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Cd11c promoter

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The CD11c promoter is a genetic element that controls the expression of the CD11c gene. CD11c is a cell surface receptor that is commonly used as a marker for dendritic cells, a type of immune cell. The CD11c promoter can be used to drive the expression of genes of interest in dendritic cells for research purposes.

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Lab products found in correlation

B6.129p2 c ccr7tm1rfor j, by Jackson ImmunoResearch (2 mentions) Human ubiquitin c promoter, by Jackson ImmunoResearch (2 mentions) C57bl 6 mice, by Jackson ImmunoResearch (2 mentions) Cd45.1 mice, by Charles River Laboratories (1 mentions) C57bl 6 background, by Charles River Laboratories (1 mentions) C57bl 6 background, by Jackson ImmunoResearch (1 mentions) B6 cg tg itgax cre 1 1reiz j, by Jackson ImmunoResearch (1 mentions)

5 protocols using cd11c promoter

1

Transgenic Mice for Immune Studies

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FcγRIIb-deficient mice on a C57BL/6 background18 (link) were kindly provided by Jeff Ravetch (Rockefeller University, New York) and Silvia Bolland (National Institutes of Health, NIAID, Bethesda, MD) and crossed to transgenic mice expressing EGFP under the control of the human ubiquitin C promoter38 (Jackson Laboratories) or transgenic mice expressing Venus EYFP under the control of the CD11c promoter39 (obtained from M. Nussenzweig, Rockefeller University, New York, NY). C57BL/6 mice were obtained from Jackson Laboratories or from Charles River Laboratories (Margate, UK). NZB/W F1 were bred in-house from NZB and NZW mice obtained from Harlan UK. CCR7-deficient mice on a C57BL/6 background (strain B6.129P2(C)-Ccr7tm1Rfor/J, stock number 006621, live repository, aged 8 weeks old) were purchased from Jackson Laboratories. Age matched C57BL/6 JAX mice were used as controls. In all experiments, both male and female mice were used. Mice were maintained in specific-pathogen-free conditions at an Association for Assessment and Accreditation of Laboratory Animal Care-accredited animal facility at NIAID or at a Home Office-approved facility in the UK. All procedures were approved by the NIAID Animal Care and Use Committee (National Institutes of Health, Bethesda, MD) or were conducted in accordance with the United Kingdom Animals (Scientific Procedures) Act 1986.
Clatworthy M.R., Aronin C.E., Mathews R.J., Morgan N., Smith K.G, & Germain R.N. (2014). Immune complexes stimulate CCR7-dependent dendritic cell migration to lymph nodes. Nature medicine, 20(12), 1458-1463.
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2

Murine Model of Langerhans Cell Histiocytosis

Cited 1 time
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All animal experiments performed in this study were approved by the Institutional Animal Care and Use Committee of Mount Sinai School of Medicine. BRAFV600ECD11c mice were created by crossing BRAFV600Eca/wt or BRAFV600Eca/ca mice (provided by M.W. Bosenberg, Yale University, New Haven, CT; Dankort et al., 2007 (link)) with mice expressing cre recombinase under the control of the CD11c promoter (C57BL/6 background; The Jackson Laboratory). BRAFV600ECD11c mice with one BRAFV600ECA allele and one CD11c-Cre allele develop a lethal LCH-like syndrome, as described (Berres et al., 2014 (link)). All animals were housed under specific pathogen-free conditions and sacrificed at the indicated time points. All experiments were controlled using littermates negative for the cre recombinase transgene construct or cre-positive littermates negative for the BRAFV600Eca construct.
BRAFV600ECD11c chimeras were generated by transplantation of 1–3 × 10^6 whole BM cells flushed from the long bones of 5–8 wk old BRAFV600ECD11c mice into lethally irradiated CD45.1 mice age 8–12 wk (C57BL/6 background; Charles River Laboratory). Mice were allowed to recover for 3 wk after transplantation before initiation of drug treatments.
Hogstad B., Berres M.L., Chakraborty R., Tang J., Bigenwald C., Serasinghe M., Lim K.P., Lin H., Man T.K., Remark R., Baxter S., Kana V., Jordan S., Karoulia Z., Kwan W.H., Leboeuf M., Brandt E., Salmon H., McClain K., Poulikakos P., Chipuk J., Mulder W.J., Allen C.E, & Merad M. (2018). RAF/MEK/extracellular signal–related kinase pathway suppresses dendritic cell migration and traps dendritic cells in Langerhans cell histiocytosis lesions. The Journal of Experimental Medicine, 215(1), 319-336.
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3

