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cxcr1 antibody  (Bioss)


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    Bioss cxcr1 antibody
    Increased <t>CXCR1</t> protein and mRNA expression in the spinal dorsal horn of BCP rats. (a–d) Immunolabeled CXCR1 (green) in the spinal cord of BCP rats. Pre-incubation of CXCR1 antibody with excessive CXCR1 blocking peptide served as the specificity control of CXCR1 antibody. Ipsilateral (Ipsi), contralateral (Contra), nucleus (blue). (e) The mRNA expression of CXCR1 was increased in the BCP group compared with the sham group. * p < 0.05, n = 7, compared to sham, Student’s t-test. (f) The protein expression of CXCR1 increased in a time-dependent manner in the BCP group compared with the sham-operated group. ** p < 0.01; n = 4, one-way ANOVA.
    Cxcr1 Antibody, supplied by Bioss, used in various techniques. Bioz Stars score: 92/100, based on 3 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/cxcr1 antibody/product/Bioss
    Average 92 stars, based on 3 article reviews
    cxcr1 antibody - by Bioz Stars, 2026-02
    92/100 stars

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    1) Product Images from "CXCR1 participates in bone cancer pain induced by Walker 256 breast cancer cells in female rats"

    Article Title: CXCR1 participates in bone cancer pain induced by Walker 256 breast cancer cells in female rats

    Journal: Molecular Pain

    doi: 10.1177/17448069221135743

    Increased CXCR1 protein and mRNA expression in the spinal dorsal horn of BCP rats. (a–d) Immunolabeled CXCR1 (green) in the spinal cord of BCP rats. Pre-incubation of CXCR1 antibody with excessive CXCR1 blocking peptide served as the specificity control of CXCR1 antibody. Ipsilateral (Ipsi), contralateral (Contra), nucleus (blue). (e) The mRNA expression of CXCR1 was increased in the BCP group compared with the sham group. * p < 0.05, n = 7, compared to sham, Student’s t-test. (f) The protein expression of CXCR1 increased in a time-dependent manner in the BCP group compared with the sham-operated group. ** p < 0.01; n = 4, one-way ANOVA.
    Figure Legend Snippet: Increased CXCR1 protein and mRNA expression in the spinal dorsal horn of BCP rats. (a–d) Immunolabeled CXCR1 (green) in the spinal cord of BCP rats. Pre-incubation of CXCR1 antibody with excessive CXCR1 blocking peptide served as the specificity control of CXCR1 antibody. Ipsilateral (Ipsi), contralateral (Contra), nucleus (blue). (e) The mRNA expression of CXCR1 was increased in the BCP group compared with the sham group. * p < 0.05, n = 7, compared to sham, Student’s t-test. (f) The protein expression of CXCR1 increased in a time-dependent manner in the BCP group compared with the sham-operated group. ** p < 0.01; n = 4, one-way ANOVA.

    Techniques Used: Expressing, Immunolabeling, Incubation, Blocking Assay

    Distribution and cellular localization of CXCR1 in the dorsal horn of the spinal cord. (a–o) Immunofluorescence data show that CXCR1 (green) was predominantly expressed in neurons (red), but not in astrocytes (red) or microglia (red). All sections were counterstained with DAPI (blue) to show nuclei. White arrows indicate possible colocalization sites. NeuN (neuronal nucleus, neuron-specific marker); GFAP (glial fibrillary acidic protein, astrocyte-specific marker); Iba-1 (ionized calcium-binding adaptor molecule 1, microglia-specific mark); n = 4. Scale bar: 50 μm.
    Figure Legend Snippet: Distribution and cellular localization of CXCR1 in the dorsal horn of the spinal cord. (a–o) Immunofluorescence data show that CXCR1 (green) was predominantly expressed in neurons (red), but not in astrocytes (red) or microglia (red). All sections were counterstained with DAPI (blue) to show nuclei. White arrows indicate possible colocalization sites. NeuN (neuronal nucleus, neuron-specific marker); GFAP (glial fibrillary acidic protein, astrocyte-specific marker); Iba-1 (ionized calcium-binding adaptor molecule 1, microglia-specific mark); n = 4. Scale bar: 50 μm.

