Clicking the images or links will redirect you to a website hosted by BenchSci that provides third-party scientific content. Neither the content nor the BenchSci technology and processes for selection have been evaluated by us; we are providing them as-is and without warranty of any kind, including for use or application of the Thermo Fisher Scientific products presented. This Antibody was verified by Relative expression to ensure that the antibody binds to the antigen stated.查看细节    Staining of C57BL/6 bone marrow cells with Anti-Human/Mouse CD45R (B220) FITC (Product # 11-0452-82) and 0.03 µg of Rat IgG2b K Isotype Control PerCP-Cyanine5-5 (Product # 45-4031-80) (left) or 0.03 µg of Anti-Mouse Ly-6G (Gr-1) PerCP-Cyanine5-5 (right).   Staining of mouse splenocytes and bone marrow cells. As expected based on known relative expression patterns, Gr-1 clone RB6-8C5 stains cells in the bone marrow myeloid gate and not in the splenocytes gate or bone marrow lymphoid gate. Details: Balb/c bone marrow cells (left) and splenocytes (middle) were surface stained with Gr-1 (clone RB6-8C5) followed by staining with 7-AAD. Viable bone marrow cells in the lymphoid (blue histogram) and myeloid (purple histogram) gates and viable splenocytes (orange histogram) were used for analysis. {RE}   Figure 4. Loss of Cemip Enhances Local Skin Inflammation in Response to S. aureus (A-F) Flow cytometry analysis of single-cell suspensions from the skin showing expression of CD11c/MHCII, Ly6G/CD11b, and LyG-C cells isolated from control, Cemip -/- control infection, and Cemip -/- infection. Cells were gated on CD3-negative. Numbers represent the percentages of the cells in the indicated gate. (G) Representative sections of skin from control and Cemip -/- mice at 3 days after S. aureus infection. Tissues are stained with red with Gr-1 antibody and blue with DAPI. Scale bar, 20 mum. (H) qRT-PCR of the relative abundance of transcripts for IL-6 as normalized to beta-actin (n = 4 for normal condition, n = 8 for infection mice/group). All error bars indicate mean +- SEM. *p    Fig. 2 VP1 recruited neutrophils into the lung. The single-cell suspensions were obtained from the lungs of mice from each experimental group and stained with anti-CD45-FITC, anti-Ly6G-PE, and anti-F4/80-APC antibodies. Flow cytometric analysis was performed and representative flow cytometry pseudocolor plots gated on neutrophils (CD45 + Ly6G + ) and macrophages (CD45 + F4/80 + ) were shown. a , b The percentage of neutrophils in the lung was markedly increased in VP1-treated mice. c , d The percentage of macrophages in the lung was slightly increased in VP1-treated mice. Values are expressed as the mean +- SEM. n = 4-6 per group. * p    Figure 4 ABT-199 alleviates PM-induced lung inflammation. After instillation of ABT-199 in the PM inflammatory model, the total BALF cells and the number of neutrophils were significantly decreased (n=5 to 7 per group) ( A ). After instillation of PM, ABT-199 also decreased the expression of CXCL-1, CXCL-2 in lung tissue ( B and C ). Apoptosis levels were determined by Annexin V and PI staining based on gating of Gr-1+/CD11b+ by flow cytometry. ABT-199 induced apoptosis of Neutrophils in BALF cells in different groups ( E - I ).   Figure 1 PM-induced lung inflammation is dominated by neutrophil accumulation, and PM reduced the apoptosis of neutrophils in BALF. We established a PM-induced lung inflammation model with instillation of PM at 100 mug/d/mouse for 2 days in WT mice (n=5 to 7 per group). PM increased the total number of macrophages, neutrophils, eosinophils, and lymphocytes in BALF. ( A ) Inflammatory cytokines such as the mouse chemokine (C-X-C motif) ligand 1 (CXCL-1) and CXCL-2 were significantly increased in WT-PM mice ( B and C ). Apoptosis in neutrophils were determined by Annexin V and PI staining based on the gating of Gr-1+/CD11b+ by flow cytometry. PM decreased the apoptosis of neutrophils in BALF cells ( D - F ).   