polyclonal goat anti mouse il 33 antibody (R&D Systems)

R&D Systems is a verified supplier

R&D Systems manufactures this product

About

News

Press Release

Team

Advisors

Partners

Contact

Bioz Stars

Bioz vStars

Buy from Supplier

Structured Review

R&D Systems polyclonal goat anti mouse il 33 antibody

<t>IL-33</t> <t>is</t> not expressed by circulating platelets or MKs. (A-B) Representative immunofluorescence images showing nonspecific IL-33 staining in bone marrow (BM)–derived MKs enriched on BSA gradient (A) and platelet-rich plasma (PRP) (B) from WT and IL-33KO mice. (C) Flow-cytometric detection of IL-33 nonspecific signal in blood platelets from WT and IL-33KO mice (PRP), using an isotype control as a negative reference. (D) Western blot analysis of IL-33 expression in platelets and MK-enriched BM cells, with total lung lysates from WT and IL-33 KO mice used as positive and negative controls, respectively. Following quantification, an equal amount of protein (20 μg) was loaded in each lane. (E) IL-33 promoter activity in total BM cells, blood platelets, and BM MK from IL-33–Citrine reporter mice assessed by flow cytometry. (F) Identification of Citrine + cells as stromal cells (CD41 − CD45 − ) in Citrine reporter mice (Citrine +/+ ) by flow cytometry. Panels A-D used a polyclonal goat anti-mouse IL-33 antibody. FL, full length; IF, immunofluorescence; KO, knockout; mIL, mouse interleukin; SSC-A, side scatter.

Polyclonal Goat Anti Mouse Il 33 Antibody, supplied by R&D Systems, used in various techniques. Bioz Stars score: 94/100, based on 290 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/goat+anti+mouse+il+33/Mouse+IL-33+Antibody/pmc13068832-46-25-30
Average 94 stars, based on 290 article reviews

polyclonal goat anti mouse il 33 antibody - by Bioz Stars, 2026-09

94/100 stars

Images

1) Product Images from "The alarmin interleukin-33 modulates platelet proteome, function, and biogenesis"

Article Title: The alarmin interleukin-33 modulates platelet proteome, function, and biogenesis

Journal: Blood Advances

doi: 10.1182/bloodadvances.2025018363

IL-33 is not expressed by circulating platelets or MKs. (A-B) Representative immunofluorescence images showing nonspecific IL-33 staining in bone marrow (BM)–derived MKs enriched on BSA gradient (A) and platelet-rich plasma (PRP) (B) from WT and IL-33KO mice. (C) Flow-cytometric detection of IL-33 nonspecific signal in blood platelets from WT and IL-33KO mice (PRP), using an isotype control as a negative reference. (D) Western blot analysis of IL-33 expression in platelets and MK-enriched BM cells, with total lung lysates from WT and IL-33 KO mice used as positive and negative controls, respectively. Following quantification, an equal amount of protein (20 μg) was loaded in each lane. (E) IL-33 promoter activity in total BM cells, blood platelets, and BM MK from IL-33–Citrine reporter mice assessed by flow cytometry. (F) Identification of Citrine + cells as stromal cells (CD41 − CD45 − ) in Citrine reporter mice (Citrine +/+ ) by flow cytometry. Panels A-D used a polyclonal goat anti-mouse IL-33 antibody. FL, full length; IF, immunofluorescence; KO, knockout; mIL, mouse interleukin; SSC-A, side scatter.

