Mouse igg1

Manufactured by BioXCell

Sourced in United States

Mouse IgG1 is a type of immunoglobulin G (IgG) antibody derived from mice. It is a commonly used laboratory reagent for various applications in immunology research and biochemical assays.

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Lab products found in correlation

Rat igg1, by BioXCell (3 mentions) Mouse igg2a, by BioXCell (3 mentions) Rat igg2b, by BioXCell (2 mentions) Rat igg2a, by BioXCell (2 mentions) Anti igf 1 ab, by R&D Systems (1 mentions) Anti ifn γ ab clone xmg1, by BioXCell (1 mentions) Armenian hamster igg, by BioXCell (1 mentions) Tumor necrosis factor (tnf), by R&D Systems (1 mentions) Tweak, by R&D Systems (1 mentions) Il 17a, by BioXCell (1 mentions) Il 17a, by R&D Systems (1 mentions) Cyclophosphamide ctx, by Merck Group (1 mentions) Mopc 1, by BioXCell (1 mentions) Ltf 2, by BioXCell (1 mentions) Rb6 8c5, by BioXCell (1 mentions) Anti cd3 cd28 dynabeads, by Thermo Fisher Scientific (1 mentions) Anti cd3 okt3, by Thermo Fisher Scientific (1 mentions) Belatacept, by Bristol-Myers Squibb (1 mentions) Anti pd 1 clone rmp1 14, by BioXCell (1 mentions) P erk, by Cell Signaling Technology (1 mentions)

Spelling variants of this product

Mouse IgG1 isotype control (clone MOPC-21, (17 citations) Mouse IgG1 isotype control (13 citations) Mouse IgG1 (clone MOPC-21; (7 citations) Mouse IgG1 isotype control antibody (clone MOPC-21) (7 citations) InVivoMAb mouse IgG1 isotype control (4 citations) Mouse IgG1 isotype control antibody (MOPC21, (3 citations) Mouse IgG1 (MOPC-21), (3 citations) Mouse IgG1 isotype control (MOPC-21; unknown specificity) (2 citations) Mouse IgG1 GIR-208 (2 citations) Anti-mouse IgG1 isotype control (clone MOPC-21) (2 citations)

13 protocols using mouse igg1

Modulating Wound Healing in Mice

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Mouse model of Vγ1D was implemented by intraperitoneal injection of 200 μg anti-Vγ1 Ab (clone 2.11; BioXcell, USA) 3 days before wound excision. Vγ4D was generated by anti-Vγ4 Ab (clone UC3-10A6; BioXcell, USA). Control mice were intraperitoneally administrated isotype control (armenian hamster IgG) (BioXcell, USA). Neutralization mouse models were conducted by injecting subcutaneously into wound margin 0, 1, and 2 days following excision with 20 μg/wound of anti-IGF-1 Ab (R&D Systems, Minneapolis, MN, USA), anti-IL-17A Ab (clone 17F3; BioXcell, USA), anti-IFN-γ Ab (clone XMG1.2; BioXcell, USA), anti-IL-1β Ab (clone B122; BioXcell, USA), anti-IL-23 Ab (clone BE0051; BioXcell, USA), anti-CCL20 Ab (clone 114906; R&D Systems, USA), respectively. IL-17A neutralization of low and high doses was performed by 2 and 200 μg/wound of anti-IL-17A Ab, respectively. Isotype control mice received equivalent doses of isotype Abs subcutaneously. Isotype control Abs of IGF-1, IL-17A, IL-1β, IL-23, CCL20 are poly goat IgG, mouse IgG1, armenian hamster IgG, rat IgG2, and rat IgG1 (BioXcell), respectively. Mouse models of recombinant cytokine addition were generated by subcutaneously injecting rIGF-1/rIL-17A/rIL-1β/rIL-23 (R&D Systems, Minneapolis, MN, USA) with the doses of 2, 20, 200 ng/wound, respectively, in the wound margin. Control mice were administrated with sterile PBS.

Li Y., Wang Y., Zhou L., Liu M., Liang G., Yan R., Jiang Y., Hao J., Zhang X., Hu X., Huang Y., Wang R., Yin Z., Wu J., Luo G, & He W. (2018). Vγ4 T Cells Inhibit the Pro-healing Functions of Dendritic Epidermal T Cells to Delay Skin Wound Closure Through IL-17A. Frontiers in Immunology, 9, 240.

