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Lyz2 cre

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Lyz2-Cre is a recombinase enzyme that specifically recognizes and cleaves DNA sequences at loxP sites, enabling targeted gene manipulation in mouse models. It is commonly used in conditional gene knockout studies.

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Lab products found in correlation

C57bl 6j, by Jackson ImmunoResearch (8 mentions) Cd11c cre, by Jackson ImmunoResearch (4 mentions) Cx3cr1cre, by Jackson ImmunoResearch (4 mentions) Mrp8 cre, by Jackson ImmunoResearch (3 mentions) Wild type c57bl 6 mice, by Charles River Laboratories (2 mentions) Ifngr, by Jackson ImmunoResearch (2 mentions) Andcasp1 11, by Jackson ImmunoResearch (2 mentions) B6.129p2 lyz2tm1 cre, by Jackson ImmunoResearch (2 mentions) Sting golden ticket stinggt gt mouse, by Jackson ImmunoResearch (2 mentions) C57bl 6j mice, by Jackson ImmunoResearch (2 mentions) Rag2 il2rg mice, by Taconic Biosciences (2 mentions) Foxp3egfp, by Jackson ImmunoResearch (2 mentions) Arg1fl fl, by Jackson ImmunoResearch (2 mentions) Rorc γt gfp gfp, by Jackson ImmunoResearch (2 mentions) Rosa26floxstop eyfp, by Jackson ImmunoResearch (2 mentions) Wild type c57bl 6j mice, by Jackson ImmunoResearch (2 mentions) Dba 1j, by Jackson ImmunoResearch (2 mentions) Ubc creert2, by Jackson ImmunoResearch (2 mentions) Villin cre, by Jackson ImmunoResearch (2 mentions) C57bl 6 wt, by Jackson ImmunoResearch (2 mentions)

45 protocols using lyz2 cre

1

Myeloid-Specific Notch Regulation in Mice

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Mice were maintained on the C57BL/6 background in a specific pathogen-free facility. RBP-J-floxed (RBP-Jf) mice (12 (link)) or ROSA-Stopf-NIC transgenic mice (14 (link)) were mated with Lyz2-Cre (#019096, Jackson Laboratory) mice to obtain mice with myeloid-specific Notch blockade (Lyz2-Cre-RBP-Jf/f, with Lyz2-Cre-RBP-J+/f as a control) or activation (Lyz2-Cre-ROSA-Stopf-NIC, with ROSA-Stopf-NIC as a control) mice, respectively. Mice were genotyped with tail DNA using polymerase chain reaction (PCR) primers listed in Table S1 in Supplementary Material. All animal experiments were approved by the Animal Experiment Administration Committee of Fourth Military Medical University.
Lin Y., Zhao J.L., Zheng Q.J., Jiang X., Tian J., Liang S.Q., Guo H.W., Qin H.Y., Liang Y.M, & Han H. (2018). Notch Signaling Modulates Macrophage Polarization and Phagocytosis Through Direct Suppression of Signal Regulatory Protein α Expression. Frontiers in Immunology, 9, 1744.
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2

Characterization of C9orf72 and STING Mice

Cited 1 time
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All mice were housed in pathogen-free facilities under 12-h light dark cycles with access to food and water ad libitum. Temperature was set 74°F +/− 2° with humidity 30–70%. C9orf72−/− mice were as previously published7 (link) and wildtype mice were purchased from Jackson Laboratories. C9orf72fl/fl mice were provided by the Pasterkamp lab12 (link) and were crossed with Cx3cr1Cre (B6J.B6N(Cg)-Cx3cr1tm1.1(cre)Jung/J) and Lyz2Cre (B6.129P2-Lyz2tm1(cre)Ifo/J) purchased from Jackson Laboratories to obtain Cx3cr1Cre;C9orf72fl/fl and Lyz2Cre;C9orf72fl/fl mice. The STING golden-ticket (STINGgt/gt) mouse was obtained from Jackson Laboratories (C57BL/6J- Tmem173gt/J). C9orf72−/− mice were crossed with STINGgt/gt to obtain C9orf72−/−;STINGgt/gt mice. All mice have the nuclear background of C57BL/6J. Mice were sex- and age-matched. For all experiments mice were grouped according to genotype. For EAE and B16 melanoma models genotypes were randomly separated into experimental groups. Researchers were blinded when scoring EAE, counting tumor burden in B16 melanoma model. Husbandry and behavioral tests were conducted in accordance with the protocols described by the National Institutes of Health’s Guide for the Care and Use of Animals and were approved by Cedars-Sinai Institutional Animal Care and Use Committees (IACUC #8161).
McCauley M.E., O’Rourke J.G., Yáñez A., Markman J.L., Ho R., Wang X., Chen S., Lall D., Jin M., Muhammad A.K., Bell S., Landeros J., Valencia V., Harms M., Arditi M., Jefferies C, & Baloh R.H. (2020). C9orf72 in myeloid cells suppresses STING-induced inflammation. Nature, 585(7823), 96-101.
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3

