Mar1 5a3

Manufactured by BioXCell

Sourced in Lebanon, United States

The MAR1-5A3 is a laboratory equipment product. It is a tool used for cell analysis and manipulation in research settings. The core function of the MAR1-5A3 is to facilitate the study and examination of cellular properties and behaviors.

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Lab products found in correlation

Mopc 21, by BioXCell (11 mentions) Ltf 2, by BioXCell (2 mentions) Rmp1 14, by BioXCell (2 mentions) αcd4 gk1, by BioXCell (2 mentions) Be0241, by BioXCell (1 mentions) Be0083, by BioXCell (1 mentions) Isotype control, by BioXCell (1 mentions) Igg control clone 2a3, by BioXCell (1 mentions) Mcc950, by Selleck Chemicals (1 mentions) Nor noha, by Cayman Chemical (1 mentions) Ifn β, by PBL Assay Science (1 mentions) Cpg odn 2088, by InvivoGen (1 mentions) Il 1β 211 11b, by Thermo Fisher Scientific (1 mentions) Tnf α, by Thermo Fisher Scientific (1 mentions) Cytofix cytoperm buffer, by BD (1 mentions) Anti cd4 antibody clone gk1, by BioXCell (1 mentions) C57bl 6j male mice, by Jackson ImmunoResearch (1 mentions) C57bl 6 mice, by Taconic Biosciences (1 mentions) Il 12, by BioLegend (1 mentions) Rmp1 14, by BioLegend (1 mentions)

Close spelling variants of this product

Clone MAR1-5A3 (5 citations) MAR1–5A3 IFNAR neutralizing antibody (4 citations) Anti-mouse IFNAR1 (Clone: MAR1-5A3) (4 citations) Anti-mouse IFNAR1 antibody (clone MAR1-5A3; (2 citations) IFNAR blocking antibody (clone MAR1–5A3 (2 citations) IFNAR-1) antibody (clone MAR1-5A3, (2 citations) αIFNAR; MAR1-5A3 (2 citations) αIFNAR antibody (MAR1–5A3; (2 citations) Anti-IFNAR1 (MAR1-5A3) (2 citations) Anti-IFNAR1 antibody (clone MAR1-5A3; (2 citations)

25 protocols using mar1 5a3

Evaluating Therapeutic Antibodies Against DENV

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Five or six 6-week old IFN-α/β/γR KO C57BL/6 mice per group were challenged i.p. with 2.0 × 10⁶ FFU of DENV-3 (P12/08) under anesthesia. Twenty hours post challenge, HuMAbs 1F11, 3G9, 3G9-LALA, 3G9-N265A, 3G9-N297A, or isotype control (500 μg/mouse) were injected i.p., and the mice were observed for 20 days. Mice were euthanized for humane purposes if they showed apparent symptoms.
Five 6-week old BALB/c mice per group were injected with 2 mg of anti-type I IFN receptor monoclonal antibody (MAR1-5A3, BioXcell, Lebanon, NH) i.p. at day 1 before initiating the viral challenge with 1.0 × 10⁶ FFU of DENV-2 (NGC) i.p. under anesthesia. Twenty hours post-challenge, HuMAb 3G9, 3G9-N297A, or isotype control (100 μg/mouse) were injected via the i.p route. Blood samples were collected at days 2 and 3 post challenge. Infectious viral particles were subjected to viral titration.

Kotaki T., Kurosu T., Grinyo-Escuer A., Davidson E., Churrotin S., Okabayashi T., Puiprom O., Mulyatno K.C., Sucipto T.H., Doranz B.J., Ono K.I., Soegijanto S, & Kameoka M. (2021). An affinity-matured human monoclonal antibody targeting fusion loop epitope of dengue virus with in vivo therapeutic potency. Scientific Reports, 11, 12987.