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Neutralizing Antibodies for Mouse Cytokines

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Neutralizing antibodies to mouse TNF (rat anti-mouse; clone XT3.11) and IL-17A (mouse anti-mouse; clone 17F3) were in vivo grade from Bio X Cell (Lebanon, NH, USA). Mouse anti-mouse TWEAK neutralizing antibody (clone mP2D10) was produced by Biogen, Inc. Isotype control antibodies were rat IgG1, mouse IgG1, and mouse IgG2a, all from Bio X Cell (Lebanon, NH, USA) for the TNF, IL-17A and TWEAK neutralizing antibodies, respectively. All recombinant human cytokines, TWEAK, TNF, and IL-17A, were from R&D Systems (Minneapolis, MN, USA).

Gupta R.K., Gracias D.T., Figueroa D.S., Miki H., Miller J., Fung K., Ay F., Burkly L, & Croft M. (2021). TWEAK Functions with TNF and IL-17 on Keratinocytes and is a Potential Target for Psoriasis Therapy. Science immunology, 6(65), eabi8823.

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Antibody characterization and in vivo use

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The 314.8 mAb (mouse IgG1 anti-human ICOS) has been described before.²¹ Isotype controls (mouse IgG1, MOPC-1; rat IgG2b, LTF-2) and anti-Gr1 mAb (rat IgG2b, RB6-8C5) were purchased from BioXcell (West Lebanon, NH, USA). The MT807R1 recombinant Ig consisting of rhesus IgG1k constant regions and CDRs derived from the anti-human CD8 antibody M-T807 grafted into rhesus variable framework regions and was provided by the Nonhuman Primate Reagent Resource (NIH contract HHSN272200900037C and grant RR016001). The antibody was expressed in vitro using serum-free medium and purified by protein-A affinity chromatography. Endotoxin was <1EU/mg. Cyclophosphamide (CTX, Sigma Aldrich) was prepared extemporaneously according to supplier technical data sheet, i.e to 20 mg/ml of injectable water. All reagents were injected intraperitoneally.

Burlion A., Ramos R.N., KC P., Sendeyo K., Corneau A., Ménétrier-Caux C., Piaggio E., Olive D., Caux C, & Marodon G. (2019). A novel combination of chemotherapy and immunotherapy controls tumor growth in mice with a human immune system. Oncoimmunology, 8(7), 1596005.

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Modulating CD4+ T cell subsets

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Fresh or frozen PBMC from healthy donors cells were cultured in 96 well flat-bottomed plates in RPMI supplemented with 10% human AB serum (Mediatech, VA) and 2.4 mM L-glutamine. Frozen PBMC were rested overnight before stimulation. Cells were stimulated with either 1 µg/mL (PBMC) or 2 µg/mL (lymph node T cells) functional grade anti-CD3 (OKT3; eBiosciences) in the presence of belatacept (100 µg/mL; Bristol-Myers Squibb, NY) or human IgG1-Fc control (BioXCell, Lebanon, NH), or with anti-CD3/CD28 Dynabeads (Invitrogen) in the presence of 10 µg/mL anti-CTLA-4 (BN13; BioXCell, Lebanon, NH) or mouse IgG1 (BioXCell, Lebanon, NH), as indicated. Cells were washed twice with media and restimulated with PMA/Iono for 4 h as described above. CD4⁺ T cell subsets were defined by the following gating strategy: CD45RA⁺ Th1, CD4⁺CD45RA⁺IFN-γ⁺; CD45RA⁻ Th1, CD4⁺CD45RA⁻ IFN-γ⁺; CD45RA⁻CCR6⁺ Th17, CD4⁺CD45RA⁻CCR6⁺IL-17⁺. The change in frequency of CD4+ populations was calculated as (% Cytokine⁺ Blockade/% Cytokine⁺ IgG)×100 of the indicated population.