Figure Legend Snippet: IL-33 is not expressed by circulating platelets or MKs. (A-B) Representative immunofluorescence images showing nonspecific IL-33 staining in bone marrow (BM)–derived MKs enriched on BSA gradient (A) and platelet-rich plasma (PRP) (B) from WT and IL-33KO mice. (C) Flow-cytometric detection of IL-33 nonspecific signal in blood platelets from WT and IL-33KO mice (PRP), using an isotype control as a negative reference. (D) Western blot analysis of IL-33 expression in platelets and MK-enriched BM cells, with total lung lysates from WT and IL-33 KO mice used as positive and negative controls, respectively. Following quantification, an equal amount of protein (20 μg) was loaded in each lane. (E) IL-33 promoter activity in total BM cells, blood platelets, and BM MK from IL-33–Citrine reporter mice assessed by flow cytometry. (F) Identification of Citrine + cells as stromal cells (CD41 − CD45 − ) in Citrine reporter mice (Citrine +/+ ) by flow cytometry. Panels A-D used a polyclonal goat anti-mouse IL-33 antibody. FL, full length; IF, immunofluorescence; KO, knockout; mIL, mouse interleukin; SSC-A, side scatter.

Techniques Used: Immunofluorescence, Staining, Derivative Assay, Clinical Proteomics, Control, Western Blot, Expressing, Activity Assay, Flow Cytometry, Knock-Out

IL-33 deficiency alters the platelet proteome. (A) Proteomic profiling of sorted platelets from WT and IL-33KO mice. (B) Volcano plot comparing IL-33KO and WT platelet proteomes. The x-axis shows log fold change (IL-33KO/WT), and the y-axis shows −log( P -value). Proteins upregulated in IL-33KO platelets are highlighted in blue; downregulated proteins in gray. (C) Number of proteins detected and significantly altered ( P < .03, fold change > 0.2). (D,F) Gene Ontology (GO) analysis of enriched biological processes among upregulated (D) and downregulated (F) proteins ( https://geneontology.org ). (E,G) Heat maps of the top 20 most abundant upregulated (E) and downregulated (G) proteins. Data were obtained from n = 5 mice per group. KO, knockout. Figure created with biorender.com . Blanchard L. (2026) https://BioRender.com/b78qj95 .

Figure Legend Snippet: IL-33 deficiency alters the platelet proteome. (A) Proteomic profiling of sorted platelets from WT and IL-33KO mice. (B) Volcano plot comparing IL-33KO and WT platelet proteomes. The x-axis shows log fold change (IL-33KO/WT), and the y-axis shows −log( P -value). Proteins upregulated in IL-33KO platelets are highlighted in blue; downregulated proteins in gray. (C) Number of proteins detected and significantly altered ( P < .03, fold change > 0.2). (D,F) Gene Ontology (GO) analysis of enriched biological processes among upregulated (D) and downregulated (F) proteins ( https://geneontology.org ). (E,G) Heat maps of the top 20 most abundant upregulated (E) and downregulated (G) proteins. Data were obtained from n = 5 mice per group. KO, knockout. Figure created with biorender.com . Blanchard L. (2026) https://BioRender.com/b78qj95 .

Techniques Used: Knock-Out

IL-33 deficiency impairs platelets adhesion to ECM components. (A) Schematic and (B) analysis of platelet adhesion assays to soluble fibrinogen, with or without ADP (1μM), assessed by flow cytometry. PRP from WT and IL-33 KO mice was analyzed, and results are expressed as a ratio relative to the WT mean. Data were obtained from n = 11 mice per group across 3 independent experiments. (C) Schematic of platelet spreading assays on fixed substrates, analyzed by immunofluorescence in WT and IL-33 KO platelets. Representative images and quantitative analyses of adherent and spreading PRP from WT or IL-33 KO mice on (D) fibrinogen, (E) podoplanin, and (F) laminin at 5 and 15 minutes following ADP (1μM) stimulation. Platelets were stained with CD41-APC. Data were obtained from n = 11 mice per group across 3 independent experiments, except for the laminin spreading assay, which was performed on n = 5 mice in a single experiment. (G-H) Platelet spreading assays without ADP stimulation on fibrinogen (G) and podoplanin (H) at 5 and 15 minutes (n = 7 mice per group per experiment). Statistical analyses were performed using t tests (D-F) and 2-way analysis of variance (ANOVA) with Sidak multiple comparisons test (B). Scale bar, 20 μm. Statistical analysis was conducted using t tests; # P < .05; ## P < .01; ### P < .001; #### P < .0001. IF, immunofluorescence. Figure created with biorender.com . Blanchard L. (2026) https://BioRender.com/z523pur .