Genetic Mouse Models for Disease Research

Cited 1 time
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C57BL/6 wild-type, Saa−/−, Lrp1fl/fl, and Lrp1ΔCd11c mice were bred and maintained in the barrier facility at the University of Texas Southwestern Medical Center. Saa−/− mice were generated using CRISPR/Cas9 genome editing on a C57BL/6J background (15 (link)). Lrp1fl/fl mice (46 (link)) on a 129S7/SvEvBrd genetic background were used to generate a CD11c+ cell-specific Lrp1 knockout (Lrp1ΔCd11c) mouse by crossing with a mouse expressing Cre recombinase under the control of the CD11c promoter (Jackson Laboratories; B6.Cg-Tg (Itgax-cre)1-1Reiz/J). Mice 8–12 weeks of age were used for all experiments and co-housed littermates were used as controls. Experiments were performed using protocols approved by the Institutional Animal Care and Use Committees of the UT Southwestern Medical Center.
Bang Y.J., Hu Z., Li Y., Gattu S., Ruhn K.A., Raj P., Herz J, & Hooper L.V. (2021). Serum amyloid A delivers retinol to intestinal myeloid cells to promote adaptive immunity. Science (New York, N.Y.), 373(6561), eabf9232.
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4

Generation and Characterization of BRAFV600E Mouse Models

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All animal experiments performed in this study were approved by the Institutional Animal Care and Use Committee (IACUC) of Mount Sinai School of Medicine. BRAFV600Elangerin mice were generated by crossing mice expressing cre recombinase under the control of the murine langerin promoter (C57BL/6 background; provided by B. Claussen, Erasmus University Medical Center, Rotterdam, Amsterdam; Zahner et al., 2011 (link)) with heterozygous mice carrying a cre-activated allele of BRAF-V600E (BRAFV600Eca/wt, C57BL/6 background) in which wild-type BRAF is expressed in both alleles in the absence of cre-mediated recombination (provided by M.W. Bosenberg, Yale University, New Haven, CT; Dankort et al., 2007 (link)). BRAFV600ECD11c mice were created by crossing BRAFV600Eca/wt mice with mice expressing cre recombinase under the control of the CD11c promoter (C57BL/6 background; The Jackson Laboratory). All animals were housed under specific pathogen-free (SPF) conditions and sacrificed at the indicated time points. All experiments were controlled using littermates negative for the cre recombinase transgene construct.
Berres M.L., Lim K.P., Peters T., Price J., Takizawa H., Salmon H., Idoyaga J., Ruzo A., Lupo P.J., Hicks M.J., Shih A., Simko S.J., Abhyankar H., Chakraborty R., Leboeuf M., Beltrão M., Lira S.A., Heym K.M., Clausen B.E., Bigley V., Collin M., Manz M.G., McClain K., Merad M, & Allen C.E. (2014). BRAF-V600E expression in precursor versus differentiated dendritic cells defines clinically distinct LCH risk groups. The Journal of Experimental Medicine, 211(4), 669-683.
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5

Transgenic Mice for Immune Studies

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FcγRIIb-deficient mice on a C57BL/6 background18 (link) were kindly provided by Jeff Ravetch (Rockefeller University, New York) and Silvia Bolland (National Institutes of Health, NIAID, Bethesda, MD) and crossed to transgenic mice expressing EGFP under the control of the human ubiquitin C promoter38 (Jackson Laboratories) or transgenic mice expressing Venus EYFP under the control of the CD11c promoter39 (obtained from M. Nussenzweig, Rockefeller University, New York, NY). C57BL/6 mice were obtained from Jackson Laboratories or from Charles River Laboratories (Margate, UK). NZB/W F1 were bred in-house from NZB and NZW mice obtained from Harlan UK. CCR7-deficient mice on a C57BL/6 background (strain B6.129P2(C)-Ccr7tm1Rfor/J, stock number 006621, live repository, aged 8 weeks old) were purchased from Jackson Laboratories. Age matched C57BL/6 JAX mice were used as controls. In all experiments, both male and female mice were used. Mice were maintained in specific-pathogen-free conditions at an Association for Assessment and Accreditation of Laboratory Animal Care-accredited animal facility at NIAID or at a Home Office-approved facility in the UK. All procedures were approved by the NIAID Animal Care and Use Committee (National Institutes of Health, Bethesda, MD) or were conducted in accordance with the United Kingdom Animals (Scientific Procedures) Act 1986.
Clatworthy M.R., Aronin C.E., Mathews R.J., Morgan N., Smith K.G, & Germain R.N. (2014). Immune complexes stimulate CCR7-dependent dendritic cell migration to lymph nodes. Nature medicine, 20(12), 1458-1463.
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