Lysm cre

Manufactured by Jackson ImmunoResearch

Sourced in United States, Montenegro, Germany

LysM-Cre is a Cre recombinase transgene that is expressed under the control of the lysozyme M (LysM) gene promoter. The LysM gene is selectively expressed in myeloid lineage cells, including macrophages and neutrophils. The LysM-Cre transgene can be used to achieve conditional gene deletion or activation in these cell types.

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LysM-Cre mice (105 citations) LysM-Cre (B6.129P2-Lyz2tm1(cre)Ifo/J) mice (13 citations) LysM-Cre transgenic mice (8 citations) Lysozyme M (LysM)-cre mice (4 citations) C57Bl/6 LysM-Cre mice (3 citations) C57Bl/6J LysM-Cre mice (2 citations) CMV-Cre or LysM-Cre mice (2 citations) C57BL/6J LysM-Cre (2 citations) LysM-cre knock in mice (2 citations) B6.129P2-Lyz2tm1(cre)lfo/J (LysM-Cre) mice (2 citations)

106 protocols using lysm cre

Generating Viable LysM-Cre:PPARγ Knockout Mice

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LysM-Cre (The Jackson Laboratory, 4781) and PPARγ^fl (The Jackson Laboratory, 4584) mice on a C57BL/6 background were interbred to generate viable homozygous LysM-Cre:PPARγ^fl/fl animals. PPARγ deletion was confirmed by PCR for DNA analysis and Western blotting for analysis of PPARγ protein expression. The parental strains were maintained in-house and used as controls. For therapeutic studies, wild-type female C57BL/6J mice were obtained from The Jackson Laboratory at 5 weeks of age and used at 9 to 12 weeks of age.

Goyal G., Wong K., Nirschl C.J., Souders N., Neuberg D., Anandasabapathy N, & Dranoff G. (2018). PPARγ Contributes to Immunity Induced by Cancer Cell Vaccines That Secrete GM-CSF. Cancer immunology research, 6(6), 723-732.

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Piezo1 Overexpression and Knockdown in Mice

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All animal procedures were approved by the Institutional Animal Care and Use Committees of The Scripps Research Institute (TSRI). All animals were housed in the same vivarium conditions at a constant temperature of 20^oC, with a 12 hour light/dark cycle.
Constitutive, RBC-specific, and macrophage specific GOF Piezo1 mice were generated by breeding mice with conditional GOF Piezo1 allele with Cmv-cre (The Jackson Laboratory stock# 006054), EpoR-cre (a gift from Dr. Klingmuller group at Max-Planck-Institute für Immunbiologie, Freiburg, Germany), and LysM-cre (The Jackson Laboratory stock# 004781). All GOF Piezo1 mice were generated at Taconic, Hudson, NY, and maintained on C57BL/6 background (Ma et al., 2018 ). Heterozygous GOF mice were used for the experiments, unless mentioned otherwise. Macrophage-specific LOF Piezo1 mice were generated by breeding mice with conditional LOF Piezo1 allele (The Jackson Laboratory stock# 029213) with the same LysM-cre. All cre driver mice were on C57BL/6 background or were backcrossed at least 10 generations to C57BL/6. Littermates with a mix of equal number of male and female mice were used for experiments. Aging mice (12months to 18months old) born from same breeders were used in the experiments.

Ma S., Dubin A.E., Zhang Y., Mousavi S.A., Wang Y., Coombs A., Loud M., Andolfo I, & Patapoutian A. (2021). A role of PIEZO1 in iron metabolism in mice and humans. Cell, 184(4), 969-982.e13.