Characterization of C9orf72 and STING Mice

Cited 1 time
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All mice were housed in pathogen-free facilities under 12-h light dark cycles with access to food and water ad libitum. Temperature was set 74°F +/− 2° with humidity 30–70%. C9orf72−/− mice were as previously published7 (link) and wildtype mice were purchased from Jackson Laboratories. C9orf72fl/fl mice were provided by the Pasterkamp lab12 (link) and were crossed with Cx3cr1Cre (B6J.B6N(Cg)-Cx3cr1tm1.1(cre)Jung/J) and Lyz2Cre (B6.129P2-Lyz2tm1(cre)Ifo/J) purchased from Jackson Laboratories to obtain Cx3cr1Cre;C9orf72fl/fl and Lyz2Cre;C9orf72fl/fl mice. The STING golden-ticket (STINGgt/gt) mouse was obtained from Jackson Laboratories (C57BL/6J- Tmem173gt/J). C9orf72−/− mice were crossed with STINGgt/gt to obtain C9orf72−/−;STINGgt/gt mice. All mice have the nuclear background of C57BL/6J. Mice were sex- and age-matched. For all experiments mice were grouped according to genotype. For EAE and B16 melanoma models genotypes were randomly separated into experimental groups. Researchers were blinded when scoring EAE, counting tumor burden in B16 melanoma model. Husbandry and behavioral tests were conducted in accordance with the protocols described by the National Institutes of Health’s Guide for the Care and Use of Animals and were approved by Cedars-Sinai Institutional Animal Care and Use Committees (IACUC #8161).
McCauley M.E., O’Rourke J.G., Yáñez A., Markman J.L., Ho R., Wang X., Chen S., Lall D., Jin M., Muhammad A.K., Bell S., Landeros J., Valencia V., Harms M., Arditi M., Jefferies C, & Baloh R.H. (2020). C9orf72 in myeloid cells suppresses STING-induced inflammation. Nature, 585(7823), 96-101.
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4

Conditional Knockout of RBP-J in Mice

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Eight-week old male mice were used in our study. All wild-type C57/BL6 and transgenic mice were maintained under specific pathogen free conditions. The Lyz2-Cre transgenic (Jackson Laboratory, Bar Harbor, ME) and RBP-J-floxed (RBP-Jf)41 (link) mice were crossed to obtain RBP-Jf/+ and RBP-Jf/f mice bearing the Lyz2-Cre transgene (hereafter referred to as control and RBP-J cKO, respectively), which were identified by polymerase chain reaction (PCR) with tail DNA as a template41 (link). Primers for Lyz2-Cre: N1: 5′-CCGGTCGATGCAACGAGTGATGAGG; N2: 5′-GCCTCCAGCTTGCATGATCTCCGG; Primers for WT: R3: 5′-GTTCTTAACCTGTTGGTCGGAACC; R4: 5′-GCTTGAGGCTTGATGTTCTGTATTGC; Primers for RBP-J-floxed: R3: 5′-GTTCTTAACCTGTTGGTCGGAACC; PGKD1: 5′-ACCGGTGATGTGGAATGTGT. All animal experiments were approved by the Animal Experiment Administration Committee of Fourth Military Medical University. All animal manipulations were carried out in accordance with the National Institutes of Health Guide for the Care and Use of Laboratory Animals (NIH Publications, eighth edition) revised in 2012, and all efforts were made to minimize animal number and their suffering.
Dou G.R., Li N., Chang T.F., Zhang P., Gao X., Yan X.C., Liang L., Han H, & Wang Y.S. (2016). Myeloid-Specific Blockade of Notch Signaling Attenuates Choroidal Neovascularization through Compromised Macrophage Infiltration and Polarization in Mice. Scientific Reports, 6, 28617.
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5

