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mouse anti il 1ri  (R&D Systems)


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    Structured Review

    R&D Systems mouse anti il 1ri
    Mouse Anti Il 1ri, supplied by R&D Systems, used in various techniques. Bioz Stars score: 94/100, based on 35 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/il+1ri/Mouse+IL-1+RI+Antibody/us12414981-314-39-42
    Average 94 stars, based on 35 article reviews
    mouse anti il 1ri - by Bioz Stars, 2026-10
    94/100 stars

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    Negative Control:

    Article Title: Cyclodextrin polysulphates repress IL-1 and promote the accumulation of chondrocyte extracellular matrix.
    Article Snippet: .. Mouse anti-human mAb (subclass: IgG1) against IGFR1, IL-1RI, IL-1RII, IL-1b and the mouse IgG1 negative control were purchased from R&D systems (Abingdon, UK; IGFR1: clone 33255.111; IL-1RI: clone 35730.111; IL-1RII: clone 34141.11; IL-1b: clone 8516.311). .. Mouse anti-human IGF-1, IL-1a and anti-human chondrocyte-specific aggrecan mAbs were purchased from Biosource Europe (Nivelles, Belgium; IGF-1: clone AHG0014; IL-1a: clone 624B3F2; aggrecan: clone 4D11-2A9).

    Incubation:

    Article Title: The role of interleukin-1 in the pathogenesis of human Intervertebral disc degeneration
    Article Snippet: After washing, non-specific binding sites were blocked at room temperature for 45 min, either with 20% w/v rabbit serum (Sigma), for IL-1Ra and IL-1RI, or with 20% w/v donkey serum (Sigma), for IL-1α, IL-1β, and ICE. .. Sections were incubated overnight at 4°C with mouse monoclonal primary antibodies against human IL-1Ra (1:200 dilution, R&D Systems, Abingdon, UK), IL-1RI (1:50 dilution, R&D Systems), and goat polyclonal primary antibodies against human IL-1α (1:300 dilution, Santa Cruz Biotechnology, Santa Cruz, CA, USA), IL-1β (1:300 dilution, SantaCruz), and ICE (1:10 dilution, SantaCruz). .. Negative controls in which mouse or goat IgGs (Dako, Cambridgeshire, UK) replaced the primary antibody (at an equal protein concentration) were used.



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    Figure 2. The relative RNA and protein expression of HMGB1, TLR4, IL-1β, <t>IL-1R</t> in epileptogenic tubers (ETs) and non-epileptogenic tubers (non-ETs) (RNA :n = 17; protein: n = 10), and wild-type and control model mice group (n = 6). Figure A showed the relative RNA level of HMGB-1 (1.40 ± 0.32, t(17) = 5.574, P < 0.0001), TLR4 (P = 0.045), IL-1β (P = 0.005), and IL-1R (P = 0.009) were significantly lower in non-ETs compared to ETs. Figure B showed the protein level of HMGB-1 (t(18) = 2.617, P = 0.017), TLR4 (t(18) = 3.074, P = 0.007), IL-1β (t(18) = 2.140, P = 0.046), and IL-1R (P = 0.043) were significantly lower in non-ETs than ETs. Figure C showed the relative RNA level of HMGB-1 (P = 0.004), TLR4 (t(10) = 4.179, P = 0.002), IL-1β (t(10) = 6.411, P < 0.0001), and IL-1R (P = 0.004) were significantly lower in wild-type control group compared to model control group. Figure D showed the protein level of HMGB-1 (t(10) = 4.461, P = 0.001), TLR4 (t(10) = 6.558, P < 0.0001), IL-1β (t(10) = 3.449, P = 0.006), and IL-1R (t(10) = 6.108, P = 0.0001) were significantly lower in wild-type control group compared to model control group (*: p < 0.05; **: p < 0.01; ***: p < 0.001; ****p < 0.0001).
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    Image Search Results