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Characterization of Il-27 Knockout Mice

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All animal studies were approved by the Duke University Institutional Animal Care and Use Committee under protocols A175-14-07, A156-17-06, and A107-20-05. C57BL6/J (The Jackson Laboratory, Stock #000664, Bar Harbor, ME), Il-27p28fl/fl;LysMCre^+/^-, Il-27p28^EGFP mice and their littermates or Il-27p28fl/fl mice were used for control. Il-27p28^EGFP mice were kindly generated (14 (link)) and provided by Dr. Ross M. Kedl. Il-27p28fl/fl mice (33 (link)) were kindly provided by Drs. Zhinan Yin (Biomedical Translational Research Institute, Jinan University) and Li Fan Lu (University of California San Diego). These mice were bred with LysMCre mice (The Jackson Laboratory, Stock #004781) to generate Il-27p28fl/fl;LysMCre^+/^- in our laboratory. Mice were maintained under regulated conditions with food and water ad libitum in the pathogenic-free facility at Duke University.

Suwanpradid J., Lee M.J., Hoang P., Kwock J., Floyd L.P., Smith J.S., Yin Z., Atwater A.R., Rajagopal S., Kedl R.M., Corcoran D.L., Zhang J.Y, & MacLeod A.S. (2021). IL-27 Derived From Macrophages Facilitates IL-15 Production and T Cell Maintenance Following Allergic Hypersensitivity Responses. Frontiers in Immunology, 12, 713304.

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Conditional Inactivation of Gnas in Mice

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All animal experiments were performed in accordance with the relevant regulations and guidelines and were approved by the Institutional Animal Care and Use Committee (IACUC), University of Pennsylvania.
CreERT2 mice (Jackson Laboratories, stock no. 008463) [12 (link)] were crossed to Gnas^fl/fl mice [4 (link)–8 (link)] to generate CreERT2;Gnas^fl/+ mice which were subsequently crossed with Gnas^fl/fl mice to obtain CreERT2;Gnas^fl/fl mice. Cre-negative mice from the same litters were used as controls. At 4 weeks of age, mice were injected intraperitoneally with tamoxifen dissolved in corn oil (1 mg/100 μl) on three successive days at 50 μg/g body weight. Three mice were harvested at 4 weeks and at 6 weeks post-injection. LysM-Cre mice (Jackson Laboratories, stock no. 004781) [13 (link)] were crossed with Gnas^fl/fl mice to generate LysM-Cre;Gnas^fl/+ mice which were subsequently crossed with Gnas^fl/fl mice to obtain LysM-Cre;Gnas^fl/fl mice and Cre-negative (Gnas^fl/fl) control mice. Mice were analyzed at 3–4 weeks of age by histology and at 12 weeks by micro-computed tomography. Both male and female mice were used in these studies. All mouse lines were maintained on a C57BL/6 background (crosses used mice from Jackson Laboratories, stock no. 000664).

Ramaswamy G., Fong J., Brewer N., Kim H., Zhang D., Choi Y., Kaplan F.S, & Shore E.M. (2017). Ablation of Gsα signaling in osteoclast progenitor cells adversely affects skeletal bone maintenance. Bone, 109, 86-90.

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Genotyping Ndel1-flox and LysM-Cre Mice

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Ndel1-flox (129S-Ndel1^tm2hr, stock number 026958) and LysM-Cre (B6.129P2-Lyz2^tm1(cre)Ifo, stock number 004781) mice on 129Sv and C57BL6 background, respectively, were procured from The Jackson Laboratory (Bar Harbor, ME, USA). Homogenous floxed mice of Ndel1 in C57BL6 background were generated by backcrossing 129Sv mice with C57BL6 mice for greater than ten generations. Mice were genotyped for Ndel1-flox and LysM-Cre using primers and protocol provided by The Jackson Laboratory.

Das B.K., Gogoi J., Kannan A., Gao L., Xing W., Mohan S, & Zhao H. (2021). The Cytoplasmic Dynein Associated Protein NDE1 Regulates Osteoclastogenesis by Modulating M-CSF and RANKL Signaling Pathways. Cells, 11(1), 13.