Genetic Mouse Models for Circadian Research

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8-10-week old male mice were used for all the experiments. Brain and muscle ARNTL-like (Bmal)1flox/flox, Lyz2cre and Icam1−/− mice were purchased from Jackson Laboratories. Neuron-glial antigen (Ng)2-cre and Ng2-DsRed (Cspg4-DsRed) mice were provided by Konstantin Stark. Lysozyme (Lyz)2-green fluorescent protein (gfp) mice were provided by Markus Sperandio. Per1−/−Per2−/− mice were provided by Urs Albrecht22 (link). Cdh5ERT2-cre mice were a gift from Ralf H. Adams. β2 adrenergic receptor (Adrb2)−/− mice were a gift from Gerard Karsenty to Paul Frenette. Nestin (Nes)-gfp mice were a gift from Grigori Enikolopov to Paul Frenette. C57BL/6 wild-type mice were obtained from Charles River. Animals were housed under a 12 h:12 h light-dark cycle with ad libitum access to food and water. All animal experimental procedures were carried out in accordance with the German Law of Animal Welfare and approved by the Regierung of Oberbayern or the Animal Care and Use Committee of the Albert Einstein College of Medicine or the Swiss Federal Veterinary Office.
de Juan A., Ince L.M., Pick R., Chen C.S., Molica F., Zuchtriegel G., Wang C., Zhang D., Druzd D., Hessenauer M.E., Pelli G., Kolbe I., Oster H., Prophete C., Hergenhan S.M., Albrecht U., Ripperger J., Montanez E., Reichel C.A., Soehnlein O., Kwak B.R., Frenette P.S, & Scheiermann C. (2019). Artery-associated sympathetic innervation drives rhythmic vascular inflammation of arteries and veins. Circulation, 140(13), 1100-1114.
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6

Genetically Modified Mouse Models

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C57BL/6N mice were purchased from Charles River Laboratories. Syk+/- mice were from Martin Turner (The Babraham Institute, UK) and bred as heterozygous. Fas<f/f> mice (kind gift from K. Rajewsky, Max Delbrück Center for Molecular Medicine, Germany) were bred with Lyz2<Cre> (Jackson Laboratory, USA) mice. Cdh5<CreERT2>mice (Ralf H. Adams, University of Münster, Germany, Wang et al., 2010b (link)) were bred with Fasl<f/f> or Fas<f/f> (Karray et al., 2004 (link)) mice. Animal experiments were performed in accordance with institutional guidelines of the German Cancer Research Center and were approved by the Regierungspräsidium Karlsruhe, Germany (Permit Number: G188/13).
Gao L., Gülcüler G.S., Golbach L., Block H., Zarbock A, & Martin-Villalba A. (2016). Endothelial cell-derived CD95 ligand serves as a chemokine in induction of neutrophil slow rolling and adhesion. eLife, 5, e18542.
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7

Conditional Deletion of Y1 Receptor

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Example 1

Lyz2-cre (The Jackson Laboratory), 2.3-kB Col1a1-cre, and Y1 flox/flox mice were used in order to remove a Y1 receptor in osteoblasts and macrophages. The mice were disposed in an experimental group by using a block randomization method. In order to eliminate prejudice, data collection and data analysis were never involved. All mice experiments were approved by Kyungpook National University Institutional Animal Care and Use Committee.

US10543254B2. Composition containing neuropeptide Y for inhibiting side effects of anticancer agents (2020-01-28). KYUNGPOOK NATIONAL UNIVERSITY INDUSTRY-ACADEMIC COOPERATION FOUNDATION [KR]. Inventors: Jae Sung Bae [KR], Hee Kyung Jin [KR], Min Hee Park [KR].
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8

