTCR mutant infection was a control. (H) Expression of TLR4 and production of TNF-α, IL-1β and IL-6 in PA14 WT-infected and ΔTCR mutant-infected MH-S cells were detected by immunoblotting. Data are representative of three experiments expressed as means SEM (n = 3, one-way ANOVA with Tukey's post hoc; *P ≤ 0.05; **P ≤ 0.005).

    Journal: Cell Research

    Article Title: Type I CRISPR-Cas targets endogenous genes and regulates virulence to evade mammalian host immunity

    doi: 10.1038/cr.2016.135

    Figure Lengend Snippet: PA14 CRISPR-Cas regulates innate immunity through TLR4/NF-κB signaling. (A) MH-S cells were infected with PA14 WT and ΔTCR mutant at an MOI of 20:1 for 2 h. qPCR primer assay of immune response-related factors in ΔTCR mutant-infected MH-S cells versus PA14 WT-infected controls. Red dots indicate increased genes and green dots indicate decreased genes (over 10-fold change and P ≤ 0.05, n = 2 biological replicates). (B) Expression of TLR2, TLR4 and indicated signaling factors in PA14 WT-, ΔTCR mutant- and complemented strain-infected MH-S cells (30 min). (C) MH-S cells were infected with PA14 WT, ΔTCR mutant and complemented strain at an MOI of 20:1 for 0, 15, 30 and 60 min. CSLM results show the translocation of p-NF-κB (p-p65) in MH-S cells using immune staining. DAPI was used for staining the nucleus (arrows showing the nuclear translocation). (D) CSLM results show the production of TLR4 in MH-S cells. (E) TLR4 expression was determined in C57BL/6J WT and TLR4 KO mice by immunoblotting. (F) Secretion of TNF-α, IL-1β and IL-6 in BALF from C57BL/6J WT and TLR4 KO mice after WT PA14, ΔTCR mutant and complemented strain infection. (G) Phagocytosis of indicated MH-S cells was measured by CFU count assay. MH-S cells were infected with an MOI of 20:1, 25:1, 30:1, 35:1 and 40:1 PA14 WT. The MOI of 20:1 ΔTCR mutant infection was a control. (H) Expression of TLR4 and production of TNF-α, IL-1β and IL-6 in PA14 WT-infected and ΔTCR mutant-infected MH-S cells were detected by immunoblotting. Data are representative of three experiments expressed as means SEM (n = 3, one-way ANOVA with Tukey's post hoc; *P ≤ 0.05; **P ≤ 0.005).

    Article Snippet: Mouse monoclonal Abs against β-actin (sc-47778), TLR4 (sc-293072), NF-κB p50 (sc-166588), p-NF-κB p50 (sc-33022), Stat6 (sc-374021), and Jak2 (sc-390539), rabbit polyclonal Abs against TLR2 (sc-10739), and p-Jak2 (sc-21870), goat polyclonal Abs against TNF-α (sc-1349), IL-6 (sc-1265), IL-1β (sc-23460) and p-Stat6 (sc-11762) were obtained from Santa Cruz Biotechnology (Dallas, TX).

    Techniques: CRISPR, Infection, Mutagenesis, Expressing, Translocation Assay, Staining, Western Blot, Control