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TIM-3 Conditional Knockout Mouse Model

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Six-to eight-week-old C57BL/6, Cd11c^cre, Zbtb46^cre, Cd4^cre, E8i^cre, Lysm^cre, Cx3cr1^cre and Foxp3-ERT2^cre mice were purchased from the Jackson Laboratory. Havcr2^fl/fl mice were generated as described in supplementary materials. TIM-3 conditional knockout mice were generated by crossing to the above cre lines. For knockin/knockout alleles (Lysm^cre) the appropriate controls were used; that is, Havcr2^fl/+ × Lysm^cre+/−, for all other cre lines fl/fl mice were used as controls. For experiments with Foxp3-ERT2^cre mice, mice were orally gavaged with 8 mg tamoxifen 3 days before tumour implantation and every 3 days thereafter for the duration of the experiments. Havcr2^+/+Foxp3-ERT2^cre were used as an additional wild-type control but results were comparable to Havcr2^fl/fl and were therefore not included. Deletion efficiency was determined by flow cytometry (not shown). Animal experiments were done in accordance with the guidelines of the institutional Animal Care and Use Committee (IACUC) at Brigham and Women’s Hospital and Harvard Medical School. All animals were euthanized before reaching humane endpoint, with tumour growth no greater than 2 cm in any one direction or of a total of 400 mm² overall. Mice of both sexes were used throughout the study; sex-matched and age-matched (8–12 weeks) controls were used in individual experiments.

Dixon K.O., Tabaka M., Schramm M.A., Xiao S., Tang R., Dionne D., Anderson A.C., Rozenblatt-Rosen O., Regev A, & Kuchroo V.K. (2021). TIM-3 restrains anti-tumour immunity by regulating inflammasome activation. Nature, 595(7865), 101-106.

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Genetically Modified Mouse Models for Investigating LRP5/6 Signaling

Cited 3 times

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Lrp5^-/- [42 (link)] and Lrp5^a214v(neo)/+ [21 (link)] mice were generated as described. Lrp5^fl/fl and Lrp6^fl/fl [22 (link)], Flk1^Breier-Cre [30 (link)], Rx-Cre [23 (link)] and CD11b-Cre [29 (link)] mice were kindly provided by Drs. Bart O. William, Kevin P. Campbell, Eric Swindell and Roland Baron, respectively. VE-Cad-Cre [24 (link)], Tie2-Cre [25 (link)], LysM-Cre [28 (link)] and tdTomato [27 (link)] mice were purchased from the Jackson Laboratory. Flk1^Breier-Cre, Rx-Cre, CD11b-Cre, VE-Cad-Cre and Tie2-Cre mice were all transgenic lines generated by fusing the Cre gene to a fragment of the promoter sequence of Flk1, Rx, CD11b, VE-Cad and Tie2, respectively. LysM-Cre mice were knock-ins, generated by targeted insertion of the Cre cDNA into the endogenous M lysozyme locus. When animals from different genetic backgrounds were crossed, littermate controls were used to avoid confounding effects.

Huang W., Li Q., Amiry-Moghaddam M., Hokama M., Sardi S.H., Nagao M., Warman M.L, & Olsen B.R. (2016). Critical Endothelial Regulation by LRP5 during Retinal Vascular Development. PLoS ONE, 11(3), e0152833.

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Conditional Deletion of Pfkfb3 in Myeloid Cells

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Mice were used in accordance with the protocol approved by the Institutional Animal Care and Use Committee of Augusta University. The floxed Pfkfb3 (Pfkfb3^flox/flox) mice were generated by Xenogen Biosciences Corporation (Cranbury, NJ, USA) (14 (link)). Myeloid-specific Pfkfb3 knockout was achieved by cross-breeding Pfkfb3^flox/flox mice with Lysm-Cre mice (stock no. 004781, The Jackson Laboratory, Bar Harbor, ME, USA) to generate Pfkfb3^flox/flox; Lysm-Cre (Pfkfb3^ΔMϕ) mice. All mice were on a C57BL/6J background.