Figure 3 Polymorfonuclear (PMN) cell infiltration in spleen, kidney, lung, liver and lymph nodes (A) Fold change in the percentage of splenic neutrophils compared to control healthy mice, which had an average neutrophil percentage of 2 to 10 % in their spleen at weeks 4 to 8 (N=3-5). Percentages of neutrophils were obtained by performing flow cytometry on single cell suspensions from the spleen. A fixed order of gating was used: first a gate was drawn to include the correct cell population and to exclude debris, a second gate excluded doublets. Next, a gate was set on the living cells, followed by a gate on the CD45 + population (leukocytes). Neutrophils were identified as CD45 + /GR1 + /CD11b + cells. (B) Pearson correlation between spleen weight (g) and the percentage of neutrophils in spleen for the three cohorts altogether. The Pearson correlation coefficient (r) and p-value for each individual group is indicated in the lower part of the figure. (C) Score of PMN infiltration in spleen (N=3) and (D) representative picture (40X magnification) of PMNs in spleen of mice from groups XNG (A)-PBS / XNG (B) and XNG (A)-CDV / XNG (B) at weeks 5 and 6. (E) Score of PMN infiltration in kidney, lung, liver and lymph nodes. The percentage of PMNs in tissue slides was microscopically (10X magnification) estimated and semi-quantified using the following scale: 0 score for = 50%. The PMN score in all organs of c   Fig 1 Decreased neutrophils in MiR125a -/- mice. (A) Flow cytometry analysis of bone marrow (upper panel) and peripheral blood (lower panel). Neutrophils were stained with CD11b-Percp cy5.5 and Ly6G-APC. Bar graphs indicated numbers of neutrophils per femur. Values were represented as mean+-s.d., n = 5 mice of each genotype. (B) Flow cytometry analysis of bone marrow neutrophils after bone marrow transplantation for 6 weeks. Bar graphs indicated total numbers of neutrophils. Values were represented as mean+-s.d.,n = 5 mice of each genotype. (C) Morphological character of neutrophils in MiR125a +/+ and MiR125a -/- mice. Peripheral blood (original magnification, x1000) of control and knockout mice were stained with Giemsa. (D) Expression of miR-125a during myeloid development (mean+-s.d.,n = 3). HSC, hematopoietic stem cells; CMP, common myeloid progenitors; GMP, granulocyte-monocyte progenitors; MEP, megakaryocyte erythroid progenitors; BM-N, bonemarrow neutrophils. ** P    Fig 2 Lower mortality and neutrophil infiltration in LPS-induced lethal septic shock in MiR125a -/- mice. (A) Flow cytometry analysis of infiltrating neutrophils from lungs of MiR125a +/+ and MiR125a -/- mice challenged with 25 mg/kg LPS after 24 hours. Single cell suspensions of lung cells were previously gated with CD45. Neutrophils were stained with CD11b-Percp cy5.5 and Ly6G-APC. Bar graph shows the average percentage of infiltrating neutrophils (mean+-s.d.,n = 3 mice of each genotype). (B) Hematoxylinand-eosin staining of lung sections from WT and KO mice 24 hours after 25 mg/kg LPS injection. Bar graph is the histopathological severity score of lung sections. Histopathological severity of randomly selected fields from the lung sections were graded as 0 (no findings or normal), 1 (mild), 2 (moderate) or 3 (severe) for each of the four parameters(congestion, edema, hemorrhage and inflammation). Theses results were confirmed by a blinded independent