    Techniques Used: Immunofluorescence, Marker, Binding Assay

    Spinal cord blockade of CXCR1 attenuates abnormal gait and mechanical hyperalgesia in BCP rats. (a-b) Relative expression of CXCR1-mRNA and CXCR2-mRNA in PC12 cells after CXCR1-siRNA transfection. *** P < 0.001. n = 3, Student's t-test. (c) Western blot results showing the reduction of CXCR1 protein levels after CXCR1-siRNA treatment. ** p < 0.01. n = 4, Student’s t-test. (d) Intrathecal injection of CXCR1-siRNA relieved tumor-induced mechanical allodynia 10 days after BCP. * p < 0.05, ** p < 0.01, compared to sham, two-way repeated measures ANOVA. (e-g) Representative CatWalk gaits, including print view, timing view, and print intensity, in sham (e), BCP+siControl (f), BCP + si-CXCR1 (g) groups. (h-j) Intrathecal injection of CXCR1-siRNA significantly attenuated tumor-induced reductions in maximum contact area (h), maximum contact maximum intensity (j), and mean intensity (i) in tumor-bearing rats. Starting on day 7 after tumor inoculation, CXCR1-siRNA was intrathecally injected daily for six consecutive days. Behavioral testing was performed 4 h after the last injection. Data were calculated as percentages of ipsilateral (left)/contralateral (right) hind paws. Data are presented as mean ± SEM * p < 0.05, ** p < 0.01, *** p < 0.001, one-way ANOVA. LH, left rear; RH, right rear.
    Figure Legend Snippet: Spinal cord blockade of CXCR1 attenuates abnormal gait and mechanical hyperalgesia in BCP rats. (a-b) Relative expression of CXCR1-mRNA and CXCR2-mRNA in PC12 cells after CXCR1-siRNA transfection. *** P < 0.001. n = 3, Student's t-test. (c) Western blot results showing the reduction of CXCR1 protein levels after CXCR1-siRNA treatment. ** p < 0.01. n = 4, Student’s t-test. (d) Intrathecal injection of CXCR1-siRNA relieved tumor-induced mechanical allodynia 10 days after BCP. * p < 0.05, ** p < 0.01, compared to sham, two-way repeated measures ANOVA. (e-g) Representative CatWalk gaits, including print view, timing view, and print intensity, in sham (e), BCP+siControl (f), BCP + si-CXCR1 (g) groups. (h-j) Intrathecal injection of CXCR1-siRNA significantly attenuated tumor-induced reductions in maximum contact area (h), maximum contact maximum intensity (j), and mean intensity (i) in tumor-bearing rats. Starting on day 7 after tumor inoculation, CXCR1-siRNA was intrathecally injected daily for six consecutive days. Behavioral testing was performed 4 h after the last injection. Data were calculated as percentages of ipsilateral (left)/contralateral (right) hind paws. Data are presented as mean ± SEM * p < 0.05, ** p < 0.01, *** p < 0.001, one-way ANOVA. LH, left rear; RH, right rear.

    Techniques Used: Expressing, Transfection, Western Blot, Injection

    BCP-induced activation of spinal JAK2/STAT3 signaling is dependent on CXCR1 in vivo and in vitro. (a–c) The phosphorylated proteins of the JAK2/STAT3 pathway were time-dependently increased in the spinal cord of rats with BCP. * p < 0.05, ** p < 0.01, *** p < 0.001, compared to sham group, one-way ANOVA. (d–f) Phosphorylated proteins of the JAK2/STAT3 pathway were reduced after intrathecal injection of CXCR1-siRNA. * p < 0.05, *** p < 0.001, compared to sham group, one-way ANOVA. (g–i) Phosphorylated protein of JAK2/STAT3 was dependent on CXCR1 activation in PC12 cells. * p < 0.05, ** p < 0.01, *** p < 0.001.
    Figure Legend Snippet: BCP-induced activation of spinal JAK2/STAT3 signaling is dependent on CXCR1 in vivo and in vitro. (a–c) The phosphorylated proteins of the JAK2/STAT3 pathway were time-dependently increased in the spinal cord of rats with BCP. * p < 0.05, ** p < 0.01, *** p < 0.001, compared to sham group, one-way ANOVA. (d–f) Phosphorylated proteins of the JAK2/STAT3 pathway were reduced after intrathecal injection of CXCR1-siRNA. * p < 0.05, *** p < 0.001, compared to sham group, one-way ANOVA. (g–i) Phosphorylated protein of JAK2/STAT3 was dependent on CXCR1 activation in PC12 cells. * p < 0.05, ** p < 0.01, *** p < 0.001.