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Streptomycin-induced EHEC infection model

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Streptomycin-treated model of EHEC infection was established as described before^{53 (link)}. Briefly, 8–16 weeks old C57BL/6 mice were treated with streptomycin sulphate (5 g/L) in drinking water for 5 days before orally gavaging with 1 × 10¹⁰ CFU EHEC or ΔEhaF. Fecal shedding of bacteria was calculated by serial dilution of fecal slurries and plating. Colon samples collected from a group of mice on days 2 and 3 post infection were homogenized in cold PBS containing protease inhibitor cocktail and the levels of cytokines in the lysates were analyzed by ELISA. Colon samples were also serially diluted and plated to assess bacterial colonization. Survival of animals following infection was assessed in a separate group of mice. For mouse studies with IFNAR antibody treatment, following streptomycin treatment as described above, mice were injected intraperitoneally with 250 µg of isotype control (In vivo Mouse IgG1 isotype control, BE0083, MOPC-21, BioXcell) or anti-IFNAR antibody (In-vivo Mouse monoclonal Anti-mouse IFNAR-1, BE0241, MAR1-5A3, BioXcell)^{70 (link)}. One day after the antibody injection mice were infected with 1 × 10¹⁰ CFU EHEC. The antibody treatment was repeated on day 1 and day 3 post infection. Fecal shedding of EHEC and survival of mice were assessed as described above.

Ta A., Ricci-Azevedo R., Vasudevan S.O., Wright S.S., Kumari P., Havira M.S., Surendran Nair M., Rathinam V.A, & Vanaja S.K. (2023). A bacterial autotransporter impairs innate immune responses by targeting the transcription factor TFE3. Nature Communications, 14, 2035.

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Zika and Supra-Lethal Infection Protocols in Mice

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For Zika infection experiments, we used 4-wk-old mice (C57BL/6) since this facilitated intracranial challenges. In all other experiments, 6–8-wk-old C57BL/6 or BALB/c mice were used. Mice were purchased from The Jackson Laboratory (approximately half males and half females). Mice were immunized intramuscularly (50 µl per quadriceps), subcutaneously (100 µl in the right flank), or intranasally (25 µl per nostril) with the indicated viral vectors. IgG isotype control (MOPC-21) or IFN-I receptor subunit 1 (IFNAR1)–blocking antibodies (MAR1-5A3) were purchased from BioXCell or Leinco and diluted in sterile PBS. 100 µg of antibody was administered, admixed together with each viral vector vaccine (as a single bolus).
Zika challenges were performed intracranially with 10⁴ PFU. Supra-lethal bacterial challenges were performed with either LM-GP33 or LM-OVA at 10⁷ CFU intravenously via lateral tail vein injection using a mouse restrainer. Other viral challenges consisted of 2 × 10⁶ PFU of VV-OVA through the intranasal route, 10⁶ PFU of YFV-17D through the intravenous route, or 10⁶ PFU of MHV coronavirus through the intranasal route. Mice were housed at the Northwestern University Center for Comparative Medicine located in downtown Chicago. All mouse experiments were performed with approval of the Northwestern University Institutional Animal Care and Use Committee.

Palacio N., Dangi T., Chung Y.R., Wang Y., Loredo-Varela J.L., Zhang Z, & Penaloza-MacMaster P. (2020). Early type I IFN blockade improves the efficacy of viral vaccines. The Journal of Experimental Medicine, 217(12), e20191220.

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IFNAR1 Blocking Antibody in Infection

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The IFN receptor (IFNAR1) blocking mAb MAR1-5A3 or isotype control (Bio X Cell) was administered by a single intraperitoneal injection of 2.5 mg mAb the day before infection with B. burgdorferi or the administration of K/B×N serum, Figs 2, 9 (20 (link), 37 (link)).

Ma Y., Bramwell K.K., Lochhead R.B., Paquette J.K., Zachary J.F., Weis J.H., Teuscher C, & Weis J.J. (2014). Borrelia burgdorferi arthritis associated locus Bbaa1 regulates Lyme arthritis and K/B×N serum transfer arthritis through intrinsic control of Type I IFN production. Journal of immunology (Baltimore, Md. : 1950), 193(12), 6050-6060.

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In vivo immune modulation for transcervical challenge

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For in vivo neutrophil depletion, 300 μg anti-L6G clone 1A8 (BioXcell) mAb or control IgG clone 2A3 (BioXcell) were administered intraperitoneally at days −2, 0 and +2, +4, +6 post transcervical challenge. For neutralization of signaling through the IFN-α/β receptor, mice were treated intraperitoneally with 500 μg per mouse of anti-IFNAR1 clone MAR1-5A3 or control IgG clone MOPC-21 (BioXcell) in phosphate-buffered saline (PBS) at days −1 and +1, +3, +5 post transcervical challenge. For neutralization of IFN-γ, 500 μg anti-IFN-γ clone XMG1.2 mAb or control IgG clone TNP6A7 (BioXcell) were administered intraperitoneally at days −1 and +2, +5 post transcervical challenge.

