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gr1  (Cell Signaling Technology Inc)


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    Structured Review

    Cell Signaling Technology Inc gr1
    Gr1, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 94/100, based on 26 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/gr1/Ly-6G%2FLy-6C+(Gr-1)+(RB6-8C5)+Rat+mAb/pm41679176-156-13-16
    Average 94 stars, based on 26 article reviews
    gr1 - by Bioz Stars, 2026-10
    94/100 stars

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    Related Articles

    Incubation:

    Article Title: MCC950 attenuates plasma cell mastitis in an MDSC-dependent manner.
    Article Snippet: .. Next, sections were incubated with the primary antibodies against CD11b (eBioscienceTM, 14–0112-82) and Gr1 (CST, 31469S) overnight at 4 ◦C. ..

    Article Title: CD31 regulates metabolic switch in Treg migration attenuates rheumatoid arthritis
    Article Snippet: .. The fixed cells were then permeabilised in a 0.1% Triton X‐100 solution on ice for 10 min and incubated overnight at 4°C with primary antibodies against DAPI (Sigma‐Aldrich, D9542), FOXP3+ (Sigma‐Aldrich, SAB5300461), CD45+ (Sigma‐Aldrich, SAB4502541), CD68+ (Invitrogen, 14‐0681‐82), GR1+ (Cell Signalling, 31469), SHP2 (Sigma‐Aldrich, SAB5700078), CD31 (Sigma‐Aldrich, SAB5700639), RNF111 (Sigma‐Aldrich, HPA038576), CD8+ (Thermo Fisher, 740029TP555), OGT (Sigma‐Aldrich, O6014), and CD4+ (Sigma‐Aldrich, SAB4503583). .. This was followed by staining with the secondary antibody which had been linked to Alexa Fluor 594 (A‐11032, Invitrogen).

    Article Title: NGR-modified cancer-associated fibroblast-derived exosomes deliver resveratrol to inhibit CXCR2/NF-κB signaling in myeloid-derived suppressor cells and reverse immune suppression in liver cancer.
    Article Snippet: Objective: This study aimed to develop NGR (Asn-Gly-Arg) peptide–modified cancer-associated fibroblast (CAF)derived exosomes for resveratrol delivery (NGR-Exos@Res) to target myeloid-derived suppressor cells (MDSCs) in the tumor microenvironment.. By inhibiting the CXCR2/NF-κB pathway, this strategy reprograms MDSC function, reverses immune suppression, restores CD8 T-cell antitumor activity, and suppresses liver cancer (LC)

    other:

    Article Title: QDPR deficiency drives immune suppression in pancreatic cancer.
    Article Snippet: Article QDPR deficiency drives im mune suppression in pancreatic cancer