    Techniques Used: Activation Assay, In Vivo, In Vitro, Injection

    BCP-induced activation of the NLRP3 inflammasome is dependent on CXCR1 in vivo and in vitro . (a–c) Elevated NLRP3, caspase1, and IL-1β proteins in BCP rats were reversed after intrathecal injection of CXCR1-siRNA. ** p < 0.01, *** p < 0.001, n = 4. (d–f) Increased protein level in NLRP3, caspase-1, and IL-1β was dependent on CXCR1 in PC12 cells. *** p < 0.001, n = 3.
    Figure Legend Snippet: BCP-induced activation of the NLRP3 inflammasome is dependent on CXCR1 in vivo and in vitro . (a–c) Elevated NLRP3, caspase1, and IL-1β proteins in BCP rats were reversed after intrathecal injection of CXCR1-siRNA. ** p < 0.01, *** p < 0.001, n = 4. (d–f) Increased protein level in NLRP3, caspase-1, and IL-1β was dependent on CXCR1 in PC12 cells. *** p < 0.001, n = 3.

    Techniques Used: Activation Assay, In Vivo, In Vitro, Injection



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    cxcr1 antibody  (Bioss)
    92
    Bioss cxcr1 antibody
    Increased <t>CXCR1</t> protein and mRNA expression in the spinal dorsal horn of BCP rats. (a–d) Immunolabeled CXCR1 (green) in the spinal cord of BCP rats. Pre-incubation of CXCR1 antibody with excessive CXCR1 blocking peptide served as the specificity control of CXCR1 antibody. Ipsilateral (Ipsi), contralateral (Contra), nucleus (blue). (e) The mRNA expression of CXCR1 was increased in the BCP group compared with the sham group. * p < 0.05, n = 7, compared to sham, Student’s t-test. (f) The protein expression of CXCR1 increased in a time-dependent manner in the BCP group compared with the sham-operated group. ** p < 0.01; n = 4, one-way ANOVA.
    Cxcr1 Antibody, supplied by Bioss, used in various techniques. Bioz Stars score: 92/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/cxcr1 antibody/product/Bioss
    Average 92 stars, based on 1 article reviews
    cxcr1 antibody - by Bioz Stars, 2026-02
    92/100 stars
    		  Buy from Supplier

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    Increased CXCR1 protein and mRNA expression in the spinal dorsal horn of BCP rats. (a–d) Immunolabeled CXCR1 (green) in the spinal cord of BCP rats. Pre-incubation of CXCR1 antibody with excessive CXCR1 blocking peptide served as the specificity control of CXCR1 antibody. Ipsilateral (Ipsi), contralateral (Contra), nucleus (blue). (e) The mRNA expression of CXCR1 was increased in the BCP group compared with the sham group. * p < 0.05, n = 7, compared to sham, Student’s t-test. (f) The protein expression of CXCR1 increased in a time-dependent manner in the BCP group compared with the sham-operated group. ** p < 0.01; n = 4, one-way ANOVA.

    Journal: Molecular Pain

    Article Title: CXCR1 participates in bone cancer pain induced by Walker 256 breast cancer cells in female rats

    doi: 10.1177/17448069221135743

    Figure Lengend Snippet: Increased CXCR1 protein and mRNA expression in the spinal dorsal horn of BCP rats. (a–d) Immunolabeled CXCR1 (green) in the spinal cord of BCP rats. Pre-incubation of CXCR1 antibody with excessive CXCR1 blocking peptide served as the specificity control of CXCR1 antibody. Ipsilateral (Ipsi), contralateral (Contra), nucleus (blue). (e) The mRNA expression of CXCR1 was increased in the BCP group compared with the sham group. * p < 0.05, n = 7, compared to sham, Student’s t-test. (f) The protein expression of CXCR1 increased in a time-dependent manner in the BCP group compared with the sham-operated group. ** p < 0.01; n = 4, one-way ANOVA.

    Article Snippet: To confirm the specificity of the CXCR1 antibody, the CXCR1 antibody was pre-adsorbed (room temperature, 1 h) against its blocking peptide (bs-1009P, Bioss) prior to incubation with spinal cord sections, by mixing the CXCR1 antibody with a ten-fold (by weight) of the blocking peptide.

