Ccr5 mice

Manufactured by Taconic Biosciences

Ccr5−/− mice, or chemokine receptor 5 knockout mice, are a laboratory animal model that have a genetic modification resulting in the deletion or inactivation of the Ccr5 gene. The Ccr5 gene encodes the CCR5 protein, which functions as a receptor for certain chemokines and plays a role in immune system processes. These mice are a useful tool for studying the biological functions of the CCR5 protein and its role in various diseases and conditions.

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Lab products found in correlation

Myd88, by Jackson ImmunoResearch (1 mentions) Cxcr2, by Jackson ImmunoResearch (1 mentions) C57bl 6j control, by Jackson ImmunoResearch (1 mentions) Swiss webster mice, by Inotiv (1 mentions) Cxcr1, by Jackson ImmunoResearch (1 mentions) C57bl 6n mice, by Taconic Biosciences (1 mentions) C57bl 6n, by Taconic Biosciences (1 mentions) C57bl 6ntac mice, by Taconic Biosciences (1 mentions) Ccl5 mice, by Jackson ImmunoResearch (1 mentions) B6.129p2 ccl5tm1hso j, by Jackson ImmunoResearch (1 mentions)

3 protocols using ccr5 mice

Murine Models for Immunological Research

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Swiss-Webster mice were purchased from Envigo. C57BL/6J Darc^−/− mice were provided by Dr. G. Scott Worthen (UPenn), re-derived and bred in-house at NYU School of Medicine. C57BL/6J controls were purchased from The Jackson Laboratory and bred in-house. Ccr5−/− mice were purchased from Taconic and bred in-house. Cxcr1−/−, Cxcr2−/−, Ccr2−/− and Myd88−/− mice were purchased from Jackson Laboratory and bred in-house. Experiments with Caspase1/11−/− mice were performed by author E.C., on animals housed at the University of California, Berkeley. Mice were maintained under specific pathogen-free conditions and used age-matched at 4–6 weeks of age for Swiss-Webster mice, and 7–11 weeks of age for C57BL/6J and all C57BL/6J background KO mice (the mice have similar weights at these respective ages). Swiss-Webster experiments were performed with all female mice, and C57BL/6J experiments were performed with female and male (sex-matched) mice. Mice were randomly mixed within their genotypes and sex and then assigned to groups.

Lubkin A., Lee W.L., Alonzo F 3.r.d., Wang C., Aligo J., Keller M., Girgis N.M., Reyes-Robles T., Chan R., O’Malley A., Buckley P., Vozhilla N., Vasquez M.T., Su J., Sugiyama M., Yeung S.T., Coffre M., Bajwa S., Chen E., Martin P., Kim S.Y., Loomis C., Worthen G.S., Shopsin B., Khanna K.M., Weinstock D., Lynch A.S., Koralov S.B., Loke P., Cadwell K, & Torres V.J. (2019). Staphylococcus aureus leukocidins target endothelial DARC to cause lethality in mice. Cell host & microbe, 25(3), 463-470.e9.

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Genetic Manipulation of CCR5 in Mice

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3-month old C57BL/6N and Ccr5 knockout (Ccr5^-/-) mice were purchased from Taconic Farms (Germantown, NY) and tested in a reverse genetic screen (Figure 1—figure supplement 1). Ccr5^-/- mice were then bred with C57BL/6N mice to generate Ccr5^+/-. Experimental WT, Ccr5^+/-, and Ccr5^-/- mice (3 to 5 months old) were generated by intercrossing Ccr5^+/- mice. Littermates were used for all experiments (except the initial reverse genetic screen). Experimental Ccr5-overexpressing transgenic mice were generated and maintained in the C57BL/6N background. Yfp⁺/Ccr5^+/- mice were generated by breeding male Thy1-YFP mice with female Ccr5^+/- mice, and 3 to 6 months old Yfp⁺/Ccr5^+/- mice and their littermates Yfp⁺/Ccr5^+/+ (Yfp⁺/WT) mice were used for the spine density experiment. 10-week-old male C57BL/6N mice were purchased from Taconic Farms (Germantown, NY) for shRNA-cont or shRNA-CCR5 AAV injections and for the V3 loop peptide experiments. Mice were group housed with free access to food and water, and maintained on a 12:12 hr light:dark cycle. All experiments were performed during the light phase of the cycle. All studies were approved by the Animal Research Committee at UCLA and University of Cardiff and carried out in compliance with the United Kingdom’s Animals (Scientific Procedures) Act 1986 where applicable.

Zhou M., Greenhill S., Huang S., Silva T.K., Sano Y., Wu S., Cai Y., Nagaoka Y., Sehgal M., Cai D.J., Lee Y.S., Fox K, & Silva A.J. (2016). CCR5 is a suppressor for cortical plasticity and hippocampal learning and memory. eLife, 5, e20985.

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CCR5 Knockout Mouse Protocol

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Ccr5 knockout (Ccr5^−/−) mice were purchased from Taconic Farms (Germantown, NY; B6.129P2-Ccr5tm1Kuz N10). Experimental WT, Ccr5^+/− and Ccr5^−/− mice (3 to 5 months old) were generated by intercrossing Ccr5^+/− mice. Littermates were used for Ccr5 KO linking test. cFos-tTa mice that express tetracycline transactivator (tTA) protein under the control of the c-Fos (also known as Fos) promoter were maintained in a C57BL/6N background. Ccrl5 knockout (Ccl5^−/−) mice were purchased from Jackson lab (B6.129P2-Ccl5tm1Hso/J). 16-month-old male C57BL/6Nia were purchased from NIA for Ccr5 expression detection and linking test. 11-week-old male C57BL/6N Tac mice were purchased from Taconic Farms (Germantown, NY) for all other experiments. Mice are housed in an AAALAC accredited facility with 12-12 light/dark cycles. Housing conforms to The Guide for the Care and Use of Laboratory Animals, 8th edition. The temperature setpoint is 72 degrees plus or minus 3 degrees; the humidity range is between 30% to 70%. All experiments were performed during the light phase of the cycle. All studies were approved by the Animal Research Committee at UCLA.

Shen Y., Zhou M., Cai D., Filho D.A., Fernandes G., Cai Y., de Sousa A.F., Tian M., Kim N., Lee J., Necula D., Zhou C., Li S., Salinas S., Liu A., Kang X., Kamata M., Lavi A., Huang S., Silva T., Do Heo W, & Silva A.J. (2022). CCR5 closes the temporal window for memory linking. Nature, 606(7912), 146-152.

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