researcher. (C) Serum concentrations of aspartate aminotransferase (ALT), blood urea nitrogen (BUN), creatine kinase (CK) and creatinine (CREA) in MiR125a +/+ and MiR125a -/- mice 24 h after injection of 25 mg/kg LPS (mean+-s.d.,n = 5 mice of each genotype,). (D) Survival of MiR125a +/+ and MiR125a -/- mice (n = 10 each genotype) intraperitoneally challenged with 45 mg/kg LPS. Data are presented as a Kaplan-Meier plot. P   Fig 4 Normal cell death but decreased cell proliferation of in MiR125a -/- neutrophils. (A) Apoptosis of bone marrow neutrophils in MiR125a +/+ and MiR125a -/- mice. 2x10 6 bone marrow cells were cultured in 10% FBS 1640 medium for 48 hours. Flow cytometry analysis of Ly6G + cell apoptosis by using Annexin V and PI staining. The bar graph shows the percentage of Annexin V + neutrophils (mean+-s.d., n = 3). (B-C) Flow cytometry analysis of neutrophils incorporating BrdU in bone marrow (B) and spleen (C) after in vivo pulsing BrdU for 72 hours. Neutrophils were previously gated with CD11b-Percp cy5.5 and Ly6G-APC. Bar graphs indicate the mean percentage of BrdU-incorporating neutrophils (mean+-s.d., n = 3). ns, none significant difference, * P    Fig 5 Decreased proliferation of immature neutrophils in MiR125a -/- mice. (A) Flow cytometry analysis of three subpopulations in CD11b + Gr-1 + neutrophils in bone marrow. Mature neutrophils (mNeu) indicate CD11b hi Gr-1 hi cells. Immature neutrophils (imNeu) indicate CD11b low Gr-1 hi cells and promyelocytes/myelocytes (pro/mye) indicate CD11b int Gr-1 int cells. The bar graph shows the average numbers of these subpopulations in MiR125a +/+ and MiR125a -/- mice. Values were represented as mean+-s.d., n = 5 mice of each genotype. (B) Flow cytometry analysis of three populations of CD11b + Gr-1 + neutrophils incorporating BrdU in bone marrow after in vivo pulsing BrdU for 72 hours. The bar graph indicates the average percentage of intensities of BrdU-incorporating cells (mean+-s.d., n = 5). Ns, none significant difference, * P    Figure 1 Silybin treatment ameliorates lipopolysaccharide (LPS)-induced acute lung injury in mice. Mice were orally administered silybin (50 or 100 mg/kg) once per day for 3 consecutive days prior to LPS sensitization as described in the Materials and methods. (A) Lung tissue were fixed in 4% formalin and subjected to hematoxylin and eosin (H&E) staining. (B) Bronchoalveolar lavage fluid (BALF) from each group was collected and the number of cells in BALF was determined. The cells were then stained with CD3-FITC, CD11b-PE, Gr1-APC and analyzed by FACS. Values were shown as the means +- SD of 8 mice. * P   Figure 2 Deletion of Otulin in Immune Cells Causes Acute Systemic Inflammation in Mice (A) OTULIN immunoblot on immune cells from wild-type mice. NK cell, natural killer cell; DC, dendritic cell; MPhi, macrophage. (B) Schematic representation of mixed bone marrow chimera generation. Wild-type (WT) B6.SJL cells are CD45.1 + , and CreERT2- Otulin flox cells are CD45.2 + . (C) Body weight following i.p. administration of tamoxifen (tx; arrows) to CreERT2- Otulin flox chimeric mice. (D) Neutrophil and lymphocyte counts from blood of CreERT2- Otulin flox chimeras and vehicle-treated controls at day 5 following tamoxifen administration. (E and F) Luminex multiplex analysis of serum cytokines and chemokines from terminal bleeds on day 5 presented as (E) a heatmap of relative changes in concentration of all analytes between CreERT2- Otulin +/flox and CreERT2- Otulin Lac Z/flox chimeras and (F) serum concentrations of cytokines and chemokines increased in CreERT2- Otulin Lac Z/flox chimeras. Data were pooled from two independent