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rabbit polyclonal anti amigo2 antibody  (Santa Cruz Biotechnology)


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    Structured Review

    Santa Cruz Biotechnology rabbit polyclonal anti amigo2 antibody
    Fig. 3. Suppression of <t>AMIGO2</t> mRNA and protein expression in LV12 cells treated with trametinib, ruxolitinib, and SP600125 and their reduced adhesion to mouse liver sinusoidal endothelial (HSE) cells. (a) LV12 cells were treated with trametinib, ruxolitinib, SP600125, or DMSO for 24 h. The relative AMIGO2 mRNA levels in each drug treatment group, compared with that in DMSO-treated LV12 cells, was determined using qRT-PCR. The bar graphs show mean ± SD from three to five independent experiments (n = 9–15, Student’s t-test). (b) Immunoreactive AMIGO2 expression was quantified as a ratio to β-actin expression using densitometry. Values represent mean ± SD (n = 7, Student’s t-test) from at least six independent experiments with similar results. (c) Typical immunoblotting performed using anti-AMIGO2 is shown in the upper panel, and the lower panel presents immunoblotting using anti-β-actin antibodies. Full-length blots were presented in Supplementary Fig. S5. (d) LV12 cells treated as described in “a” were labeled with PKH67 fluorescent dye and placed on HSE cells. The percentage of adherent cells was determined by measuring the fluorescence intensity. The graph shows mean ± SD (n = 4 in each group, Student’s t-test) from four independent experiments with similar results.
    Rabbit Polyclonal Anti Amigo2 Antibody, supplied by Santa Cruz Biotechnology, used in various techniques. Bioz Stars score: 93/100, based on 18 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/rabbit+polyclonal+anti+amigo2+antibody/AMIGO2+Antibody/pm39548119-218-26-14
    Average 93 stars, based on 18 article reviews
    rabbit polyclonal anti amigo2 antibody - by Bioz Stars, 2026-09
    93/100 stars

    Images

    1) Product Images from "Prevention of liver metastasis via the pharmacological suppression of AMIGO2 expression in tumor cells."

    Article Title: Prevention of liver metastasis via the pharmacological suppression of AMIGO2 expression in tumor cells.

    Journal: Scientific reports

    doi: 10.1038/s41598-024-71827-z

    Fig. 3. Suppression of AMIGO2 mRNA and protein expression in LV12 cells treated with trametinib, ruxolitinib, and SP600125 and their reduced adhesion to mouse liver sinusoidal endothelial (HSE) cells. (a) LV12 cells were treated with trametinib, ruxolitinib, SP600125, or DMSO for 24 h. The relative AMIGO2 mRNA levels in each drug treatment group, compared with that in DMSO-treated LV12 cells, was determined using qRT-PCR. The bar graphs show mean ± SD from three to five independent experiments (n = 9–15, Student’s t-test). (b) Immunoreactive AMIGO2 expression was quantified as a ratio to β-actin expression using densitometry. Values represent mean ± SD (n = 7, Student’s t-test) from at least six independent experiments with similar results. (c) Typical immunoblotting performed using anti-AMIGO2 is shown in the upper panel, and the lower panel presents immunoblotting using anti-β-actin antibodies. Full-length blots were presented in Supplementary Fig. S5. (d) LV12 cells treated as described in “a” were labeled with PKH67 fluorescent dye and placed on HSE cells. The percentage of adherent cells was determined by measuring the fluorescence intensity. The graph shows mean ± SD (n = 4 in each group, Student’s t-test) from four independent experiments with similar results.
    Figure Legend Snippet: Fig. 3. Suppression of AMIGO2 mRNA and protein expression in LV12 cells treated with trametinib, ruxolitinib, and SP600125 and their reduced adhesion to mouse liver sinusoidal endothelial (HSE) cells. (a) LV12 cells were treated with trametinib, ruxolitinib, SP600125, or DMSO for 24 h. The relative AMIGO2 mRNA levels in each drug treatment group, compared with that in DMSO-treated LV12 cells, was determined using qRT-PCR. The bar graphs show mean ± SD from three to five independent experiments (n = 9–15, Student’s t-test). (b) Immunoreactive AMIGO2 expression was quantified as a ratio to β-actin expression using densitometry. Values represent mean ± SD (n = 7, Student’s t-test) from at least six independent experiments with similar results. (c) Typical immunoblotting performed using anti-AMIGO2 is shown in the upper panel, and the lower panel presents immunoblotting using anti-β-actin antibodies. Full-length blots were presented in Supplementary Fig. S5. (d) LV12 cells treated as described in “a” were labeled with PKH67 fluorescent dye and placed on HSE cells. The percentage of adherent cells was determined by measuring the fluorescence intensity. The graph shows mean ± SD (n = 4 in each group, Student’s t-test) from four independent experiments with similar results.