    Figure 2. The relative RNA and protein expression of HMGB1, TLR4, IL-1β, IL-1R in epileptogenic tubers (ETs) and non-epileptogenic tubers (non-ETs) (RNA :n = 17; protein: n = 10), and wild-type and control model mice group (n = 6). Figure A showed the relative RNA level of HMGB-1 (1.40 ± 0.32, t(17) = 5.574, P < 0.0001), TLR4 (P = 0.045), IL-1β (P = 0.005), and IL-1R (P = 0.009) were significantly lower in non-ETs compared to ETs. Figure B showed the protein level of HMGB-1 (t(18) = 2.617, P = 0.017), TLR4 (t(18) = 3.074, P = 0.007), IL-1β (t(18) = 2.140, P = 0.046), and IL-1R (P = 0.043) were significantly lower in non-ETs than ETs. Figure C showed the relative RNA level of HMGB-1 (P = 0.004), TLR4 (t(10) = 4.179, P = 0.002), IL-1β (t(10) = 6.411, P < 0.0001), and IL-1R (P = 0.004) were significantly lower in wild-type control group compared to model control group. Figure D showed the protein level of HMGB-1 (t(10) = 4.461, P = 0.001), TLR4 (t(10) = 6.558, P < 0.0001), IL-1β (t(10) = 3.449, P = 0.006), and IL-1R (t(10) = 6.108, P = 0.0001) were significantly lower in wild-type control group compared to model control group (*: p < 0.05; **: p < 0.01; ***: p < 0.001; ****p < 0.0001).

    Journal: Science progress

    Article Title: HMGB1 mediates inflammation response of epileptogenicity in tuberous sclerosis complex-related epilepsy.

    doi: 10.1177/00368504251338653

    Figure Lengend Snippet: Figure 2. The relative RNA and protein expression of HMGB1, TLR4, IL-1β, IL-1R in epileptogenic tubers (ETs) and non-epileptogenic tubers (non-ETs) (RNA :n = 17; protein: n = 10), and wild-type and control model mice group (n = 6). Figure A showed the relative RNA level of HMGB-1 (1.40 ± 0.32, t(17) = 5.574, P < 0.0001), TLR4 (P = 0.045), IL-1β (P = 0.005), and IL-1R (P = 0.009) were significantly lower in non-ETs compared to ETs. Figure B showed the protein level of HMGB-1 (t(18) = 2.617, P = 0.017), TLR4 (t(18) = 3.074, P = 0.007), IL-1β (t(18) = 2.140, P = 0.046), and IL-1R (P = 0.043) were significantly lower in non-ETs than ETs. Figure C showed the relative RNA level of HMGB-1 (P = 0.004), TLR4 (t(10) = 4.179, P = 0.002), IL-1β (t(10) = 6.411, P < 0.0001), and IL-1R (P = 0.004) were significantly lower in wild-type control group compared to model control group. Figure D showed the protein level of HMGB-1 (t(10) = 4.461, P = 0.001), TLR4 (t(10) = 6.558, P < 0.0001), IL-1β (t(10) = 3.449, P = 0.006), and IL-1R (t(10) = 6.108, P = 0.0001) were significantly lower in wild-type control group compared to model control group (*: p < 0.05; **: p < 0.01; ***: p < 0.001; ****p < 0.0001).

    Article Snippet: The primary antibodies HMGB1 (1:250; Abcam; cat. no. ab79823), TLR4 (1:100; Abcam; cat. no. ab22048), IL-1β (1:50; Abcam; cat. no. ab315084), and IL-1R (1:50; Santa Cruz Biotechnology; cat. no. sc-66054) were incubated overnight at 4°C.