experiments. (G and H) Flow cytometry analysis of CD11b + Gr-1 + neutrophils in total cellular infiltrate (CD45.1 + and CD45.2 + ) in peritoneal lavage (PL), spleen, and liver from CreERT2- Otulin flox chimeras presented as (G) representative dot plots with percentage of cells in gate indicated and (H) total cell number. (I) Micrographs of hematoxylin and eosin (H&E) stained sections reveal inflammatory foci (arrowheads) in liver parenchyma. Micrographs are re   Figure 3 Neutralization of TNF Ameliorates Inflammation Caused by OTULIN Deficiency (A-J) Measurements from tamoxifen (tx)-treated (arrows) CreERT2- Otulin flox bone marrow chimeras injected with (A-C) anti-TNF neutralizing antibodies (alphaTNF) (data were pooled from two independent experiments), (D-F) anti-G-CSF-neutralizing antibodies (alphaG-CSF), (G-I) anti-IL-6-neutralizing antibodies (alphaIL-6), or isotype control as indicated. (A, D, and G) Body weight of CreERT2- Otulin flox chimeric mice treated with neutralizing antibodies as indicated. (B, E, and H) Blood neutrophil counts from CreERT2- Otulin flox chimeric mice treated as indicated. (C, F, and I) Total number of infiltrating CD11b + Gr-1 + neutrophils in spleen and peritoneal lavage (PL) measured by flow cytometry from CreERT2- Otulin flox chimeric mice treated as indicated. (J) Heatmap of Luminex multiplex analysis of cytokines and chemokines in serum from terminal bleeds on days 6 or 7 from chimeric mice treated as indicated. Numbers indicate relative change compared to isotype-treated del/flox mice within each experiment. G-CSF levels for alphaG-CSF and alphaIL-6 were measured by ELISA. Asterisks ( * ) indicate the level of statistical significance. (K) Model of TNF-driven systemic inflammation and the contributions from different cytokines in OTULIN-deficient mice. (A-J) Data are presented as mean +- SEM, and n represents number of mice. See also Figure S3 .   Figure S2 Generation of OTULIN-Targeted Mice, OTULIN Expression, Genotyping, and Reconstitution of Bone Marrow Chimeric Mice, Related to Figure 2 (A) Schematic showing the strategy to generate conditional and cell-type-specific knockouts of Otulin . SA, splice acceptor; neo, neomycin-resistance cassette; pA, polyA signal; PGK, murine PGK-1 promoter; DTA, diphtheria toxin A selection cassette; KanR, Kanamycin-resistance cassette. (B) Genotyping of mouse strains. PCR reactions showing the expected products from each genotype. (C) E13.5 embryos stained with X-gal for beta-galactosidase activity and cleared by methyl salicylate shows Otulin promoter activity in multiple tissues. Pictures are representative of five embryos of each genotype from two independent experiments. (D) Immunoblot analysis showing OTULIN expression in multiple tissues from adult wild-type C57BL/6 mice. Blots are representative of three independent experiments. (E) Ratio of CD45.1 + (wild-type B6.SJL) and CD45.2 + (CreERT2- Otulin +/flox or CreERT2- Otulin Lac Z/flox C57BL/6) expressing splenocytes determined by flow cytometry at the termination of chimera experiments. Data were pooled from two independent experiments. (F) Genotyping of bone marrow cells or blood leukocytes from CreERT2- Otulin flox chimeras treated with tamoxifen or vehicle shows complete or near-complete conversion of flox alleles to del alleles upon tamoxifen treatment. Note that WT(+) products are present in all reactions as BJ6.SJL WT c   Figure S5 Flow Cytometry Plots and Quantification of Cell Populations in Mice Lacking Otulin in Myeloid Cells, Related to Figure 5 (A-D) Flow cytometry analysis of (A-B) CD11b + Gr-1 + neutrophils and CD11b + Gr-1 - macrophages, and (C-D) CD8 + T cells in liver, peritoneal lavage (PL), spleen, lung, and kidney from from 4-9 month old LysMCre- Otulin flox mice presented as (A and C) representative dot plots or (B and D) total cell number or frequency of infiltrating cells. Missing graphs of total number of infiltrating cells in (B) and (D) are shown in main Figure 5 D. (A-D) Data were pooled from two independent experiments. Data are presented as mean +- SEM, and n represents number of mice.   