Figure Legend Snippet: IL-33 deficiency impairs platelets adhesion to ECM components. (A) Schematic and (B) analysis of platelet adhesion assays to soluble fibrinogen, with or without ADP (1μM), assessed by flow cytometry. PRP from WT and IL-33 KO mice was analyzed, and results are expressed as a ratio relative to the WT mean. Data were obtained from n = 11 mice per group across 3 independent experiments. (C) Schematic of platelet spreading assays on fixed substrates, analyzed by immunofluorescence in WT and IL-33 KO platelets. Representative images and quantitative analyses of adherent and spreading PRP from WT or IL-33 KO mice on (D) fibrinogen, (E) podoplanin, and (F) laminin at 5 and 15 minutes following ADP (1μM) stimulation. Platelets were stained with CD41-APC. Data were obtained from n = 11 mice per group across 3 independent experiments, except for the laminin spreading assay, which was performed on n = 5 mice in a single experiment. (G-H) Platelet spreading assays without ADP stimulation on fibrinogen (G) and podoplanin (H) at 5 and 15 minutes (n = 7 mice per group per experiment). Statistical analyses were performed using t tests (D-F) and 2-way analysis of variance (ANOVA) with Sidak multiple comparisons test (B). Scale bar, 20 μm. Statistical analysis was conducted using t tests; # P < .05; ## P < .01; ### P < .001; #### P < .0001. IF, immunofluorescence. Figure created with biorender.com . Blanchard L. (2026) https://BioRender.com/z523pur .

Techniques Used: Flow Cytometry, Immunofluorescence, Staining

IL-33 deficiency reduces thrombus formation under high shear stress. (A) Schematic representation of the thrombus formation assay on collagen during arterial flow of whole blood from WT or IL-33 KO mice. (B) Representative images and quantitative analysis of thrombus volume, expressed as a percentage relative to the WT mean, formed on collagen under physiological arterial shear rate (1500 s ˗1 ) using whole blood from WT or IL-33 KO mice. (C) Representative images and quantitative analysis of thrombus volume, expressed as a percentage relative to the WT mean, formed on collagen under pathological arterial shear rate (3000 s ˗1 ) using whole blood from WT or IL-33 KO mice. Data are representative of 3 independent experiments (n = 4-5 mice/group). Statistical analysis was performed using 2-way ANOVA with Sidak multiple comparisons test, # P < .05. Investigators were blinded to genotype during the thrombus formation assay. Figure created with biorender.com . Blanchard L. (2026) https://BioRender.com/tt7i113 .

Figure Legend Snippet: IL-33 deficiency reduces thrombus formation under high shear stress. (A) Schematic representation of the thrombus formation assay on collagen during arterial flow of whole blood from WT or IL-33 KO mice. (B) Representative images and quantitative analysis of thrombus volume, expressed as a percentage relative to the WT mean, formed on collagen under physiological arterial shear rate (1500 s ˗1 ) using whole blood from WT or IL-33 KO mice. (C) Representative images and quantitative analysis of thrombus volume, expressed as a percentage relative to the WT mean, formed on collagen under pathological arterial shear rate (3000 s ˗1 ) using whole blood from WT or IL-33 KO mice. Data are representative of 3 independent experiments (n = 4-5 mice/group). Statistical analysis was performed using 2-way ANOVA with Sidak multiple comparisons test, # P < .05. Investigators were blinded to genotype during the thrombus formation assay. Figure created with biorender.com . Blanchard L. (2026) https://BioRender.com/tt7i113 .