Krummey S.M., Cheeseman J.A., Conger J.A., Jang P.S., Mehta A.K., Kirk A.D., Larsen C.P, & Ford M.L. (2014). High CTLA-4 Expression on Th17 Cells Results in Increased Sensitivity to CTLA-4 Coinhibition and Resistance to Belatacept. American journal of transplantation : official journal of the American Society of Transplantation and the American Society of Transplant Surgeons, 14(3), 607-614.

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B16 and 4T1 Tumor Models for Antibody Blockade

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Cells were washed and resuspended in sterile PBS. For most intravenous and subcutaneous B16 experiments, 2 × 10⁵ cells in 200 μl were injected. For some intravenous injection experiments (noted in figure legend), 2 × 10⁴ B16 cells in 200 μl were injected. For intravenous and subcutaneous 4T1 experiments, 1 × 10⁵ cells in 200 μl were injected. Subcutaneous tumor growth was measured using calipers, and tumor volume was estimated using the formula V = (L*W²)/2. Tumor growth in the lungs from intravenous injection was quantified via macroscopic examination. For antibody blockade experiments, anti-KLRG1 (clone 1F10, generated as described below, 200 μg/mouse), anti-PD-1 (clone RMP1-14, BioXcell Cat# BE0146, 200 μg/mouse), or control antibody (rat IgG2a, BioXcell Cat# BE0089, 200 μg/mouse, mouse IgG1, BioXcell Cat# BE0083, 200 μg/mouse) were intraperitoneally injected on day 7, 10, 13, and 16 post-tumor cell injection. Animals were monitored daily and tumor growth was measured every third day. Animals were euthanized on day 21 post-intravenous injection and on day 19 or 22 post-subcutaneous injection or when tumor volume reached 2000 mm³.

Tata A., Dodard G., Fugère C., Leget C., Ors M., Rossi B., Vivier E, & Brossay L. (2021). Combination blockade of KLRG1 and PD-1 promotes immune control of local and disseminated cancers. Oncoimmunology, 10(1), 1933808.

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Immune Profiling of Tumor Microenvironment

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PD-L1 (1:400; Cell Signaling Technology; #13684), CD47 (1:200; Sigma; HPA044659), GAPDH (1:2000; Cell Signaling Technology; #5174), CD3 (1:200; Thermo Fisher; 14-0038-80), CD4 (1:150; Thermo Fisher; 14-0041-82), CD8 (1:100; Thermo Fisher; 14-0081-82), SIRPα (1:200; Abcam; ab267409), CD20 (1:100; Abcam; ab78237), FoxP3 (1:300; Abcam; ab20034), Ki-67 (1:200; Abcam; ab16667), EGFR (1:50; Cell Signaling Technology; #2085), p-ERK (1:400; Cell Signaling Technology; #3074), total-ERK (1:500; Cell Signaling Technology; #4695), β-catenin (1:200; Abcam; ab32572), CD68 (1:100; Abcam; ab213363), EMA (1:300; Abcam; ab109185), Anti-CD47 antibody (Clone: MIAP301) (100μg/day in vivo; BioXcell), Anti-CD47 antibody (Clone: B6H12) (10μg/mL in vitro and 100μg/day in vivo; BioXcell), isotype control (mouse IgG1, BioXcell).

Liu X., Zhang H., Wang C., Li Z., Zhu Q., Feng Y., Fan J., Qi S., Wu Z, & Liu Y. (2023). Tumor-selective Blockade of CD47 Signaling with CD47 Antibody for Enhanced Anti-tumor Activity in Malignant Meningioma. Current Neuropharmacology, 21(10), 2159-2173.

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Depletion and inhibition of viral infection

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Mice were infected with 10⁷ PFUs intranasally (i.n.) for WR and subcutaneously (s.c.; flank skin) for MVA, unless mentioned otherwise. Body weights were measured daily, and animals were sacrificed upon losing more than 30% of their initial weight. For CD8 T cell depletion studies, mice were injected intraperitoneally with 200 μg of anti-CD8β antibody (Clone 53-5.8: BioXCell BE0223) or isotype control (Clone HRPN: BioXCell BE0088) at day −6 and −3 and 100 μg at day 0, 4 and 8 of WR challenge. For IFNAR1 inhibition, 400 μg of anti-IFNAR-1 antibody (Clone MAR1-5A3: BioXCell BE0241) or isotype control (mouse IgG1: BioXCell BE0083) was administered intraperitoneally at 6 h before and after both MVA and WR infection (4 times in total).