Genetic Manipulation of Autophagy Genes

Cited 4 times
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Atg5f/f and
Atg5f/f-Lyz2cre+/−mice were generated as described previously in an enhanced barrier
facility17 (link),56 (link).
Becn1f/f-
Lyz2cre+/−57 (link),
Fip200f/f-
Lyz2cre+/−58 (link),
Atg7f/f-Lyz2cre+/−51 (link), and
Atg16l1f/f-
Lyz2cre+/− 59 (link) were generated in the same way as
Atg5f/f-
Lyz2cre+/−.
Becn1f/f-
CD11c-cre+/−, and
Becn1f/f-
Mrp8-cre+/− were generated by breeding
Becn1f/f to CD11c-
cre+/− (#007567) and
Mrp8-cre+/− (#021614) from the Jackson
Laboratory. Rag1−/− (#002216),
Ifngr−/− (#003288), and
Casp1/11−/− (#016621) mice were
from the Jackson Laboratory.
Rubicon−/− knockout mice were
kindly provided by Doug Green and Jennifer Martinez25 (link). All mice used for experimental
procedures were backcrossed in house to B6/J except for
Rubicon−/− mice. 8–12 weeks
of age and sex-matched littermates were used unless specified otherwise and were
subject to randomization. Statistical consideration was not used to determine
mouse sample sizes. Mice were housed and bred at Washington University in St.
Louis in specific pathogen-free conditions in accordance with federal and
university guidelines, and protocols were approved by the Animal Studies
Committee of Washington University.
Wang Y.T., Zaitsev K., Lu Q., Li S., Schaiff W.T., Kim K.W., Droit L., Wilen C.B., Desai C., Balce D.R., Orchard R.C., Orvedahl A., Park S., Kreamalmeyer D., Handley S.A., Pfeifer J.D., Baldridge M.T., Artyomov M.N., Stallings C.L, & Virgin H.W. (2020). Select autophagy genes maintain quiescence of tissue-resident macrophages and increase susceptibility to Listeria monocytogenes. Nature microbiology, 5(2), 272-281.
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9

Myeloid-Specific Bmal1 and Hif1a Knockout Mice

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All animal studies were approved by the Harvard Medical Area Standing Committee on Animal Research. Animals were housed in a pathogen-free barrier facility at the Harvard T.H. Chan School of Public Health. Bmal1fl/fl (stock # 007668), Hif1a fl/fl (stock # 007561), and Lyz2-Cre (stock # 004781) mice in the C57BL/6J background were obtained from Jackson laboratories and were originally contributed by Drs Charles Weitz, Dmitriy Lukashev, and Irmgard Foerster, respectively. Floxed mice were crossed with Lyz2-Cre mice to generate myeloid-specific Bmal1 and Hif1a knockout mice. Myeloid-specific Bmal1 knockout mice were crossed with Hif1afl/fl mice, and the resulting heterozygotes were crossed to generate myeloid-specific Bmal1 and Hif1a double-knockout mice. The genotypes were validated by both DNA genotyping and mRNA expression. Gender- and age-matched mice of between 8–24 weeks of age were used for experiments. Similar results were obtained from male and female mice.
Alexander R.K., Liou Y.H., Knudsen N.H., Starost K.A., Xu C., Hyde A.L., Liu S., Jacobi D., Liao N.S, & Lee C.H. (2020). Bmal1 integrates mitochondrial metabolism and macrophage activation. eLife, 9, e54090.
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10

Generation of LysM-Cre Tgfbr2 Knockout Mice

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All mice were bred and maintained under specific pathogen‐free conditions at Karolinska Institutet or at the University of Zurich. All animal experiments were approved and performed in accordance with national and cantonal animal care guidelines and ethical permits. We generated two lines of LysMCreTgfbr2fl/fl mice: Tgfbr2fl/fl mice were imported from Dr. Ming Li at Sloan Kettering Institute, or obtained from Dr. Per Levéen, Lund University. LysMCre mice were obtained from The Jackson Laboratory (Lyz2‐Cre) or directly from Dr. Irmgard Förster, University of Cologne, and bred to obtain LysMCreTgfbr2fl/fl mice (LysMCre/+Tgfbr2fl/fl) and littermate controls (LysMCre/+TGFbR2fl/wt or LysM+/+TGFbR2fl/fl). The animals were crossed for >10 generations to C57BL6.
Parsa R., Lund H., Tosevski I., Zhang X., Malipiero U., Beckervordersandforth J., Merkler D., Prinz M., Gyllenberg A., James T., Warnecke A., Hillert J., Alfredsson L., Kockum I., Olsson T., Fontana A., Suter T, & Harris R.A. (2016). TGFβ regulates persistent neuroinflammation by controlling Th1 polarization and ROS production via monocyte‐derived dendritic cells. Glia, 64(11), 1925-1937.
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