Techniques Used: Shear, Tube Formation Assay

IL-33 treatment in vivo modifies platelet morphology and activation, expands the MK-biased LT-HSC pool, and enhances platelet release within lung capillaries. (A) Schematic overview of the IL-33 treatment protocol: WT mice received 3 intranasal doses of recombinant human IL-33 or PBS. (B) Flow cytometry analysis of platelet morphology in WT mice following IL-33 or PBS treatment. (C) Quantification of platelet counts by flow cytometry in IL-33- or PBS-treated WT mice. Data are from n = 14 mice per group, collected across 3 independent experiments. (D) Flow cytometry assessment of platelet degranulation, measuring alpha granule (P-selectin) and dense granule (CD63) expression after IL-33 or PBS administration. (E) Plasma levels of sCD40L, measured by ELISA in IL-33–treated or PBS-treated WT mice. (D-E) Data are from n = 8 to 9 mice per group, collected across 2 independent experiments. (F) Quantification of BM LT-HSC, separated into CD41 ˗ (canonical) and CD41 + (MK-biased) populations, shown as a percentage of LSK cells. Data are obtained from n = 22 mice per group, collected across 5 independent experiments. (G) Lung intravital microscopy was performed in PF4-mTmG mice treated with IL-33 or PBS, 24 hours after the first (IL-33 1×) or third (IL-33 3×) administration to assess MKs/proplatelets generating platelets. (H) Representative time-lapse intravital lung microscopy images showing PF4 + small proplatelets and large proplatelet/MK structures releasing platelets within pulmonary capillaries. Scale bar, 50 μm. (I-J) Quantification of proplatelet structures producing platelets per hour per ROI in the lung, categorized as small (<200 platelet volume equivalent), medium (200-1000 platelets), and large (>1000 platelets). (K) Total platelet release per hour across the entire lung. Statistical analysis was performed using t test; # P < .05, ## P < .01. A total of n = 5 to 21 videos were analyzed, collected from 3 to 11 mice per group across 5 independent experiments. ns, not significant. Figure created with biorender.com . Blanchard L. (2026) https://BioRender.com/qdgtyov .

Figure Legend Snippet: IL-33 treatment in vivo modifies platelet morphology and activation, expands the MK-biased LT-HSC pool, and enhances platelet release within lung capillaries. (A) Schematic overview of the IL-33 treatment protocol: WT mice received 3 intranasal doses of recombinant human IL-33 or PBS. (B) Flow cytometry analysis of platelet morphology in WT mice following IL-33 or PBS treatment. (C) Quantification of platelet counts by flow cytometry in IL-33- or PBS-treated WT mice. Data are from n = 14 mice per group, collected across 3 independent experiments. (D) Flow cytometry assessment of platelet degranulation, measuring alpha granule (P-selectin) and dense granule (CD63) expression after IL-33 or PBS administration. (E) Plasma levels of sCD40L, measured by ELISA in IL-33–treated or PBS-treated WT mice. (D-E) Data are from n = 8 to 9 mice per group, collected across 2 independent experiments. (F) Quantification of BM LT-HSC, separated into CD41 ˗ (canonical) and CD41 + (MK-biased) populations, shown as a percentage of LSK cells. Data are obtained from n = 22 mice per group, collected across 5 independent experiments. (G) Lung intravital microscopy was performed in PF4-mTmG mice treated with IL-33 or PBS, 24 hours after the first (IL-33 1×) or third (IL-33 3×) administration to assess MKs/proplatelets generating platelets. (H) Representative time-lapse intravital lung microscopy images showing PF4 + small proplatelets and large proplatelet/MK structures releasing platelets within pulmonary capillaries. Scale bar, 50 μm. (I-J) Quantification of proplatelet structures producing platelets per hour per ROI in the lung, categorized as small (<200 platelet volume equivalent), medium (200-1000 platelets), and large (>1000 platelets). (K) Total platelet release per hour across the entire lung. Statistical analysis was performed using t test; # P < .05, ## P < .01. A total of n = 5 to 21 videos were analyzed, collected from 3 to 11 mice per group across 5 independent experiments. ns, not significant. Figure created with biorender.com . Blanchard L. (2026) https://BioRender.com/qdgtyov .