    Techniques: Expressing, Immunolabeling, Incubation, Blocking Assay

    Distribution and cellular localization of CXCR1 in the dorsal horn of the spinal cord. (a–o) Immunofluorescence data show that CXCR1 (green) was predominantly expressed in neurons (red), but not in astrocytes (red) or microglia (red). All sections were counterstained with DAPI (blue) to show nuclei. White arrows indicate possible colocalization sites. NeuN (neuronal nucleus, neuron-specific marker); GFAP (glial fibrillary acidic protein, astrocyte-specific marker); Iba-1 (ionized calcium-binding adaptor molecule 1, microglia-specific mark); n = 4. Scale bar: 50 μm.

    Journal: Molecular Pain

    Article Title: CXCR1 participates in bone cancer pain induced by Walker 256 breast cancer cells in female rats

    doi: 10.1177/17448069221135743

    Figure Lengend Snippet: Distribution and cellular localization of CXCR1 in the dorsal horn of the spinal cord. (a–o) Immunofluorescence data show that CXCR1 (green) was predominantly expressed in neurons (red), but not in astrocytes (red) or microglia (red). All sections were counterstained with DAPI (blue) to show nuclei. White arrows indicate possible colocalization sites. NeuN (neuronal nucleus, neuron-specific marker); GFAP (glial fibrillary acidic protein, astrocyte-specific marker); Iba-1 (ionized calcium-binding adaptor molecule 1, microglia-specific mark); n = 4. Scale bar: 50 μm.

    Article Snippet: To confirm the specificity of the CXCR1 antibody, the CXCR1 antibody was pre-adsorbed (room temperature, 1 h) against its blocking peptide (bs-1009P, Bioss) prior to incubation with spinal cord sections, by mixing the CXCR1 antibody with a ten-fold (by weight) of the blocking peptide.

    Techniques: Immunofluorescence, Marker, Binding Assay

    Spinal cord blockade of CXCR1 attenuates abnormal gait and mechanical hyperalgesia in BCP rats. (a-b) Relative expression of CXCR1-mRNA and CXCR2-mRNA in PC12 cells after CXCR1-siRNA transfection. *** P < 0.001. n = 3, Student's t-test. (c) Western blot results showing the reduction of CXCR1 protein levels after CXCR1-siRNA treatment. ** p < 0.01. n = 4, Student’s t-test. (d) Intrathecal injection of CXCR1-siRNA relieved tumor-induced mechanical allodynia 10 days after BCP. * p < 0.05, ** p < 0.01, compared to sham, two-way repeated measures ANOVA. (e-g) Representative CatWalk gaits, including print view, timing view, and print intensity, in sham (e), BCP+siControl (f), BCP + si-CXCR1 (g) groups. (h-j) Intrathecal injection of CXCR1-siRNA significantly attenuated tumor-induced reductions in maximum contact area (h), maximum contact maximum intensity (j), and mean intensity (i) in tumor-bearing rats. Starting on day 7 after tumor inoculation, CXCR1-siRNA was intrathecally injected daily for six consecutive days. Behavioral testing was performed 4 h after the last injection. Data were calculated as percentages of ipsilateral (left)/contralateral (right) hind paws. Data are presented as mean ± SEM * p < 0.05, ** p < 0.01, *** p < 0.001, one-way ANOVA. LH, left rear; RH, right rear.

    Journal: Molecular Pain

    Article Title: CXCR1 participates in bone cancer pain induced by Walker 256 breast cancer cells in female rats

    doi: 10.1177/17448069221135743

    Figure Lengend Snippet: Spinal cord blockade of CXCR1 attenuates abnormal gait and mechanical hyperalgesia in BCP rats. (a-b) Relative expression of CXCR1-mRNA and CXCR2-mRNA in PC12 cells after CXCR1-siRNA transfection. *** P < 0.001. n = 3, Student's t-test. (c) Western blot results showing the reduction of CXCR1 protein levels after CXCR1-siRNA treatment. ** p < 0.01. n = 4, Student’s t-test. (d) Intrathecal injection of CXCR1-siRNA relieved tumor-induced mechanical allodynia 10 days after BCP. * p < 0.05, ** p < 0.01, compared to sham, two-way repeated measures ANOVA. (e-g) Representative CatWalk gaits, including print view, timing view, and print intensity, in sham (e), BCP+siControl (f), BCP + si-CXCR1 (g) groups. (h-j) Intrathecal injection of CXCR1-siRNA significantly attenuated tumor-induced reductions in maximum contact area (h), maximum contact maximum intensity (j), and mean intensity (i) in tumor-bearing rats. Starting on day 7 after tumor inoculation, CXCR1-siRNA was intrathecally injected daily for six consecutive days. Behavioral testing was performed 4 h after the last injection. Data were calculated as percentages of ipsilateral (left)/contralateral (right) hind paws. Data are presented as mean ± SEM * p < 0.05, ** p < 0.01, *** p < 0.001, one-way ANOVA. LH, left rear; RH, right rear.