    Techniques Used: Expressing, Quantitative RT-PCR, Western Blot, Labeling, Fluorescence

    Related Articles

    Incubation:

    Article Title: Prevention of liver metastasis via the pharmacological suppression of AMIGO2 expression in tumor cells
    Article Snippet: Twenty to forty micrograms of protein was subjected to 10% SDS-PAGE under reducing conditions and then blotted onto a polyvinylidene fluoride membrane (ISEQ00010; Merck Millipore, Darmstadt, Germany). .. For LV12 cells, the membranes were incubated with mouse monoclonal anti-AMIGO2 antibody (G-7; sc-373699, Santa Cruz Biotechnology, Santa Cruz, CA, USA) at a 1:50 dilution or rabbit polyclonal anti-AMIGO2 antibody (LS-C401236; LS Bio, Shirley, MA, USA) at a 1:1,000 dilution, and then with peroxidase-conjugated goat polyclonal anti-mouse IgG antibody at a 1:2,000 dilution (PM009-7; Medical & Biological Laboratories, Nagoya, Japan) or peroxidase-conjugated goat polyclonal anti-rabbit IgG antibody at a 1:2,000 dilution (ab97080; Abcam, Cambridge, UK), respectively. .. For MKN45 cells, the membranes were incubated with rat monoclonal anti-AMIGO2 antibody at a 1:10,000 dilution (rTNK1A0012) , and then incubated with peroxidase-conjugated goat polyclonal anti-rat IgG antibody diluted 1:10,000 (ab98425; Abcam).

    Article Title: Prevention of liver metastasis via the pharmacological suppression of AMIGO2 expression in tumor cells.
    Article Snippet: Twenty to forty micrograms of protein was subjected to 10% SDS-PAGE under reducing conditions and then blotted onto a polyvinylidene fluoride membrane (ISEQ00010; Merck Millipore, Darmstadt, Germany). .. For LV12 cells, the membranes were incubated with mouse monoclonal anti-AMIGO2 antibody (G-7; sc-373699, Santa Cruz Biotechnology, Santa Cruz, CA, USA) at a 1:50 dilution or rabbit polyclonal anti-AMIGO2 antibody (LS-C401236; LS Bio, Shirley, MA, USA) at a 1:1,000 dilution, and then with peroxidase-conjugated goat polyclonal anti-mouse IgG antibody at a 1:2,000 dilution (PM009-7; Medical & Biological Laboratories, Nagoya, Japan) or peroxidase-conjugated goat polyclonal anti-rabbit IgG antibody at a 1:2,000 dilution (ab97080; Abcam, Cambridge, UK), respectively. .. For MKN45 cells, the membranes were incubated with rat monoclonal anti-AMIGO2 antibody at a 1:10,000 dilution (rTNK1A0012)12, and then incubated with peroxidase-conjugated goat polyclonal anti-rat IgG antibody diluted 1:10,000 (ab98425; Abcam).



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    Santa Cruz Biotechnology rabbit polyclonal anti amigo2 antibody
    Fig. 3. Suppression of <t>AMIGO2</t> mRNA and protein expression in LV12 cells treated with trametinib, ruxolitinib, and SP600125 and their reduced adhesion to mouse liver sinusoidal endothelial (HSE) cells. (a) LV12 cells were treated with trametinib, ruxolitinib, SP600125, or DMSO for 24 h. The relative AMIGO2 mRNA levels in each drug treatment group, compared with that in DMSO-treated LV12 cells, was determined using qRT-PCR. The bar graphs show mean ± SD from three to five independent experiments (n = 9–15, Student’s t-test). (b) Immunoreactive AMIGO2 expression was quantified as a ratio to β-actin expression using densitometry. Values represent mean ± SD (n = 7, Student’s t-test) from at least six independent experiments with similar results. (c) Typical immunoblotting performed using anti-AMIGO2 is shown in the upper panel, and the lower panel presents immunoblotting using anti-β-actin antibodies. Full-length blots were presented in Supplementary Fig. S5. (d) LV12 cells treated as described in “a” were labeled with PKH67 fluorescent dye and placed on HSE cells. The percentage of adherent cells was determined by measuring the fluorescence intensity. The graph shows mean ± SD (n = 4 in each group, Student’s t-test) from four independent experiments with similar results.
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    Fig. 3. Suppression of <t>AMIGO2</t> mRNA and protein expression in LV12 cells treated with trametinib, ruxolitinib, and SP600125 and their reduced adhesion to mouse liver sinusoidal endothelial (HSE) cells. (a) LV12 cells were treated with trametinib, ruxolitinib, SP600125, or DMSO for 24 h. The relative AMIGO2 mRNA levels in each drug treatment group, compared with that in DMSO-treated LV12 cells, was determined using qRT-PCR. The bar graphs show mean ± SD from three to five independent experiments (n = 9–15, Student’s t-test). (b) Immunoreactive AMIGO2 expression was quantified as a ratio to β-actin expression using densitometry. Values represent mean ± SD (n = 7, Student’s t-test) from at least six independent experiments with similar results. (c) Typical immunoblotting performed using anti-AMIGO2 is shown in the upper panel, and the lower panel presents immunoblotting using anti-β-actin antibodies. Full-length blots were presented in Supplementary Fig. S5. (d) LV12 cells treated as described in “a” were labeled with PKH67 fluorescent dye and placed on HSE cells. The percentage of adherent cells was determined by measuring the fluorescence intensity. The graph shows mean ± SD (n = 4 in each group, Student’s t-test) from four independent experiments with similar results.
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    Image Search Results


    Primary antibodies, pretreatment, and dilutions used for immunohistochemistry.

