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Tlr4 knockout mice

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TLR4 knockout mice are a laboratory animal model in which the Toll-like receptor 4 (TLR4) gene has been genetically modified to be non-functional. TLR4 is a key receptor involved in the innate immune response to various pathogens. The absence of a functional TLR4 receptor in these mice can be used to study the role of TLR4 signaling in different biological processes.

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Lab products found in correlation

Nod scid nod cg prkdcscid mice, by Jackson ImmunoResearch (2 mentions) C57bl 6 cd45.1 pepboyj, by Japan SLC (2 mentions) Rompun, by Bayer (1 mentions)

Spelling variants of this product

Tlr4−/− mice (12 citations) C57BL/10 TLR4 knockout mice (TLR4−/−; C57BL/10ScNJ) (2 citations)

5 protocols using tlr4 knockout mice

1

Myeloid-Specific FAK Knockout Mice

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The generation of myeloid-specific conditional FAK knockout mice and their control littermates have been described previously [26] (link). TLR4 knockout mice were purchased from Jackson Laboratories (stock # 007227) and gp91phox−/− mice were a kind gift from Dr. Borna Mehrad, University of Virginia, Charlottesville, VA. Mice were kept in pathogen-free conditions and allowed free access to food and water.
Owen K.A., Meyer C.B., Bouton A.H, & Casanova J.E. (2014). Activation of Focal Adhesion Kinase by Salmonella Suppresses Autophagy via an Akt/mTOR Signaling Pathway and Promotes Bacterial Survival in Macrophages. PLoS Pathogens, 10(6), e1004159.
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2

Congenic Murine Transplantation Model

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C57BL/6-CD45.2 and C57BL/6-CD45.1 (PepboyJ) mice were purchased from Japan SLC, Sankyo-Lab Service, Jackson Laboratories (000664, 002014), or bred in-house. For congenic transplantation experiments, 8–12 week-old male mice were used as donors and 8–12 week-old female mice were used as recipients. TLR2-knockout mice, TLR4-knockout mice, and NOD/Scid (NOD.Cg-Prkdcscid) mice were purchased from Jackson Laboratories (004650, 007227, 005557, and 001303, respectively). NG (NOD.Cg-Prkdcscid Il-2rγnull/SzJ) mice were purchased from In Vivo Science Inc. All mice were housed in a specific pathogen-free (SPF) condition with free access to food and water. All animal protocols were approved by the Animal Care and Use Committee of the Institute of Medical Science University of Tokyo, the Animal Care and Use Committee of RIKEN Tsukuba Branch, and/or the Administrative Panel on Laboratory Animal Care at Stanford University.
Wilkinson A.C., Ishida R., Kikuchi M., Sudo K., Morita M., Crisostomo R.V., Yamamoto R., Loh K.M., Nakamura Y., Watanabe M., Nakauchi H, & Yamazaki S. (2019). Long-term ex vivo hematopoietic stem cell expansion affords nonconditioned transplantation. Nature, 571(7763), 117-121.
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3

Congenic Murine Transplantation Model

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C57BL/6-CD45.2 and C57BL/6-CD45.1 (PepboyJ) mice were purchased from Japan SLC, Sankyo-Lab Service, Jackson Laboratories (000664, 002014), or bred in-house. For congenic transplantation experiments, 8–12 week-old male mice were used as donors and 8–12 week-old female mice were used as recipients. TLR2-knockout mice, TLR4-knockout mice, and NOD/Scid (NOD.Cg-Prkdcscid) mice were purchased from Jackson Laboratories (004650, 007227, 005557, and 001303, respectively). NG (NOD.Cg-Prkdcscid Il-2rγnull/SzJ) mice were purchased from In Vivo Science Inc. All mice were housed in a specific pathogen-free (SPF) condition with free access to food and water. All animal protocols were approved by the Animal Care and Use Committee of the Institute of Medical Science University of Tokyo, the Animal Care and Use Committee of RIKEN Tsukuba Branch, and/or the Administrative Panel on Laboratory Animal Care at Stanford University.
Wilkinson A.C., Ishida R., Kikuchi M., Sudo K., Morita M., Crisostomo R.V., Yamamoto R., Loh K.M., Nakamura Y., Watanabe M., Nakauchi H, & Yamazaki S. (2019). Long-term ex vivo hematopoietic stem cell expansion affords nonconditioned transplantation. Nature, 571(7763), 117-121.
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4

Comparative Evaluation of Murine Immunology

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Seven- to eight-week-old C57BL/6 and BALB/c female mice were purchased from KOATECH (Pyeongtaek, Korea) and maintained in a specific pathogen-free biosafety level-2 facility at the Korea Research Institute of Bioscience and Biotechnology (KRIBB). TLR4 knockout mice were purchased from The Jackson Laboratory (Bar Harbor, Maine, USA). Only 8- to 12-week-old female mice were used in this study. All animal experiments were approved by the Institutional Animal Use and Care Committee of KRIBB (KRIBB-AEC-19173) and performed in accordance with the Guide for the Care and Use of Laboratory Animals published by the US National Institutes of Health.
Kim C.U., Lim D., Kim Y.S., Ku B, & Kim D.J. (2023). Influenza viral matrix 1 protein aggravates viral pathogenicity by inducing TLR4-mediated reactive oxygen species production and apoptotic cell death. Cell Death & Disease, 14(3), 228.
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5

Resistin's Effects on Mouse Brain

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Adult male C57BL6J mice (27-32 g) and TLR-4-knockout mice (Jackson Laboratories) were treated with resistin or vehicle via intracerebroventricular infusion during 3 days. Briefly, mini-osmotic pumps (model 2002; Alzet, Charles River, L'Arbresle, France) were implanted under ketamine (150 mg/kg; Vibrac, Lyon, France)/xylazine (5 mg/kg; Rompun; Bayer) anesthesia. Brain infusion cannulas were stereotaxically placed into the lateral brain ventricle. The osmotic pumps were housed in a subcutaneous pocket on the dorsal surface of the animal. The mice were then infused with either vehicle or resistin (1.2 µg/12 µL/day; pumping rate 0.5 µL/h) for 3 days. All animals were overnight starved and then were killed (n = 6, per group). The hypothalami were manually dissected and immediately frozen into liquid nitrogen and conserved at -80°C. The quality of the dissection was verified by the measurement of POMC and NPY expression known to be specific to the hypothalamus. All procedures were conducted according to the guidelines of laboratory animal care and were approved by the local government commission for animal research: Ethics Committee for animal experimentation of Paris Center and South # 59 (France), with authorization # 91-467.
Miao J., Benomar Y., Al Rifai S., Poizat G., Riffault L., Crépin D, & Taouis M. (2018). Resistin inhibits neuronal autophagy through Toll-like receptor 4. The Journal of endocrinology, 238(1).
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