Figure 4 Increased survival and reduced cardiac fibrosis in c-Kit TgD814Y mutants after CI. ( a ) Kaplan-Meier survival analysis in c-Kit +/+ ( n =20) and c-Kit TgD814Y ( n =12) mice. Survival of c-Kit TgD814Y mice was statistically significant compared with c-Kit +/+ 5 days after injury (100% c-Kit TgD814Y versus 57% wt). Mice that died during surgery were not considered for the survival curve. ( b ) Timeline showing blood samplings before and after CI and hearts collection. Myocardial regeneration was assessed at 1, 4 and 6 weeks post CI. ( c - e ) Cytofluorimetric analyses on blood samples harvested 1 week before CI and every week until the mice were killed stained for GR-1 and CD11b surface Markers. Representative plotting of GR-1 and CD11b staining of blood harvested from c-Kit +/+ and c-Kit TgD814Y mice 7 days before (upper panels) and 30 days after (lower panels) CI. ( c ) Curves representing the mean values of CD11b + GR-1 + ( d ) and CD11b + GR-1 - ( e ) blood cells ( n =8 mice for each group). Data are reported+-S.E. Significance respect to the first blood sampling either for c-Kit +/+ and c-Kit TgD814Y is reported, # P    Figure 2 Differentiation of iPSCs into Mphi (A) Schematic representation of the three step EB-based protocol employed for hematopoietic differentiation. (1) embryoid bodies (EBs) are formed for 8 days in the presence of 10 ng/ml IL-3 with 30 ng/ml SCF added from day 5 onward; (2) EBs are dissociated to single cells and CD41 + cells are isolated by fluorescence-activated cell sorting; and (3) terminal differentiation is achieved by 10-15 days of adherent culture in the presence of 30% M-CSF containing supernatant (L929 cells). (B) Representative picture of EBs at day 8. Scale bar, 500 mum. (C) Flow cytometric analysis of CD41 expression on day 8 and representative picture of May-Grunwald/Giemsa-stained cytospins of CD41 + cells. Scale bar, 50 mum. (D) Approximately 10-fold increase in cell number during differentiation (independent experiments, n = 3, mean +- SD). (E and F) Representative pictures of (E) BMlin - -Mphi and (F) CD45.1 iPSC-Mphi in bright-field and in May-Grunwald/Giemsa-stained cytospins. Scale bars, 100 mum and 20 mum. (G and H) Exemplary flow cytometry plots for expression of surface markers F4/80, CD11b, CD14, CD11c, Gr-1, CD45.1, CD45.2, CD41, CD3, and B220 on BMlin - -Mphi (G) and CD45.1iPSC-Mphi (H).   Figure 5 Differentiation of miPAP1 into Mphi (A and B) Representative picture of (A) bright-field EBs at day 8 of differentiation (scale bar, 500 mum) and (B) flow cytometric analysis of CD41 expression. (C) Representative pictures of (upper picture; scale bar, 100 mum) bright-field microscopy and (lower picture; scale bar, 20 mum) May-Grunwald/Giemsa-stained cytospins of miPAP1-Mphi. (D) Flow cytometric analysis of surface marker expression (data for F4/80, CD11b, CD14, CD11c, Gr-1, CD45.1, CD45.2, CD41, CD3, and B220).   