Techniques Used: In Vivo, Activation Assay, Recombinant, Flow Cytometry, Expressing, Clinical Proteomics, Enzyme-linked Immunosorbent Assay, Intravital Microscopy, Microscopy

IL-33 in vivo treatment alters platelet proteome, modulating inflammatory and coagulation-related pathways. (A) Proteomic profiling of sorted platelets from WT mice treated with PBS or recombinant (rIL-33). (B) Volcano plot comparing human rIL-33 and PBS-treated mice platelet proteomes. The x-axis shows log fold change (IL-33KO/WT), and the y-axis shows ˗log( P -value). Proteins upregulated in IL-33 treated mice platelets are highlighted in orange; downregulated proteins in gray. (C) Number of proteins detected and significantly altered ( P < .03, fold change > 0.2). (D,F) Gene Ontology (GO) analysis of enriched biological processes among upregulated (D) and downregulated (F) proteins ( https://geneontology.org ). (E,G) Heat maps of the top 20 most abundant upregulated (E) and downregulated (G) proteins. Data represent n = 10 mice per group, collected from 2 independent experiments. Figure created with biorender.com . Blanchard L. (2026) https://BioRender.com/og48c3y .

Figure Legend Snippet: IL-33 in vivo treatment alters platelet proteome, modulating inflammatory and coagulation-related pathways. (A) Proteomic profiling of sorted platelets from WT mice treated with PBS or recombinant (rIL-33). (B) Volcano plot comparing human rIL-33 and PBS-treated mice platelet proteomes. The x-axis shows log fold change (IL-33KO/WT), and the y-axis shows ˗log( P -value). Proteins upregulated in IL-33 treated mice platelets are highlighted in orange; downregulated proteins in gray. (C) Number of proteins detected and significantly altered ( P < .03, fold change > 0.2). (D,F) Gene Ontology (GO) analysis of enriched biological processes among upregulated (D) and downregulated (F) proteins ( https://geneontology.org ). (E,G) Heat maps of the top 20 most abundant upregulated (E) and downregulated (G) proteins. Data represent n = 10 mice per group, collected from 2 independent experiments. Figure created with biorender.com . Blanchard L. (2026) https://BioRender.com/og48c3y .

Techniques Used: In Vivo, Coagulation, Recombinant

Staining:

Article Title: Foxp3 and Bcl6 deficiency synergistically induces spontaneous development of atopic dermatitis-like skin disease.
Article Snippet: 1Laboratory of Pharmaceutical Immunology, Department of Medicinal and Life Sciences, Faculty of Pharmaceutical Sciences, Tokyo University of Science, Noda, Chiba 278-8510, Japan 2Department of Applied Biological Science, Faculty of Science and Technology, Tokyo University of Science, Noda, Chiba 278-8510, Japan 3Laboratory of Molecular Medical Science, Department of Medicinal and Life Sciences, Faculty of Pharmaceutical Sciences, Tokyo University of Science, Noda, Chiba 278-8510, Japan 4Division of Immunology, Health Science Faculty, International Centre for Genetic Engineering and Biotechnology (ICGEB), Cape Town Component & Institute of Infectious Diseases and Molecular Medicine (IDM), University of Cape Town, Cape Town 7701, South Africa 5Division of Integrated Research, Research Institute for Biomedical Sciences, Tokyo University of Science, Noda, Chiba 2780022, Japan

Incubation:

Article Title: Complement-producing adventitial fibroblasts form an IL-33 alarmin hub that maintains ILC2s during airway allergy.
Article Snippet: .. After blocking, the primary antibodies: goat anti-mouse IL-33 (R&D Systems; AF3626-SP) 10 μg/mL, rabbit anti-mouse COL1A1 (Cell Signaling Technology; 28368) 1:100, rat anti-mouse GATA3 (BioLegend; 386902) 1:100, Armenian Hamster anti-mouse CD3e (eBioscience; 14-0031-82) 1:100, Alpaca GFP-Booster (ChromoTek; gb2AF488) 1:500, were incubated overnight at 4 ◦ C. Before adding secondary antibodies, the sections were washed three times with 0.5% Triton X-100/PBS. .. The secondary antibodies, donkey anti-rat 647 (Invitrogen; A78947), donkey anti-goat Alexa Fluor 488 (Invitrogen- A32814), donkey anti-goat Alexa Fluor 647 (Invitrogen; A21447), goat anti-Armenian hamster Alexa Fluor 568 (Invitrogen; A78965), were incubated for 1–2 h at room temperature, followed by 0.5% Triton X-100/PBS washes.

