Nlrp3

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Nlrp3−/−, is a type of genetically modified mouse that has a disruption in the Nlrp3 gene. This gene is involved in the formation of the NLRP3 inflammasome, a protein complex that plays a role in the immune response. The Nlrp3−/− mouse is a useful tool for studying the function of the NLRP3 inflammasome in various biological processes.

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NLRP3−/− mice (19 citations) NLRP3 KO mice (4 citations) NLRP3 KO (4 citations) B6.Nlrp3−/−, (2 citations) Nlrp3−/− C57BL/6J female mice (2 citations) B6.129S6-Nlrp3™1Bhk/J (2 citations) NLRP3 KO (B6.129S6-Nlrp3/Jtm1Bhk) (2 citations)

33 protocols using nlrp3

Genetic Manipulation of Mouse Autophagy

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Wild-type C57BL/6 mice and mice with floxed Atg7 (Atg7F/F) [37 (link)], with hepatic deletion of Atg7 (Atg7−/− mice) [15 (link)], with constitutively activated Nrf2 (CaNRF2) [47 (link)], or with Alb-Cre expression [48 (link)] (The Jackson Laboratory, Cat#003574) have been described previously. These mice were further crossed with mice deficient in Caspase-11(The Jackson Laboratory, Cat#024698), in Nlrp3 (The Jackson Laboratory, Cat#021302), or in Gasdermin D [14 (link)] to generate Atg7/Caspase11 −/− or Atg7/Nlrp3 −/−, or Atg7/GsdmD −/− doubly deficient mice as previously described [3 (link)]. Both male and female mice were used at the ages between 6-12 weeks. Mice were housed in a pathogen-free facility and were maintained on a 12-hour light/12-hour dark cycle with free access to food and water. The Institutional Animal Care and Use Committee (IACUC) of Tulane University and Indiana University approved all animal studies.

Khambu B., Cai G., Liu G., Bailey N.T., Mercer A.A., Baral K., Ma M., Chen X., Li Y, & Yin X.M. (2023). NRF2 transcriptionally regulates Caspase-11 expression to activate HMGB1 release by Autophagy-deficient hepatocytes. Cell Death Discovery, 9, 270.

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Myeloid-specific Sirt1 Deficiency Mice

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C57BL/6 (Orient Bio) and Nlrp3^-/- (Jackson Laboratory) mice were bred at Yonsei University College of Medicine under specific pathogen-free conditions. To obtain myeloid-specific Sirt1-deficient mice (Sirt1^fl/fl;LysM Cre mice), homozygous Sirt1^fl/fl mice (C57BL/6) were crossed with LysM Cre transgenic mice (C57BL/6, Jackson laboratory). Mice aged 9–12 weeks were used in the experiments. All experimental procedures were approved by the Institutional Ethical Committee, Yonsei University College of Medicine. Animal experiments were performed in accordance with the guidelines of the Institutional Ethical Committee. Mice were shaved 24 h prior to injection, and intradermally administered with FK866 (7 mg/kg) once a day, for two consecutive days. After the last FK866 injection, ATP was intradermally administered (12.5 mg/kg) at the same injection site. Six hours after ATP injection, the mice were sacrificed and subjected to various analyses.

Shim D.W., Cho H.J., Hwang I., Jung T.Y., Kim H.S., Ryu J.H, & Yu J.W. (2021). Intracellular NAD+ Depletion Confers a Priming Signal for NLRP3 Inflammasome Activation. Frontiers in Immunology, 12, 765477.

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Genetic Manipulation for Inflammasome Study

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Aim2^−/−, Nlrp3^−/−, Il18^−/−, Caspase-1^−/− (Caspase-1/11^−/−) and WT (C57Bl6/J) mice were purchased from Jackson Laboratory. Il1β^−/− mice (Shornick et al., 1996 (link)) were kindly shared by Dr. Chandrashekhar Pasare at UT Southwestern. All mice are maintained in a specific pathogen free (SPF) facility. All studies were approved by the Institutional Animal Care and Use Committee (IACUC) of UT Southwestern Medical Center and were conducted in accordance with the IACUC guidelines and the National Institutes of Health Guide for the Care and Use of Laboratory Animals. All experiments were conducted with sex and age-matched mice and both male and female mice were included.

Hu S., Peng L., Kwak Y.T., Tekippe E.M., Pasare C., Malter J.S., Hooper L.V, & Zaki M.H. (2015). The DNA Sensor AIM2 Maintains Intestinal Homeostasis via Regulation of Epithelial Antimicrobial Host Defense. Cell reports, 13(9), 1922-1936.