Fig. 8 Flow cytometry analysis of immune cells in blood and lungs. Blood samples and lungs from infected C57BL/6J (grey bars), CAST/EiJ (green bars) and 129S1/SvImJ (pink bars) mice (1 x 10 1 FFU) were prepared. Cell suspensions were analyzed by flow cytometry on days 0, 3 and 5 p.i.. After excluding dead cells fluorochrome-labeled antibodies were used to differentiate various immune cell populations in blood ( a ) and lungs ( b ): CD4 pos (T helper cells); CD8 pos (cytotoxic cells); CD19 pos (B cells), NKp46 pos (NK cells), CD11b pos Ly6G pos (granulocytes), CD115 pos (monocytes) and F4/80 pos (macrophages). The number of individual cell populations over time (mean +/-SEM) was determined. For each measurement lungs and blood samples from individual animals were used. Data from two independent experiments were combined (n = 6 per time point). Data of different time points were analyzed for statistically significant differences using non-parametric Mann-Whitney- U -test (*: p -value    Figure 4 BMSC exosomes mainly induce the survival of CD11b + Ly6G low Ly6C + cells A. Naive ( n = 3) or 5T33 CD11b + cells ( n = 3) were cultured with BMSC exosomes (BMSC exo, 100 mug/ml) in 5% serum medium for 48 hours and then stained with anti-CD11b-PE-Cy7 and anti-Gr-1-APC. Mean fluorescence intensities of CD11b and Gr-1 were measured by flow cytometry. B. Subpopulations of naive or 5T33 CD11b + cells were determined using anti-Ly6G-PE-Cy7 and anti-Ly6C-APC staining. C. Naive ( n = 3) or D. 5T33 CD11b + cells ( n = 3) were treated with BMSC exosomes (100 mug/ml) in 5% serum medium for 48 hours and then stained with anti-Ly6G-PE-Cy7, anti-Ly6C-APC, and Annexin V-FITC. The percentages of living (Annexin-V - ) cells in Ly6G low Ly6C + and Ly6G high Ly6C int subsets were determined by flow cytometry. * = p    Figure 7 BMSC exosomes activate MDSCs in vivo and enhance their capability of T cell suppression A. 200 mug RGFCS-labeled BMSC exosomes (BMSC exo) or RGFCS control were intravenously injected into week 2 5T33MM mice ( n = 3) for 24 hours. The BM cells were isolated and stained with anti-CD11b-PE-Cy7. Mean florescence intensities of RGFCS in the total BM cells (in average) and CD11b + cells were determined by flow cytometry. B. and C. 200 mug BMSC exosomes or PBS (control) were intravenously injected into week 2 5T33MM mice ( n = 4) for 24 hours. Thereafter, the bone marrow and spleen cells were isolated and stained with anti-CD11b-PE-Cy7, anti-Gr-1-APC, anti-p-Stat3-Alexa Fluor 488, and anti-p-Stat1-PE. Mean fluorescence intensities of (B) p-Stat3 or (C) p-Stat1 in CD11b + Gr-1 + cells were measured by flow cytometry. D. CD11b + cells isolated from 5T33MM mice ( n = 3) were cultured with BMSC exosomes for 48 hours and the concentration of NO in supernatant was measured. E. Splenocytes obtained from naive mice were labeled with CFSE, stimulated with CD3/CD28 Dynabeads, and cultured with indicated ratio of CD11b + cells obtained from week 2 5T33MM mice ( n = 8) intravenously injected with PBS (control) or 200 mug BMSC exosomes. After 3 days of culture, the cells were stained with anti-CD3-PE-Cy7 and 7-AAD and the percentage of proliferating cells within gated CD3 + 7-AAD - cells was determined by flow cytometry. * = p    Figure 3 Differentiation of iPSCs toward the Hematopoietic Lineage (A) Methylcellulose colony assays were performed at the end of the hematopoietic differentiation procedure with cKit + cells purified from cultures initiated by WT, oc/oc , or oc/oc BAC-corrected iPSCs. Pictures on the left represent erythroid (BFU-E), myeloid (CFU-GM and CFU-M), and mixed (CFU-GEMM) colonies obtained from differentiated WT iPSCs; pictures on the right show CFU-GM colonies from one oc/oc and one corrected iPSC clone (scale bars, 400 mum). Colony assays were performed with all nine clones, for a total of 16-30 independent replicates/group (WT, oc/oc , and BAC-corrected). Once scored, some individual colonies were cytospun and stained with May-Grunwald