Yang C., Lei L., Collins J.W., Briones M., Ma L., Sturdevant G.L., Su H., Kashyap A.K., Dorward D., Bock K.W., Moore I.N., Bonner C., Chen C.Y., Martens C.A., Ricklefs S., Yamamoto M., Takeda K., Iwakura Y., McClarty G, & Caldwell H.D. (2021). Chlamydia evasion of neutrophil host defense results in NLRP3 dependent myeloid-mediated sterile inflammation through the purinergic P2X7 receptor. Nature Communications, 12, 5454.

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Pulmonary Delivery of Immune Modulators

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Mice were anesthetized with isoflurane and treated i.ph. with 30 – 50μL injection-grade saline containing TLR agonists (10μg CpG ODN 2088, CpG type B, Invivogen, #tlrl-1826; 50μg Pam3CSK4 (Pm3), Invivogen, #vac-pms) or recombinant cytokines (5μg TNFα, PeproTech, #315-01A; 2.0x10⁴U IFNβ, PBL, #12400-1; 200U IL-1α #211-11A, 200U IL-1β #211-11B or both together at 200U total, PeproTech) to allow for pulmonary delivery one week (unless otherwise stated in the figure legends) prior to SCV2 infection. For neutralization of cytokine signaling, mice were i.p. injected with 500μg anti-TNFα (BioXCell clone XT3.11), 500μg anti-IFNAR1 (BioXCell clone MAR1-5A3) and/or 500μg IgG1 isotype control (BioXCell clone MOPC-21) in injection-grade saline. For inhibition of Nlrp3, mice were injected i.p. with 600μg MCC950 (SelleckChem #S7809) on the day of SCV2 infection and again two days later. For inhibition of arginase-1, mice were administered 100μg Nor-NOHA (Cayman Chemical #10006861) i.n. once daily on the day before, the day of, and two days following SCV2 infection.

Baker P.J., Bohrer A.C., Castro E., Amaral E.P., Snow-Smith M., Torres-Juárez F., Gould S.T., Queiroz A.T., Fukutani E.R., Jordan C.M., Khillan J.S., Cho K., Barber D.L., Andrade B.B., Johnson R.F., Hilligan K.L, & Mayer-Barber K.D. (2024). The inflammatory microenvironment of the lung at the time of infection governs innate control of SARS-CoV-2 replication. bioRxiv.

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Intravenous and Intramuscular Vaccine Delivery

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SNP vaccines were prepared in sterile PBS (Gibco) and administered intravenously by tail vein injection (100 μl). For ChAdOx1 vaccinations, viral stocks were thawed on ice and then resuspended in PBS at a concentration that yielded 1 × 10⁸ IU per 100 μl IV dose or 1 × 10⁸ IU per 50μl IM dose. For IFNα receptor blockade, mice were treated 500μg of anti-IFNα receptor 1 antibody (MAR1–5A3; Bio X Cell) in 100μl of PBS via intraperitoneal injection. Mice were also treated with 200μg of anti-PD-L1 antibody in 100μl of PBS via intraperitoneal injection (10F.9G2; BioXcell).

van Dijk K, & Nelson E.B. (2000). Fatty Acid Competition as a Mechanism by Which Enterobacter cloacae Suppresses Pythium ultimum Sporangium Germination and Damping-Off. Applied and Environmental Microbiology, 66(12), 5340-5347.

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Dissecting DC Activation and Tumor Antigen Uptake