Blocking Assay:

Immunopeptidomics:

Article Title: Immunomodulatory Functions of Intercalated Cells in Kidney Autoimmunity
Article Snippet: Cryosections of 5, 10, or 16 μm thickness were generated using a Reichert Frigocut microtome and mounted on Fisherbrand Superfrost Plus slides (Fisher Scientific, Pittsburgh, PA). .. The primary antibody panel included rat anti-mouse-F4/80 , rabbit anti-V-ATPase B1 subunit , rat anti MHC Class II (I-A/I-E) (0.2 μg/mL, M5/114.15.2, 12-5321-81, Thermo Fisher Scientific), rat anti AQP1 (200 μg/mL, sc-32737, Santa Cruz Biotechnology), goat anti-mouse-IgG1 (1mg/mL, A10551, Invitrogen), goat anti-mouse-IgG2c (0.8mg/mL, 115-035-208, Jackson ImmunoResearch), donkey anti-mouse-IgM (0.8mg/mL, 715-035-020, Jackson ImmunoResearch), Armenian Hamster anti-mouse-CD3 (0.5mg/mL, 100303, Bioegend), rat anti-mouse-IgD (0.5mg/mL, 405702, Biolegend), goat anti-mouse-CD20 (0.5mg/mL, sc-7735, Santa Cruz), goat anti-mouse IL-33 (0.2 mg/mL; Polyclonal; AF3626, R&D Systems), rat anti-mouse CD138 (0.2 mg/ml; Clone 281-2, 563192, BD Biosciences) and Alexa Fluor 488 rat anti-mouse-CD45 (0.5mg/ml; Clone 30-F11, 103121, BD Biosciences). .. Secondary antibodies comprised Alexa Fluor 488 goat anti-rabbit IgG (1:800 dilution; 111-545-144, Jackson ImmunoResearch), DyLight 649 goat anti-hamster (STAR104D649, AbD Serotec), Cy3 donkey anti-rabbit IgG (7.5 μg/ml; 711-165-152, Jackson ImmunoResearch), Cy3 donkey anti-rat IgG (1:800 dilution; 712-166-153, Jackson ImmunoResearch), Alexa Fluor 647 donkey anti-mouse (1:800 dilution; 715-606-151, Jackson ImmunoResearch), Cy3 donkey anti-goat IgG (1:800 dilution; 705-166-147, Jackson ImmunoResearch), Cy3 donkey anti-goat IgG(H+L) (1:800 dilution; 705-165-147, Jackson ImmunoResearch), Alexa Fluor 488 Donkey Anti-Goat IgG (H+L) (1.5mg/ml; 705-545-147, Jackson ImmunoResearch).

Western Blot:

Article Title: Natterin-Induced Neutrophilia Is Dependent on cGAS/STING Activation via Type I IFN Signaling Pathway
Article Snippet: After running, the proteins were transferred to a nitrocellulose membrane (Novex, no. IB301001, Thermo Fisher Scientific) using the iBlot Dry Blotting system (no. 10072147, Invitrogen Thermo Fisher Scientific, Waltham, MA, USA) for 7 min or by the traditional transfer method using Mighty Small Transphor (Sigma-Aldrich Chemie GmbH, no. 80620426). .. Specific proteins were detected according to Grund et al. [ ] using the goat anti-mouse IL-33 (processed form: 18 to 20 kDa, no. 842875 at 1 μg/mL, R&D Systems, Inc., Minneapolis, MI, USA) followed by the second antibody donkey anti-goat IgG-HRP (no. sc 2033 at 1/2000, Santa Cruz Biotechnology Inc., Dallas, TX, USA) and anti-β-tubulin (no. IMG-5810A at 0.6 μg/mL, IMGENEX, Novus Biologicals LLC, Littleton, CO, USA) followed by secondary antibody mouse anti-rabbit IgG HRP True Blot (no. 18-8816-33 at 1/500, Rockland, Hamburg, Germany) for 3 h on the iBindTM Flex Western System apparatus using iBind Cards (Invitrogen Thermo Fisher Scientific, no. SLF2010). .. The development was performed by adding an ECL chemiluminescence kit (Novex, no. WP20005, Thermo Fisher Scientific) mixing equal parts of substrates solution.