and Giemsa. The insert shows a representative example of a cytospin preparation of a CFU-GEMM colony showing macrophages (M), monocytes (Mo), granulocytes (Gr), and erythrocytes (Er) (scale bar, 50 mum). In other experiments, FACS analysis was performed on pooled colonies to confirm the presence of TER119 + erythroid cells, CD11b + F4/80 + macrophages, TER119 - CD11b + Ly6G + polymorphonucleated (PMN) granulocytes. On the PMN - gate monoblasts, Pro-monocytes and monocytes were defined as CD31 + Ly6C - , CD31 + Ly6C + , and CD31 - Ly6C + , respectively. Three clones for each group (WT, oc/oc and BAC-corrected) were used, and results are pooled (five to 15 independent replicates/group) and shown in the bar graph. (B) Representative FACS analyses sho   Figure 5 Infiltrating cell functions and numbers are reduced in B7-1-deficient mice six months following pristane inoculation. Expression of CD11b, CD11c, Gr1 and CD21 on cells in spleens from each group were detected using FACS. CD86 and MHC-II expression in CD21 + B cells from spleens of each group were also detected using FACS. *P Description: The RB6-8C5 monoclonal antibody reacts with mouse Ly-6G, a 21-25 kDa protein also known as the myeloid differentiation antigen Gr-1. A GPI-linked protein, Gr-1 is expressed by the myeloid lineage in a developmentally regulated manner in the bone marrow. While monocytes only express Gr-1 transiently during their bone marrow development, the expression of Gr-1 on bone marrow granulocytes as well as on peripheral neutrophils is a good marker for these populations.eBioscience testing indicates that in the bone marrow and lysed whole blood, the antibody clone RB6-8C5 also stains cells that express the highest levels of Ly6c (as defined by staining with antibody clone HK1.4). It is recommended that 1A8-Ly6G (cat. 9668) be used when looking at Ly-6G specific targets.Applications Reported: This RB6-8C5 antibody has been reported for use in flow cytometric analysis.Applications Tested: This RB6-8C5 antibody has been tested by flow cytometric analysis of mouse bone marrow cells. This can be used at less than or equal to 0.06 µg per test. A test is defined as the amount (µg) of antibody that will stain a cell sample in a final volume of 100 µL. Cell number should be determined empirically but can range from 10^5 to 10^8 cells/test. It is recommended that the antibody be carefully titrated for optimal performance in the assay of interest.Excitation: 488 nm; Emission: 695 nm; Laser: Blue Laser.Filtration: 0.2 µm post-manufacturing filtered. Granulocytes are a category of white blood cells characterised by the presence of granules in their cytoplasm. They are also called polymorphonuclear leukocytes (PMN or PML) because of the varying shapes of the nucleus, which is usually lobed into three segments. In common parlance, the term polymorphonuclear leukocyte often refers specifically to neutrophil granulocytes, the most abundant of the granulocytes. Granulocytes or PMN are released from the bone marrow by the regulatory complement proteins. 蛋白别名: Granulocyte Marker; Ly-6C1; Ly-6C2; Ly-6G; Ly-6G.1; lymphocyte antigen 6 complex, locus C; lymphocyte antigen 6C precursor (Ly-6C); Lymphocyte antigen 6C1; Lymphocyte antigen 6C2; Lymphocyte antigen 6G; Lymphocyte antigen Ly-6C; lymphocyte differentiation antigen; PML; PMN 基因别名: AA682074; AA959465; Gr-1; Gr1; Ly-6C; Ly-6C.2; Ly-6C1; Ly-6C2; Ly-6G; Ly6c; Ly6c1; Ly6c2; Ly6g Host server : magellan-srch-2-prod-green:8080/10.253.227.78:8080. git-commit: 2cd8645d2fc6bfe4ccb4abfa14772b0a94f68e98 git-url: http://victoria.invitrogen.com:8333/magellan/core.git git-branch: origin/release/1.27.0-2021.08.32-1.0