    Journal: International Journal of Molecular Sciences

    Article Title: Impact of Astrocyte Depletion upon Inflammation and Demyelination in a Murine Animal Model of Multiple Sclerosis

    doi: 10.3390/ijms20163922

    Figure Lengend Snippet: Primary antibodies, pretreatment, and dilutions used for immunohistochemistry.

    Article Snippet: Amigo2 , 0.5% triton , 1:200 , polyclonal rabbit , Bioss Antibodies Inc., Woburn, Massachusetts, USA , ABIN138654.

    Techniques: Immunohistochemistry

    Fig. 3. Suppression of AMIGO2 mRNA and protein expression in LV12 cells treated with trametinib, ruxolitinib, and SP600125 and their reduced adhesion to mouse liver sinusoidal endothelial (HSE) cells. (a) LV12 cells were treated with trametinib, ruxolitinib, SP600125, or DMSO for 24 h. The relative AMIGO2 mRNA levels in each drug treatment group, compared with that in DMSO-treated LV12 cells, was determined using qRT-PCR. The bar graphs show mean ± SD from three to five independent experiments (n = 9–15, Student’s t-test). (b) Immunoreactive AMIGO2 expression was quantified as a ratio to β-actin expression using densitometry. Values represent mean ± SD (n = 7, Student’s t-test) from at least six independent experiments with similar results. (c) Typical immunoblotting performed using anti-AMIGO2 is shown in the upper panel, and the lower panel presents immunoblotting using anti-β-actin antibodies. Full-length blots were presented in Supplementary Fig. S5. (d) LV12 cells treated as described in “a” were labeled with PKH67 fluorescent dye and placed on HSE cells. The percentage of adherent cells was determined by measuring the fluorescence intensity. The graph shows mean ± SD (n = 4 in each group, Student’s t-test) from four independent experiments with similar results.

    Journal: Scientific reports

    Article Title: Prevention of liver metastasis via the pharmacological suppression of AMIGO2 expression in tumor cells.

    doi: 10.1038/s41598-024-71827-z

    Figure Lengend Snippet: Fig. 3. Suppression of AMIGO2 mRNA and protein expression in LV12 cells treated with trametinib, ruxolitinib, and SP600125 and their reduced adhesion to mouse liver sinusoidal endothelial (HSE) cells. (a) LV12 cells were treated with trametinib, ruxolitinib, SP600125, or DMSO for 24 h. The relative AMIGO2 mRNA levels in each drug treatment group, compared with that in DMSO-treated LV12 cells, was determined using qRT-PCR. The bar graphs show mean ± SD from three to five independent experiments (n = 9–15, Student’s t-test). (b) Immunoreactive AMIGO2 expression was quantified as a ratio to β-actin expression using densitometry. Values represent mean ± SD (n = 7, Student’s t-test) from at least six independent experiments with similar results. (c) Typical immunoblotting performed using anti-AMIGO2 is shown in the upper panel, and the lower panel presents immunoblotting using anti-β-actin antibodies. Full-length blots were presented in Supplementary Fig. S5. (d) LV12 cells treated as described in “a” were labeled with PKH67 fluorescent dye and placed on HSE cells. The percentage of adherent cells was determined by measuring the fluorescence intensity. The graph shows mean ± SD (n = 4 in each group, Student’s t-test) from four independent experiments with similar results.

    Article Snippet: For LV12 cells, the membranes were incubated with mouse monoclonal anti-AMIGO2 antibody (G-7; sc-373699, Santa Cruz Biotechnology, Santa Cruz, CA, USA) at a 1:50 dilution or rabbit polyclonal anti-AMIGO2 antibody (LS-C401236; LS Bio, Shirley, MA, USA) at a 1:1,000 dilution, and then with peroxidase-conjugated goat polyclonal anti-mouse IgG antibody at a 1:2,000 dilution (PM009-7; Medical & Biological Laboratories, Nagoya, Japan) or peroxidase-conjugated goat polyclonal anti-rabbit IgG antibody at a 1:2,000 dilution (ab97080; Abcam, Cambridge, UK), respectively.

    Techniques: Expressing, Quantitative RT-PCR, Western Blot, Labeling, Fluorescence