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Genetically Engineered Mice for Immunology

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The Vsig4-deficient (Vsig4^−/−) mice were provided by M. van Lookeren Campagne (Department of Immunology, Genentech, CA, USA). Nlrp3^−/− (#017970), Il-1R1^−/− (#003245), and C57BL/6 WT were purchased from the Jackson laboratory (Bar Harbor, Maine, USA). The Ms4a6d^−/− mice were generated by Cyagen Biosciences (Guangzhou, China) using the CRISPR/Cas9 technique (fig. S10). Vsig4^−/− mice were crossed with Nlrp3^−/− and Il-1R1^−/− mice to develop Vsig4^−/−Nlrp3^−/− and Vsig4^−/−Il-1R1^−/− DKO mice. All mice were backcrossed 10 times onto the B6 background to avoid unpredictable confounders. Mice were maintained in microisolator cages, fed with standard laboratory chow diet and water, and housed in the animal colony at the animal center of the Third Military Medical University (TMMU). All animals received humane care according to the criteria outlined in the Guide for the Care and Use of Laboratory Animals prepared by the National Academy of Sciences and published by the National Institutes of Health (NIH publication 86-23, revised 1985). All of the experiments comply with the animal study protocol approved by the Laboratory Animal Welfare and Ethics Committee of the TMMU (no. SYXK-PLA-20120031).

Huang X., Feng Z., Jiang Y., Li J., Xiang Q., Guo S., Yang C., Fei L., Guo G., Zheng L., Wu Y, & Chen Y. (2019). VSIG4 mediates transcriptional inhibition of Nlrp3 and Il-1β in macrophages. Science Advances, 5(1), eaau7426.

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Intranasal Pneumococcal Infection in Mice

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Wild-type C57BL/6J mice and congenic knockout mice (muMT^-/-, Tlr2^-/-, Nod2^-/-, Ifnar^-/-, Ccr2^-/-, Il1r^-/-, Nlrp3^-/-) were obtained from Jackson Laboratories (Bar Harbor, ME), and bred and maintained in a conventional animal facility. The Il1a^-/- and Il1b^-/- mice were generously provided by Dr. Yoichiro Iwakura at the Tokyo University of Science [23 (link)]. Pups were housed with a dam until weaned at the age of 3.5 weeks. During colonization, all mice appeared healthy and demonstrated normal weight gain similar to uninfected controls.
Pups at day 4 of life were infected with 10³−10⁴ CFU of S. pneumoniae in 3 μl PBS by intranasal (i.n.) instillation divided over both nares without the use of anesthesia. At the time points indicated following challenge, mice were euthanized by CO₂ asphyxiation followed by cardiac puncture. The trachea was lavaged with 200 μl sterile PBS collected from the nares to determine URT colonization density of S. pneumoniae. A second URT lavage with 600 μL RLT lysis buffer (Qiagen) + 1% β-mercaptoethanol was performed to obtain host RNA from the URT epithelia for gene expression analyses.

Kuipers K., Lokken K.L., Zangari T., Boyer M.A., Shin S, & Weiser J.N. (2018). Age-related differences in IL-1 signaling and capsule serotype affect persistence of Streptococcus pneumoniae colonization. PLoS Pathogens, 14(10), e1007396.

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Murine Plasmodium Infection Model

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Female mice of C57BL/6 (WT), Aim2^−/−, Casp1^−/−, Myd88^−/−, Nlrp3^−/−, Il1r1^−/− and Zbtb46-DTR mice were purchased from The Jackson Laboratory. Traf3^flox/flox mice were kindly gifted from Dr. Shao-Cong Sun (University of Texas, MD Anderson Cancer Center) and cross with CD11c-cre (The Jackson Laboratory) to generate Traf3^f/f CD11c-cre mice, Irf3^−/−:Irf7^−/− mice were from Dr. Kate Fitzgerald (University of Massachusetts Medical School) and Dr. Tadatsugo Taniguchi (The University of Tokyo), and crossed with C57BL/6 mice to get Irf3^−/− mice. For plasmodium infection, 0.5 × 10⁶ iRBCs (otherwise, indicated specifically in the figure legend) suspended in 200 µl PBS from the donor mice were intraperitoneally injected into experimental mice. All mouse-related procedures were performed according to experimental protocols approved by the Animal Care and Welfare Committee at Houston Methodist Research Institute and in accordance with NIH-approved animal study protocol LMVR-11E.

Yu X., Du Y., Cai C., Cai B., Zhu M., Xing C., Tan P., Lin M., Wu J., Li J., Wang M., Wang H.Y., Su X.Z, & Wang R.F. (2018). Inflammasome activation negatively regulates MyD88-IRF7 type I IFN signaling and anti-malaria immunity. Nature Communications, 9, 4964.