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    A: Representative histological (H & E) and immunofluorescence images of TA muscle cross-sections at day 1 post-injury following treatment with vehicle (VEH), indomethacin (INDO), aspirin (ASA), or a combination of INDO + ASA. Sections are stained for <t>Ly6G</t> (neutrophils, red), CD68 (total macrophages, green), CD206 (M2-like macrophages, red), with DAPI (nuclei, blue) and Laminin (LAM, white) to visualize fiber boundaries. B-E : Quantification of day 1 post-injury inflammatory markers including Ly6G + cell density ( B ), CD68 + cell density ( C ), the ratio of Ly6G + to total CD68 + cells ( D ), and the M1/M2 macrophage ratio ( E ). F: Representative H & E and immunofluorescence images at day 3 post-injury for the same treatment groups and markers. G-J: Quantitative analysis of inflammatory cell dynamics at day 3 post-injury, including Ly6G + cell density ( G ), CD68 + cell area as a percentage of total tissue ( H ), CD206 + cell densities ( I ), and the M1/M2 ratio ( J ). All data are presented as mean ± SEM. Statistical significance was determined by one-way ANOVA followed by Holm-Šídák post hoc tests. Groups labeled with different letters are significantly different from one another, while groups sharing a common letter are not significantly different.
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    A: Representative histological (H & E) and immunofluorescence images of TA muscle cross-sections at day 1 post-injury following treatment with vehicle (VEH), indomethacin (INDO), aspirin (ASA), or a combination of INDO + ASA. Sections are stained for <t>Ly6G</t> (neutrophils, red), CD68 (total macrophages, green), CD206 (M2-like macrophages, red), with DAPI (nuclei, blue) and Laminin (LAM, white) to visualize fiber boundaries. B-E : Quantification of day 1 post-injury inflammatory markers including Ly6G + cell density ( B ), CD68 + cell density ( C ), the ratio of Ly6G + to total CD68 + cells ( D ), and the M1/M2 macrophage ratio ( E ). F: Representative H & E and immunofluorescence images at day 3 post-injury for the same treatment groups and markers. G-J: Quantitative analysis of inflammatory cell dynamics at day 3 post-injury, including Ly6G + cell density ( G ), CD68 + cell area as a percentage of total tissue ( H ), CD206 + cell densities ( I ), and the M1/M2 ratio ( J ). All data are presented as mean ± SEM. Statistical significance was determined by one-way ANOVA followed by Holm-Šídák post hoc tests. Groups labeled with different letters are significantly different from one another, while groups sharing a common letter are not significantly different.
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    A: Representative histological (H & E) and immunofluorescence images of TA muscle cross-sections at day 1 post-injury following treatment with vehicle (VEH), indomethacin (INDO), aspirin (ASA), or a combination of INDO + ASA. Sections are stained for <t>Ly6G</t> (neutrophils, red), CD68 (total macrophages, green), CD206 (M2-like macrophages, red), with DAPI (nuclei, blue) and Laminin (LAM, white) to visualize fiber boundaries. B-E : Quantification of day 1 post-injury inflammatory markers including Ly6G + cell density ( B ), CD68 + cell density ( C ), the ratio of Ly6G + to total CD68 + cells ( D ), and the M1/M2 macrophage ratio ( E ). F: Representative H & E and immunofluorescence images at day 3 post-injury for the same treatment groups and markers. G-J: Quantitative analysis of inflammatory cell dynamics at day 3 post-injury, including Ly6G + cell density ( G ), CD68 + cell area as a percentage of total tissue ( H ), CD206 + cell densities ( I ), and the M1/M2 ratio ( J ). All data are presented as mean ± SEM. Statistical significance was determined by one-way ANOVA followed by Holm-Šídák post hoc tests. Groups labeled with different letters are significantly different from one another, while groups sharing a common letter are not significantly different.
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    Image Search Results


    Tumor growth kinetics following anti–PD-1, chemotherapy, and anti-Gr1 treatment in LLC tumor–bearing mice. (A): Diagram representing the therapeutic scheme followed for the in vivo experiment. LLC cells were injected subcutaneously on day 0 to establish tumours. Treatments were administered intraperitoneally on days 11, 14, and 17 after tumor cell inoculation, with anti-GR1 administered one day prior to each treatment cycle. The therapeutic regimens included anti-PD1 (100 μg/mouse), anti-GR1 (200 μg/mouse), and chemotherapy consisting of cisplatin (3 mg/kg) plus pemetrexed (100 mg/kg). (B): Growth curves of LLC cells subcutaneously injected into immunocompetent mice, comparing tumour volumes between control and (B) anti-PD-1 treatment, (C) anti-Gr1 treatment, (D) chemotherapy consisting on cisplatin plus pemetrexed, plus anti-PD-1 treatment, (E) chemotherapy plus anti-PD-1 plus anti-Gr1 treatment. *: p <0.05; ***: p <0.001; ****: p <0.0001.

    Journal: Translational Oncology

    Article Title: Circulating low-density neutrophils as biomarkers of resistance to first-line anti-PD-1/PD-L1 immunotherapy in non-small cell lung cancer

    doi: 10.1016/j.tranon.2026.102755

    Figure Lengend Snippet: Tumor growth kinetics following anti–PD-1, chemotherapy, and anti-Gr1 treatment in LLC tumor–bearing mice. (A): Diagram representing the therapeutic scheme followed for the in vivo experiment. LLC cells were injected subcutaneously on day 0 to establish tumours. Treatments were administered intraperitoneally on days 11, 14, and 17 after tumor cell inoculation, with anti-GR1 administered one day prior to each treatment cycle. The therapeutic regimens included anti-PD1 (100 μg/mouse), anti-GR1 (200 μg/mouse), and chemotherapy consisting of cisplatin (3 mg/kg) plus pemetrexed (100 mg/kg). (B): Growth curves of LLC cells subcutaneously injected into immunocompetent mice, comparing tumour volumes between control and (B) anti-PD-1 treatment, (C) anti-Gr1 treatment, (D) chemotherapy consisting on cisplatin plus pemetrexed, plus anti-PD-1 treatment, (E) chemotherapy plus anti-PD-1 plus anti-Gr1 treatment. *: p <0.05; ***: p <0.001; ****: p <0.0001.