Xu J., Wang L., Yang Q., Ma Q., Zhou Y., Cai Y., Mao X., Da Q., Lu T., Su Y., Bagi Z., Lucas R., Liu Z., Hong M., Ouyang K, & Huo Y. (2021). Deficiency of Myeloid Pfkfb3 Protects Mice From Lung Edema and Cardiac Dysfunction in LPS-Induced Endotoxemia. Frontiers in Cardiovascular Medicine, 8, 745810.

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Myeloid-Specific C/EBPα Deletion in Tumor Microenvironment

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All mouse studies have been conducted according to Animal Welfare Act and the Public Health Service Policy and approved by Vanderbilt University Institution Animal Care and Use Committee (IACUC) and NCI. The animals were housed in pathogen-free units, in compliance with IACUC regulations. C57BL/6 J and LysMCre mice were purchased from Jackson Labs. Mice with a floxed Cebpa gene, called Cebpa^flox/flox, were developed as described^{26 (link)}. We generated mice with myeloid-specific deletion of Cebpa by breeding Cebpa^flox/flox mice to LysMCre mice, which express Cre recombinase under the control of murine lysozyme M promoter. C/EBPα^flox/flox;LysMCre (+/−) (CebpaΔ/Δ) and littermate control mice C/EBPα^flox/flox; LysMCre (−/−) (WT) were used in the study.
The 32D myeloid cell line, Lewis lung cancer derivative cell line (3LL), B16 melanoma cell line and HUVECs were purchased from ATCC and maintained per standard cell culture techniques.
B16 or 3LL cells (5 × 10⁵ cells), with or without purified Gr1+CD11b+ cells (0.5 × 10⁵ cells), were injected subcutaneously (s.c.) into the left flank of C57Bl/6 mice. The size of tumors was determined by measurement of tumor dimensions at 2–3 day intervals using a caliper. The equation volume = length × (width)² × 0.5 was used to calculate tumor volume.

Mackert J.R., Qu P., Min Y., Johnson P.F., Yang L, & Lin P.C. (2017). Dual negative roles of C/EBPα in the expansion and pro-tumor functions of MDSCs. Scientific Reports, 7, 14048.

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Generation of STAT3 Myeloid Knockout Mice

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Mice homozygous for the loxP-flanked (floxed) Stat3 gene (STAT3^fl/fl) were kindly gifted from Dr S Akira. Mice carrying a Cre transgene under the control of the distal LysM promoter (LysM-Cre^+/+) were purchased from the Jackson Laboratory (Bar Harbor, ME). Mice with a STAT3 deletion in myeloid cells were generated by crossing mice with the floxed STAT3 allele with mice expressing Cre under the control of the LysM promoter. Genomic DNA was isolated from tail tips using a NucleoSpin genomic DNA purification kit (Macherey-Nagel GmbH, Duren, North Rhine-Westphalia, Germany). The PCR reaction was performed using AccuPower PCR premix (Bioneer, Daejeon, Korea) with the primers, which are specific for exons 22 and 23 of STAT3 and Cre transgene, according to the manufacturer’s instructions. All experiments were performed with male mice aged 8–10 weeks. Experimental animals were maintained under specific pathogen-free conditions and 22±1 °C with a reversed 12 h light–dark cycle (lights on at 0700 h). All experimental procedures were reviewed and approved by the Institutional Animal Care and Use Committee at the College of Medicine, Seoul National University.

Kwon S.H., Han J.K., Choi M., Kwon Y.J., Kim S.J., Yi E.H., Shin J.C., Cho I.H., Kim B.H., Jeong Kim S, & Ye S.K. (2017). Dysfunction of Microglial STAT3 Alleviates Depressive Behavior via Neuron–Microglia Interactions. Neuropsychopharmacology, 42(10), 2072-2086.

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