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Genetic Knockout Mice for Inflammation

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The p47^phox-deficient (p47^phox-/-, #004742), NLRP3^-/- (#017970), Caspase-1^-/- (#016621), IL-18^-/- (#004130), IL-1R1^-/- (#003245) and wild type (WT) mice were on C57BL/6 background and were purchased from the Jackson Laboratory (Bar Harbor, Maine, USA). Mice were maintained in micro-isolator cages, fed with standard laboratory chow diet and water, and housed in the animal colony at the animal center of the Third Military Medical University (TMMU). Mice approximately 12 weeks of age were used for these experiments. All animals received humane care according to the criteria outlined in the "Guide for the Care and Use of Laboratory Animals" prepared by the National Academy of Sciences and published by the National Institutes of Health (NIH publication 86–23 revised 1985).

Guo S., Yang C., Diao B., Huang X., Jin M., Chen L., Yan W., Ning Q., Zheng L., Wu Y, & Chen Y. (2015). The NLRP3 Inflammasome and IL-1β Accelerate Immunologically Mediated Pathology in Experimental Viral Fulminant Hepatitis. PLoS Pathogens, 11(9), e1005155.

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Genetically Engineered Mouse Models for Inflammasome Study

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C57BL/6, Nlrp3^−/−, Nlrp6^−/− and Nlrp12^−/− mice were purchased from Jackson Laboratories. Asc^−/− (Pycard^−/−) mice were provided by Millennium Pharmaceuticals. Caspase-1 deficient mice (Casp1^−/−) were provided by A. Hise (Case Western Reserve), Ctsb^−/− by T. Reinheckel (University of Freiburg) and Ctsl^−/− by H. Ploegh (MIT). Aim2^+/+ and Aim2^−/− were generated as described in Ref. (Rathinam et al., 2010 (link)), Tlr9^−/− mice were a gift of S. Akira (Osaka Univesrity). UNC93B1 mutant (3d) mice were from by B. Beutler (University of Texas Southwestern). Mice 6–8 weeks of age were used in all experiments. All mouse strains were bred and maintained under specific pathogen-free conditions at the University of Massachusetts Medical School.

Kalantari P., DeOliveira R.B., Chan J., Corbett Y., Rathinam V., Stutz A., Latz E., Gazzinelli R.T., Golenbock D.T, & Fitzgerald K.A. (2014). Dual engagement of the NLRP3 and AIM2 inflammasomes by plasmodial-derived hemozoin and DNA during malaria. Cell reports, 6(1), 196-210.

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NLRP3 Knockout Mice: C57Bl/6 Model

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All experiments were performed on age-matched, 8- to 10-week-old male mice on a C57Bl/6 background. C57Bl/6 (WT controls) and NLRP3^−/− animals were purchased from the Jackson Laboratory and housed under SPF conditions. C57Bl/6 germ-free mice were bred at the University of Utah, and sterility was checked by anaerobic and aerobic microbial plating and PCR. All animal use was in compliance with federal regulations and guidelines set by the University of Utah’s Institutional Animal Care and Use Committee (protocol #14-05009).

Chiaro T.R., Soto R., Stephens W.Z., Kubinak J.L., Petersen C., Gogokhia L., Bell R., Delgado J.C., Cox J., Voth W., Brown J., Stillman D.J., O’Connell R.M., Tebo A.E, & Round J.L. (2017). A member of the gut mycobiota modulates host purine metabolism exacerbating colitis in mice. Science translational medicine, 9(380), eaaf9044.

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Genetically Modified Mice Protocols

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All protocols for animal care were approved by the Institutional Animal Care and Use Committee of the University of Pennsylvania. Unless otherwise specified, mice were 4 to 12 wk of age at the time of experimentation. While age and sex were controlled for each experiment, male and female mice were used indiscriminately for experiments as we have not seen a difference in infection. C57BL/6, Casp1/11^−/−, Asc^−/−, Casp11^−/−, Aim2^−/−, Nlrp1b^−/−, Nlrp3^−/−, and Il18^−/− mice were purchased from Jackson Laboratories. Nlrc4^−/−, Il1α^−/−, and Il1β^−/− mice were provided by Sunny Shin, University of Pennsylvania, Philadelphia, PA. Nlrp6^−/− mice were obtained from Maayan Levy, University of Pennsylvania, Philadelphia, PA, but originated from the laboratory of Richard Flavell, Yale University, New Haven, CT. Casp1^fl/fl and Casp1^fl/fl-vilCRE mice were bred in-house.

Sateriale A., Gullicksrud J.A., Engiles J.B., McLeod B.I., Kugler E.M., Henao-Mejia J., Zhou T., Ring A.M., Brodsky I.E., Hunter C.A, & Striepen B. (2020). The intestinal parasite Cryptosporidium is controlled by an enterocyte intrinsic inflammasome that depends on NLRP6. Proceedings of the National Academy of Sciences of the United States of America, 118(2), e2007807118.

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