Kadoki M., Patil A., Thaiss C.C., Brooks D.J., Pandey S., Deep D., Alvarez D., von Andrian U.H., Wagers A.J., Nakai K., Mikkelsen T.S., Soumillon M, & Chevrier N. (2017). Organism-level analysis of vaccination reveals networks of protection across tissues. Cell, 171(2), 398-413.e21.

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In vivo Murine Klebsiella pneumoniae Infection

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For infection experiments, mice were i.n. challenged with 5 × 10⁴ CFUs of K. pneumoniae in 30 μl of sterile PBS. For in vivo antibody-mediated blocking experiments, mice were intraperitoneally (i.p.) injected with the following antibodies 24–48 h before infection: αMR1 (150 μg/mouse; clone 26.5; Biolegend, Mouse IgG2a), αIFNAR1 (200 μg/mouse; clone MAR1-5A3; BioXCell, Mouse IgG1), αSiglecH (150 μg/mouse; clone 440c; BioXCell, Rat IgG2b), or their respective isotype controls: Mouse IgG2a (150 μg/mouse; clone MOPC-173; Biolegend), Mouse IgG1 (200 μg/mouse; clone MOPC-21; BioXCell), and Rat IgG2b (150 μg/mouse; clone LTF-2; BioXCell). When indicated, MAIT cell expansion in vivo was performed through a repeated i.n. inoculation (3×) of 5-OP-RU (100 μM) and LPS (17.4 μg/mouse; Invivogen).
Bacterial loads were determined by counting CFUs after plating 100-fold dilution series of tissue homogenates obtained from bacteria-infected mice. Colonies were counted at 24 h.

López-Rodríguez J.C., Hancock S.J., Li K., Crotta S., Barrington C., Suárez-Bonnet A., Priestnall S.L., Aubé J., Wack A., Klenerman P., Bengoechea J.A, & Barral P. (2023). Type I interferons drive MAIT cell functions against bacterial pneumonia. The Journal of Experimental Medicine, 220(10), e20230037.

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Evaluating 14-25-9 for HNSCC Tumor Inhibition

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To study the effect of 14-25-9 on tumor growth, we employed PDX models
from two HNSCC patients. Mice were randomly allocated to three groups (n=5). On
day 0, mice were given 250cGy total body irradiation by x-ray (45 (link)). On day 1, mice from two groups were infused IV
with 5 million NK92-NKp44-1-GFP cells. Vehicle group received 15mg/Kg of mouse
IgG1 (BioXcell, USA, cat noBE0083) and treatment group received 15mg/Kg of
14-25-9 IV on day 1 and every other day for 10 days. Both groups also received
10μg/mouse human recombinant IL2 (modified and lab produced) IP in three
rounds- on day 1, 3 and 5. The third group received only the IL2 on the same
schedule. Tumor volumes were measured every other day using digital calipers. At
the end of the experiment on day 10, tumor volumes were measured, mice were
sacrificed, and tumors were excised for further immunohistochemical
analysis.

Kundu K., Ghosh S., Sarkar R., Edri A., Brusilovsky M., Gershoni-Yahalom O., Yossef R., Shemesh A., Soria J.C., Lazar V., Ben-Zion J., Campbell K.S., Elkabets M, & Porgador A. (2019). Inhibition of the NKp44-PCNA Immune Checkpoint Using a mAb to PCNA. Cancer immunology research, 7(7), 1120-1134.

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Anti-TIGIT Antibody Treatment During LCMV Infection

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Mice were injected i.p. with either 100 μg mouse IgG1 (BioXCell) or anti-TIGIT Abs (1G9 or 1B4 clone) as described previously^{31 (link)}. Injections were given on days 0, 2, 4, 10, 17, and 24 after infection if not stated otherwise during chronic LCMV infection. The treatment regimen was shortened accordingly during acute infections.

Schorer M., Rakebrandt N., Lambert K., Hunziker A., Pallmer K., Oxenius A., Kipar A., Stertz S, & Joller N. (2020). TIGIT limits immune pathology during viral infections. Nature Communications, 11, 1288.

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