    Article Snippet: To confirm the specificity of the CXCR1 antibody, the CXCR1 antibody was pre-adsorbed (room temperature, 1 h) against its blocking peptide (bs-1009P, Bioss) prior to incubation with spinal cord sections, by mixing the CXCR1 antibody with a ten-fold (by weight) of the blocking peptide.

    Techniques: Expressing, Transfection, Western Blot, Injection

    BCP-induced activation of spinal JAK2/STAT3 signaling is dependent on CXCR1 in vivo and in vitro. (a–c) The phosphorylated proteins of the JAK2/STAT3 pathway were time-dependently increased in the spinal cord of rats with BCP. * p < 0.05, ** p < 0.01, *** p < 0.001, compared to sham group, one-way ANOVA. (d–f) Phosphorylated proteins of the JAK2/STAT3 pathway were reduced after intrathecal injection of CXCR1-siRNA. * p < 0.05, *** p < 0.001, compared to sham group, one-way ANOVA. (g–i) Phosphorylated protein of JAK2/STAT3 was dependent on CXCR1 activation in PC12 cells. * p < 0.05, ** p < 0.01, *** p < 0.001.

    Journal: Molecular Pain

    Article Title: CXCR1 participates in bone cancer pain induced by Walker 256 breast cancer cells in female rats

    doi: 10.1177/17448069221135743

    Figure Lengend Snippet: BCP-induced activation of spinal JAK2/STAT3 signaling is dependent on CXCR1 in vivo and in vitro. (a–c) The phosphorylated proteins of the JAK2/STAT3 pathway were time-dependently increased in the spinal cord of rats with BCP. * p < 0.05, ** p < 0.01, *** p < 0.001, compared to sham group, one-way ANOVA. (d–f) Phosphorylated proteins of the JAK2/STAT3 pathway were reduced after intrathecal injection of CXCR1-siRNA. * p < 0.05, *** p < 0.001, compared to sham group, one-way ANOVA. (g–i) Phosphorylated protein of JAK2/STAT3 was dependent on CXCR1 activation in PC12 cells. * p < 0.05, ** p < 0.01, *** p < 0.001.

    Article Snippet: To confirm the specificity of the CXCR1 antibody, the CXCR1 antibody was pre-adsorbed (room temperature, 1 h) against its blocking peptide (bs-1009P, Bioss) prior to incubation with spinal cord sections, by mixing the CXCR1 antibody with a ten-fold (by weight) of the blocking peptide.

    Techniques: Activation Assay, In Vivo, In Vitro, Injection

    BCP-induced activation of the NLRP3 inflammasome is dependent on CXCR1 in vivo and in vitro . (a–c) Elevated NLRP3, caspase1, and IL-1β proteins in BCP rats were reversed after intrathecal injection of CXCR1-siRNA. ** p < 0.01, *** p < 0.001, n = 4. (d–f) Increased protein level in NLRP3, caspase-1, and IL-1β was dependent on CXCR1 in PC12 cells. *** p < 0.001, n = 3.

    Journal: Molecular Pain

    Article Title: CXCR1 participates in bone cancer pain induced by Walker 256 breast cancer cells in female rats

    doi: 10.1177/17448069221135743

    Figure Lengend Snippet: BCP-induced activation of the NLRP3 inflammasome is dependent on CXCR1 in vivo and in vitro . (a–c) Elevated NLRP3, caspase1, and IL-1β proteins in BCP rats were reversed after intrathecal injection of CXCR1-siRNA. ** p < 0.01, *** p < 0.001, n = 4. (d–f) Increased protein level in NLRP3, caspase-1, and IL-1β was dependent on CXCR1 in PC12 cells. *** p < 0.001, n = 3.

    Article Snippet: To confirm the specificity of the CXCR1 antibody, the CXCR1 antibody was pre-adsorbed (room temperature, 1 h) against its blocking peptide (bs-1009P, Bioss) prior to incubation with spinal cord sections, by mixing the CXCR1 antibody with a ten-fold (by weight) of the blocking peptide.

    Techniques: Activation Assay, In Vivo, In Vitro, Injection