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Splenocytes from untreated or Flt3L-treated mice were co-cultured with uninfected or NDV-preinfected GFP⁺ A20 cells at a 4:1 or 1:1 ratio for DC activation and tumor Ag uptake analysis, respectively, for 24 h. DC activation was analyzed by a 25-color spectral flow cytometry panel by staining with the following antibodies: CD132-PE, CD80-PE-Cy7, CD16.2-Pacific Blue, Sca-1-AlexaFluor 700, CCR7-PE-Cy5, MHC1b Qa-2-AlexaFluor 647, TCRβ-BV421, CD49b-BV421, CD317-BV605, F4/80-BV510, XCR1-BV650, PD-L1-BV711, CD25-BV785, Ly6G-BV570, Ly6C-PerCP-Cy5.5, CD169-PEDazzle-594, B220-BV750, CD11b-APC-Cy7, I-Ad-FITC, CD8-Pacific Orange, CD86-BV480, Galectin-9-PerCP-eFluor710, and CD11c-AlexaFluor 532 (details are listed in Supplementary Table 2). Viability was assessed by 7AAD. For T cell activation and T cell and DC blockade experiments splenocytes from Flt3L-treated mice were co-cultured with uninfected or NDV-preinfected A20 cells at a 4:1 ratio. Where indicated, splenocytes were treated with 20 μg/ml Clec9A-blocking antibodies (7H11, BioXCell), 20 μg/ml IFNAR-blocking antibodies (MAR1-5A3, BioXCell) or isotype control antibodies 1 h before co-culture, or 1 μM of the AXL inhibitor R428 (S2841, Selleckchem) 24 h and 30 min before co-culture with A20 cells. Blockade experiments and tumor Ag uptake experiments were analyzed by conventional flow cytometry.

Svensson-Arvelund J., Cuadrado-Castano S., Pantsulaia G., Kim K., Aleynick M., Hammerich L., Upadhyay R., Yellin M., Marsh H., Oreper D., Jhunjhunwala S., Moussion C., Merad M., Brown B.D., García-Sastre A, & Brody J.D. (2022). Expanding cross-presenting dendritic cells enhances oncolytic virotherapy and is critical for long-term anti-tumor immunity. Nature Communications, 13, 7149.

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IFNAR1 Blockade in HFD-Fed Mice

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For the IFNAR1-blockade experiments, 12-week-old male vTreg53 TCR-tg mice were fed with HFD, and were injected i.p. with 250 µg anti-mouse IFNAR1 mAb (BioXCell, clone MAR1–5A3) or mouse IgG1 isotype control (BioXCell, clone MOPC-21) twice a week for 8 weeks. Any effects of the Ab treatments on metabolic parameters were determined 7 weeks after the introduction of HFD, and the mice were euthanized for flow cytometric analysis 8 weeks after HFD introduction.

Li C., Wang G., Sivasami P., Ramirez R.N., Zhang Y., Benoist C, & Mathis D. (2021). Interferon-α-producing plasmacytoid dendritic cells drive the loss of adipose-tissue regulatory T cells during obesity. Cell metabolism, 33(8), 1610-1623.e5.

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Innate Cytokine-Driven CD8+ T Cell Function

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To analyze innate function of naive CD8⁺ T cell subsets, splenocytes or thymocytes from indicated mice were plated in 96-well cell culture plates (1 × 10⁶ cells/well) and cultured for 12–24 h with IL-12 (10 ng/ml), IL-18 (10 ng/ml), and with or without IL-2 (50 ng/ml). In some experiments, spleens of B6 previously transferred with CD44^loLy6C⁻ CD8⁺ Ly5.1/5.2 T cells or spleens of B6 i.p. injected with anti-IFNAR (MAR1-5A3; BioXCell) every other day for 10 days (200–300 μg/once/mice) were used. Cultured cells were harvested and stained for cell surface markers, fixed and permeabilized using BD Cytofix/Cytoperm buffer (BD Biosciences) and then stained with fluorochrome-conjugated anti-IFN-γ antibody. To analyze cytokine production after peptide restimulation, CD5^lo, Ly6C⁻, and Ly6C⁺ CD8⁺ T cells were purified from P14.Rag1^–/– Ly5.1/5.2 mice and transferred to B6 hosts (10⁴ cells/mice). Mice were infected with LCMV (2 × 10⁵ pfu/mice) day after transfer and assessed 7 days later. Splenocytes were prepared from infected mice and plated in 96-well cell culture plate (10⁶ cells/well). Cells were stimulated with titrated dose of gp33 peptide (10⁻⁴–10⁻¹ μM) for 5 h. GolgiPlμg (BD Biosciences) was added after the first hour. Cells were harvested and stained with fluorochrome-conjugated anti-IFN-γ, anti-IL-2, and anti-TNF antibodies as described elsewhere.

Ju Y.J., Lee S.W., Kye Y.C., Lee G.W., Kim H.O., Yun C.H, & Cho J.H. (2021). Self-reactivity controls functional diversity of naive CD8+ T cells by co-opting tonic type I interferon. Nature Communications, 12, 6059.

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