    Article Snippet: For the murine experiments, LLC cells were obtained from ATCC (#CRL-1642); anti-mouse Gr1 antibody (#BE0075, clone RB6-8C5) and anti-PD-1 antibody (#BE0273, clone RMP1-14) were purchased from BioXCell; pemetrexed (1000 mg/40 mL, 25 mg/mL) was obtained from TEVA; and cisplatin (#232120) was purchased from Sigma-Aldrich.

    Techniques: In Vivo, Injection, Control

    A: Representative histological (H & E) and immunofluorescence images of TA muscle cross-sections at day 1 post-injury following treatment with vehicle (VEH), indomethacin (INDO), aspirin (ASA), or a combination of INDO + ASA. Sections are stained for Ly6G (neutrophils, red), CD68 (total macrophages, green), CD206 (M2-like macrophages, red), with DAPI (nuclei, blue) and Laminin (LAM, white) to visualize fiber boundaries. B-E : Quantification of day 1 post-injury inflammatory markers including Ly6G + cell density ( B ), CD68 + cell density ( C ), the ratio of Ly6G + to total CD68 + cells ( D ), and the M1/M2 macrophage ratio ( E ). F: Representative H & E and immunofluorescence images at day 3 post-injury for the same treatment groups and markers. G-J: Quantitative analysis of inflammatory cell dynamics at day 3 post-injury, including Ly6G + cell density ( G ), CD68 + cell area as a percentage of total tissue ( H ), CD206 + cell densities ( I ), and the M1/M2 ratio ( J ). All data are presented as mean ± SEM. Statistical significance was determined by one-way ANOVA followed by Holm-Šídák post hoc tests. Groups labeled with different letters are significantly different from one another, while groups sharing a common letter are not significantly different.

    Journal: bioRxiv

    Article Title: Aspirin hastens resolution of skeletal muscle inflammation and promotes recovery of muscle strength following acute injury

    doi: 10.64898/2026.04.21.719989

    Figure Lengend Snippet: A: Representative histological (H & E) and immunofluorescence images of TA muscle cross-sections at day 1 post-injury following treatment with vehicle (VEH), indomethacin (INDO), aspirin (ASA), or a combination of INDO + ASA. Sections are stained for Ly6G (neutrophils, red), CD68 (total macrophages, green), CD206 (M2-like macrophages, red), with DAPI (nuclei, blue) and Laminin (LAM, white) to visualize fiber boundaries. B-E : Quantification of day 1 post-injury inflammatory markers including Ly6G + cell density ( B ), CD68 + cell density ( C ), the ratio of Ly6G + to total CD68 + cells ( D ), and the M1/M2 macrophage ratio ( E ). F: Representative H & E and immunofluorescence images at day 3 post-injury for the same treatment groups and markers. G-J: Quantitative analysis of inflammatory cell dynamics at day 3 post-injury, including Ly6G + cell density ( G ), CD68 + cell area as a percentage of total tissue ( H ), CD206 + cell densities ( I ), and the M1/M2 ratio ( J ). All data are presented as mean ± SEM. Statistical significance was determined by one-way ANOVA followed by Holm-Šídák post hoc tests. Groups labeled with different letters are significantly different from one another, while groups sharing a common letter are not significantly different.

    Article Snippet: Primary antibodies used include MyHC type I [Developmental Studies Hybridoma Bank (DSHB), BA-D5c, 1:100], MyHC type IIA (DSHB, SC-71c, 1:100), MyHC type IIB (DSHB, BF-F3c, 1:100), eMHC (DSHB, F1.652s, 1:20), Ly6G (GR1) (Bio-Rad, MCA2387, 1:50), CD68 (Bio-Rad, MCA1957, 1:200), CD206 (Bio-Rad, MCA2387, 1:50), and laminin (Abcam, ab7463, 1:200).

    Techniques: Immunofluorescence, Staining, Labeling