    Techniques: Expressing, Control

    Figure 3. Immunofluorescence of HMGB1,TLR4, lL-1β and IL-1R in ETs and non-ETs. Positive expression of HMGB1 is green, and positive expression of TLR4 is red on the image of immunofluorescence in ETs and non-ETs (Figure 3A, magnifications: × 4 and ×40). The percentages of positive cells (positive area) (n = 9) of HMGB1 (t(16) = 2.770, P = 0.014) and TLR4 (t(16) = 4.884, P = 0.0002)were larger in ETs than them in non-ETs (Figure 3B) and, the fluorescence intensity (n = 15) of either HMGB1 (t(28) = 2.285, P = 0.030) or TLR4 (t(28) = 2.857, P = 0.008) was higher in ETs than them in non-ETs (Figure 3C). Positive expression of IL-1β is green, and positive expression of IL-1R is red on the image of immunofluorescence in ETs and non-ETs (Figure 3D, magnifications: × 4 and ×40). The positive area (n = 9) of IL-1R (P = 0.031) was larger in ETs than non-ETs (Figure 3E), and the fluorescence intensity (n = 15) of either IL-1β (t(28) = 5.055, P < 0.0001) or IL-1R (t(28) = 2.111, P = 0.043) were higher in ETs non-ETs (Figure 3F).

    Journal: Science progress

    Article Title: HMGB1 mediates inflammation response of epileptogenicity in tuberous sclerosis complex-related epilepsy.

    doi: 10.1177/00368504251338653

    Figure Lengend Snippet: Figure 3. Immunofluorescence of HMGB1,TLR4, lL-1β and IL-1R in ETs and non-ETs. Positive expression of HMGB1 is green, and positive expression of TLR4 is red on the image of immunofluorescence in ETs and non-ETs (Figure 3A, magnifications: × 4 and ×40). The percentages of positive cells (positive area) (n = 9) of HMGB1 (t(16) = 2.770, P = 0.014) and TLR4 (t(16) = 4.884, P = 0.0002)were larger in ETs than them in non-ETs (Figure 3B) and, the fluorescence intensity (n = 15) of either HMGB1 (t(28) = 2.285, P = 0.030) or TLR4 (t(28) = 2.857, P = 0.008) was higher in ETs than them in non-ETs (Figure 3C). Positive expression of IL-1β is green, and positive expression of IL-1R is red on the image of immunofluorescence in ETs and non-ETs (Figure 3D, magnifications: × 4 and ×40). The positive area (n = 9) of IL-1R (P = 0.031) was larger in ETs than non-ETs (Figure 3E), and the fluorescence intensity (n = 15) of either IL-1β (t(28) = 5.055, P < 0.0001) or IL-1R (t(28) = 2.111, P = 0.043) were higher in ETs non-ETs (Figure 3F).

    Article Snippet: The primary antibodies HMGB1 (1:250; Abcam; cat. no. ab79823), TLR4 (1:100; Abcam; cat. no. ab22048), IL-1β (1:50; Abcam; cat. no. ab315084), and IL-1R (1:50; Santa Cruz Biotechnology; cat. no. sc-66054) were incubated overnight at 4°C.

    Techniques: Expressing

    Figure 4. The expression pattern of relative RNA and protein of HMGB1, TLR4, IL-1β, IL-1R, and the frequency of abnormal discharge and seizure attacks in mouse model. (red line: P50; blue line: P57). Figure (5A-5D) shows the relative RNA content of HMGB-1, TLR4, IL-1β and IL-1R in wild-type control group, model control group, HMGB1 prevention group, IL-1β prevention group, HMGB1 intervention group, and IL-1β intervention group. The relative RNA content of IL-1β in HMGB1-intervention group was lower compared to model control group (t(10)=2.645, P =0.025) and higher than wild-type group. Figure (5E-5H) showed the protein levels of HMGB-1, TLR4, IL-1β and IL-1R in wild-type control group, model control group, HMGB1 prevention group, IL-1β prevention group, HMGB1 intervention group, and IL-1β intervention group. The protein content of HMGB1 (t(10) =4.461, P=0.001), TLR4 (t(10) = 6.558, P<0.0001), IL-1β (t(10)=3.449, P<0.006), and IL-1R (t(10) =6.108, P=0.001) in wild-type control group was significantly lower than model control group. Figure (5I-5J): The frequency of seizure attacks at P50 in the HMGB1- prevention (P =0.007) and -intervention (P=0.027) groups was significantly decreased compared with the model control group. The frequency of seizure attacks at P50 in the IL-1β- prevention (P=0.009) and -intervention (P=0.046) groups were significantly decreased compared with the model control group. The frequency of abnormal discharge on EEG at P50 in the HMGB1- prevention (P=0.007) and -intervention (P =0.023) groups were significantly decreased compared with the model control group. The frequency of abnormal discharge on EEG at P50 in the IL-1β- prevention (P=0.002) and -intervention (P=0.011) groups were significantly decreased compared with the model control group. The frequency of abnormal discharge on EEG (P< 0.0001) and seizure attacks (P=0.0004) at P50 in the wild-type control group were significantly decreased compared with the model control group. The frequency of abnormal discharge on EEG (P =0.018) and seizure attacks (P=0.021) at P57 in the wild-type control group were significantly decreased compared with the model control group (*: p<0.05; **: p<0.01; ***: p<0.001; ****p< 0.0001).