Immunostaining:

Article Title: Eosinophils regulate intra-adipose axonal plasticity
Article Snippet: .. Primary antibodies used for immunostaining were rabbit anti-TH (Millipore catalog no. AB152, RRID: AB_390204), rabbit anti-STMN2 (Novus Biologicals catalog no. NBP1-49461, RRID: AB_10011568), mouse anti-Tuj1 (BioLegend catalog no. 801202, RRID: AB_10063408), rabbit anti-Tuj1 (Cell Signaling Technology catalog no. 5568, RRID: AB_10694505), rabbit anti-PGP9.5/UCHL1 (Proteintech catalog no. 14730–1-AP, RRID: AB_2210497), goat anti-VAChT (Millipore catalog no. ABN100, RRID: AB_2630394), rabbit anti-UCP1 (Abcam catalog no. ab10983, RRID: AB_2241462), goat anti-mouse IL-33 (R&D Systems catalog no. AF3626, RRID: AB_884269), goat anti-human IL-33 (R&D Systems catalog no. AF3625, RRID: AB_1151900), mouse anti-human Siglec-8 (BioLegend catalog no. 347102, RRID: AB_2239311), rat anti-Siglec-F-PE (BD Biosciences catalog no. 552126, RRID: AB_394341), rat anti-mouse CD45-PE (BioLegend catalog no. 103106, RRID: AB_312971), rat anti-human CD45-FITC (BioLegend catalog no. 368508, RRID: AB_2566368), rat anti-CD31 (BD Biosciences catalog no. 553370, RRID: AB_394816). .. In addition, Alexa Fluor dye–conjugated secondary antibodies were from Thermo Fisher Scientific.

Membrane:

Article Title: CEBPA restricts alveolar type 2 cell plasticity during development and injury-repair
Article Snippet: For immunofluorescence, the following antibodies were used: rabbit anti-CCAAT/enhancer binding protein alpha (C/EBPA, 1:500, 8178P, Cell Signaling Technology), chicken anti-green fluorescent protein (GFP, 1:5000, AB13970, Abcam), rabbit anti-NK homeobox 2-1 (NKX2-1, 1:1000, sc-13040, Santa Cruz), rabbit anti-pro-surfactant protein C (SFTPC, 1:1000, AB3786, Millipore), goat anti-SOX9 (SOX9, 1:1000, AF3075, R&D Systems), rabbit ani-SOX9 (SOX9, 1:1000, AB5535, Millipore). .. Goat Anti-Mouse Il-33 (IL33, 1:500, R&D, AF3626). rabbit anti-homeodomain only protein (HOPX, 1:500, sc-30216, Santa Cruz). mouse anti-homeodomain only protein (HOPX, 1:250, sc-398703 AF647, Santa Cruz). rat anti-KI67 (KI67, 1:1000, 14-5698-82, Invitrogen), guinea pig anti-lysosomal associated membrane protein 3 (LAMP3, 1:500, 391005, SySy), rat anti-epithelial cadherin (ECAD, 1:1000, 13190, Invitrogen). .. The following antibodies were used for FACS: PE/Cy7 rat anti-CD45 (CD45, 1:250, 103114, BioLegend), PE rat anti-epithelial cadherin (ECAD, 1:250, 147304, BioLegend), BV421 rat anti-epithelial cell adhesion molecule (EPCAM, 1:250, 118225, BioLegend), and AF647 rat anti-Intercellular adhesion molecule 2 (ICAM2, 1:250, A15452, Thermo Fisher).

Review