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C57bl 6 lysm cre mice

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The C57Bl/6 LysM-Cre mice are a genetically modified mouse strain that expresses Cre recombinase under the control of the lysozyme M (LysM) promoter. This results in Cre expression in myeloid cells, including macrophages and neutrophils.

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C57BL/6 mice (4025 citations) C57BL/6 (2462 citations) LysM-Cre (106 citations) LysM-Cre mice (105 citations)

3 protocols using c57bl 6 lysm cre mice

1

Generating Tie2-KO Myeloid Cells in Mice

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Tie2-KO mice were generated by breeding C57Bl/6 LysM-Cre mice (Jackson Laboratory, #004781) with Tie2flox/flox mice (26 (link)). C57BL/6 Rosa26-YFPfl/fl mice were crossed with C57Bl/6 LysM-Cre to constitutively label myeloid cells. For all experiments, 8- to 12-week-old mice of both genders were used if not otherwise indicated. Mice were housed in sterile cages, maintained in a temperature-controlled room and fed autoclaved water and food ad libitum. All animals were monitored daily for signs of disease. Ear punches were used for genotyping and tail tips were collected for re-genotyping after experiments. Mice were euthanized by cervical dislocation. All experiments were performed according to the guidelines of the institutional and governmental Animal Care and Use Committees and approved by the Regierungspräsidium Karlsruhe (permits G287/16, DKFZ305, DKFZ370).
Jakab M., Rostalski T., Lee K.H., Mogler C, & Augustin H.G. (2022). Tie2 Receptor in Tumor-Infiltrating Macrophages Is Dispensable for Tumor Angiogenesis and Tumor Relapse after Chemotherapy. Cancer Research, 82(7), 1353-1364.
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2

Genetically Modified Mouse Models

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BALB/c mice of SHIP1 wild type (+/+) or SHIP1 knockout (-/-) were kindly provided by Dr. Gerald Krystal (BC Cancer Research Centre, Vancouver, BC). C57BL/6 STAT3-/- mice were generated by crossing C57BL/6 STAT3flox/flox mice (Dr. Shizuo Akira, Hyogo College of Medicine, Nishinomiya, Japan) with C57BL/6 LysMCre mice (Jackson Laboratory). Offspring of these mice were heterozygous on both alleles, and were then crossed with homozygous STAT3flox/flox mice to generate mice with a genotype of STAT3flox/flox /LysMCre+/-. Then, STAT3flox/flox /LysMCre+/- mice were crossed with STAT3flox/flox mice to generate both STAT3flox/flox /LysMCre+/- mice (STAT3-/- mice) and STAT3flox/flox mice (STAT3+/+ mice) in the same litters. For mRNA analysis and immunoblotting studies, BALB/c mice +/+ or -/- for SHIP1 and C57BL/6 LysMCre mice +/+ or -/- for STAT3 were used. Both male and female were used, aged between 6–20 weeks old. All mice were housed and maintained in accordance with the ethic protocols approved by the University of British Columbia Animal Care Committee.
Samiea A., Yoon J.S., Cheung S.T., Chamberlain T.C, & Mui A.L. (2020). Interleukin-10 contributes to PGE2 signalling through upregulation of EP4 via SHIP1 and STAT3. PLoS ONE, 15(4), e0230427.
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3

Conditional Knockout Mice for AHR and CD39

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C57BL/6, LysM-Cre mice were purchased from Jackson Laboratories. AHRmut mice have been previously described50 . CD39loxP/loxP will be described elsewhere (S.R. and S.C.R., submitted); requests for CD39loxP/loxP should be addressed to S.C.R. (srobson@bidmc.harvard.edu). Mice in which AHR or CD39 is specifically deleted in macrophages were generated by crossing LysM-Cre mice with AHRloxP/loxP or CD39loxP/loxP mice, respectively. The deletion of AHR and CD39 in macrophages was verified by PCR, western blotting and flow cytometry (Supplementary Figs. 3 and 5). Mice were kept in a conventional, pathogen-free facility at the Harvard Institutes of Medicine and the Building for Transformative Medicine. All mouse experiments were carried out in accordance with guidelines prescribed by the Institutional Animal Care and Use Committee at Harvard Medical School.
Takenaka M.C., Gabriely G., Rothhammer V., Mascanfroni I.D., Wheeler M.A., Chao C.C., Gutiérrez-Vázquez C., Kenison J., Tjon E.C., Barroso A., Vandeventer T., de Lima K.A., Rothweiler S., Mayo L., Ghannam S., Zandee S., Healy L., Sherr D., Farez M.F., Prat A., Antel J., Reardon D.A., Zhang H., Robson S.C., Getz G., Weiner H.L, & Quintana F.J. (2019). Control of tumor-associated macrophages and T cells in glioblastoma via AHR and CD39. Nature neuroscience, 22(5), 729-740.
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