    Journal: Science progress

    Article Title: HMGB1 mediates inflammation response of epileptogenicity in tuberous sclerosis complex-related epilepsy.

    doi: 10.1177/00368504251338653

    Figure Lengend Snippet: Figure 4. The expression pattern of relative RNA and protein of HMGB1, TLR4, IL-1β, IL-1R, and the frequency of abnormal discharge and seizure attacks in mouse model. (red line: P50; blue line: P57). Figure (5A-5D) shows the relative RNA content of HMGB-1, TLR4, IL-1β and IL-1R in wild-type control group, model control group, HMGB1 prevention group, IL-1β prevention group, HMGB1 intervention group, and IL-1β intervention group. The relative RNA content of IL-1β in HMGB1-intervention group was lower compared to model control group (t(10)=2.645, P =0.025) and higher than wild-type group. Figure (5E-5H) showed the protein levels of HMGB-1, TLR4, IL-1β and IL-1R in wild-type control group, model control group, HMGB1 prevention group, IL-1β prevention group, HMGB1 intervention group, and IL-1β intervention group. The protein content of HMGB1 (t(10) =4.461, P=0.001), TLR4 (t(10) = 6.558, P<0.0001), IL-1β (t(10)=3.449, P<0.006), and IL-1R (t(10) =6.108, P=0.001) in wild-type control group was significantly lower than model control group. Figure (5I-5J): The frequency of seizure attacks at P50 in the HMGB1- prevention (P =0.007) and -intervention (P=0.027) groups was significantly decreased compared with the model control group. The frequency of seizure attacks at P50 in the IL-1β- prevention (P=0.009) and -intervention (P=0.046) groups were significantly decreased compared with the model control group. The frequency of abnormal discharge on EEG at P50 in the HMGB1- prevention (P=0.007) and -intervention (P =0.023) groups were significantly decreased compared with the model control group. The frequency of abnormal discharge on EEG at P50 in the IL-1β- prevention (P=0.002) and -intervention (P=0.011) groups were significantly decreased compared with the model control group. The frequency of abnormal discharge on EEG (P< 0.0001) and seizure attacks (P=0.0004) at P50 in the wild-type control group were significantly decreased compared with the model control group. The frequency of abnormal discharge on EEG (P =0.018) and seizure attacks (P=0.021) at P57 in the wild-type control group were significantly decreased compared with the model control group (*: p<0.05; **: p<0.01; ***: p<0.001; ****p< 0.0001).

    Article Snippet: The primary antibodies HMGB1 (1:250; Abcam; cat. no. ab79823), TLR4 (1:100; Abcam; cat. no. ab22048), IL-1β (1:50; Abcam; cat. no. ab315084), and IL-1R (1:50; Santa Cruz Biotechnology; cat. no. sc-66054) were incubated overnight at 4°C.

    Techniques: Expressing, Control