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Vav cre

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Vav-Cre is a Cre recombinase enzyme expressed under the control of the Vav1 promoter. It is commonly used in genetically modified mouse models to induce Cre-mediated recombination in hematopoietic cells.

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Lab products found in correlation

Mx1 cre, by Jackson ImmunoResearch (6 mentions) Vav cre mice, by Jackson ImmunoResearch (4 mentions) Lysm cre, by Jackson ImmunoResearch (4 mentions) Notch2fl fl, by Jackson ImmunoResearch (2 mentions) Cd11c cre, by Jackson ImmunoResearch (2 mentions) Cd11c cre mice, by Jackson ImmunoResearch (1 mentions) C57bl 6j, by Charles River Laboratories (1 mentions) C57bl 6j wt, by Jackson ImmunoResearch (1 mentions) Cmv cre, by Jackson ImmunoResearch (1 mentions) Itgax cre, by Jackson ImmunoResearch (1 mentions) B6 ly5.1 cr mice, by Charles River Laboratories (1 mentions) Nsg sgm3, by Jackson ImmunoResearch (1 mentions) Polyinosinic polycytidylic acid pipc, by Merck Group (1 mentions) Mx cre, by Jackson ImmunoResearch (1 mentions) Idtr mice, by Jackson ImmunoResearch (1 mentions) Ncr1 cre mice, by Biocytogen (1 mentions) C57bl 6 tg cag egfp 1osb j, by Jackson ImmunoResearch (1 mentions) β catenin, by Jackson ImmunoResearch (1 mentions) Nod scid il2rg nsg mice, by Jackson ImmunoResearch (1 mentions) Cas9 ki, by Jackson ImmunoResearch (1 mentions)

Spelling variants of this product

Vav-Cre mice (19 citations) VAV-Cre transgenic mice (5 citations) Vav‐Cre strain (CD45.2) (2 citations)

27 protocols using vav cre

1

Genetic Models for Notch and Wnt Signaling

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FoxO1fl/fl, α1(I)Collagen-Cre [α1(I)Col-Cre], and Catnb+/lox(ex3) mice have been reported 33 (link)–36 (link). Specific deletion of Notch1 and Notch2 in hematopoietic cells was obtained by breeding Notch1fl/fl42 (link) (Purchased from Jax, Stock# 007181) or Notch2fl/fl mice 37 (link) (purchased from the Jackson Laboratory, Stock# 010525) with Vav-cre transgenic mice 38 (link) (purchased from the Jackson Laboratory Stock# 008610). The comparative analysis of all histological and flow cytometry measurements was performed at 1 month of age because Ctnnb1CAosb and Ctnnb1CAosb;FoxO1osb−/− mice die between 4 and 6 weeks of age. Additional details are provided in the supplementary Information. All the protocols and experiments were conducted according to the guidelines of the Institute of Comparative Medicine, Columbia University.
Kode A., Mosialou I., Manavalan S.J., Rathinam C.V., Friedman R.A., Teruya-Feldstein J., Bhagat G., Berman E, & Kousteni S. (2015). FoxO1-Dependent Induction of Acute Myeloid Leukemia by Osteoblasts in Mice. Leukemia, 30(1), 1-13.
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2

Conditional Deletion of TRAF6 and IKKβ in Mice

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All mice were bred, housed, and handled in the Association for Assessment and Accreditation of Laboratory Animal Care-accredited animal facility of Cincinnati Children’s Hospital Medical Center (CCHMC) or Memorial Sloan Kettering Cancer Center (MSKCC). Animal care was in strict compliance with the institutional guidelines established by CCHMC and MSKCC, the Guide for the Care and Use of Animals, and the Association for Assessment and Accreditation of Laboratory Animal Care International. TRAF6fl/fl mice (C57BL/6) were a kind gift from Dr. Yongwon Choi (University of Pennsylvania) (Han et al., 2013 (link)). Traf6fl/fl mice were crossed with Mx1Cre (Jackson Laboratory, 003556) and VavCre mice (Jackson Laboratory, 008610) for inducible or conditional deletion of TRAF6 (Traf6fl/fl;Mx1Cre) and (Traf6fl/fl; VavCre), respectively. To delete TRAF6, Cre transgene expression in Traf6fl/fl;Mx1Cre mice was induced by pIpC. IKKβfl/fl mice were previously described and a kind gift from Dr. Albert Baldwin (University of North Carolina) (Mankan et al., 2011 (link)). To delete IKKβ in hematopoietic cells, IKKβfl/fl mice were crossed with VavCre mice. BM cells were obtained by crushing the femur, tibia, and pelvic bone, and maintained in RPMI1640 with 10% fetal bovine serum.
Fang J., Muto T., Kleppe M., Bolanos L.C., Hueneman K.M., Walker C.S., Sampson L., Wellendorf A.M., Chetal K., Choi K., Salomonis N., Choi Y., Zheng Y., Cancelas J.A., Levine R.L, & Starczynowski D.T. (2018). TRAF6 Mediates Basal Activation of NF-κB Necessary for Hematopoietic Stem Cell Homeostasis. Cell reports, 22(5), 1250-1262.
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3

Generation of WASH Conditional Mice

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Generation of mice with conditional Wash allele has been described previously [9] (link), [11] (link), [44] (link). In brief, the endogenous Wash gene was floxed (WASHfl/fl) by standard gene targeting technology and bred to LysM-Cre [44] (link), [45] (link) (Jackson Labs), Vav-Cre (Gift from Dr. Thomas Graf, Albert Einstein College) or CD11c-Cre mice [45] (link), [46] (link) (Jackson Labs). OT-II mice were a gift from H. Virgin (Washington University, St Louis, MO). Mice were bred on a C57BL/6 background.
Graham D.B., Osborne D.G., Piotrowski J.T., Gomez T.S., Gmyrek G.B., Akilesh H.M., Dani A., Billadeau D.D, & Swat W. (2014). Dendritic Cells Utilize the Evolutionarily Conserved WASH and Retromer Complexes to Promote MHCII Recycling and Helper T Cell Priming. PLoS ONE, 9(6), e98606.
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4

Genetic Manipulation of Dpy30 and P21 in Mice

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All animal procedures were approved by the Institutional Animal Care and Use Committee at the University of Alabama at Birmingham. All mice were maintained under specific pathogen-free conditions and housed in individually ventilated cages. Dpy30+/− mice were generated in our laboratory as reported previously (Yang et al., 2016 (link)) and were crossed to Mx1-Cre (Jackson Laboratory, JAX 003556) and Vav-Cre (Jackson Laboratory, JAX 008610) mice to produce Cre; Dpy30+/− Mice. These mice were further crossed with Dpy30F/F mice to produce Cre; Dpy30F/+ and Cre; Dpy30F/− littermates for experimental use. All transplant recipient mice were C57Bl/6J and CD45.1+, and purchased from Charles River Laboratories. P21−/− (129S2-Cdkn1atm1Tyj/J) mice (Jackson Laboratory, JAX 003263) were further crossed with Mx1-Cre and Dpy30F/F to generate the littermates of Dpy30F/F; P21+/−; Mx1-Cre and Dpy30F/F; P21−/−; Mx1-Cre.
Yang Z., Shah K., Khodadadi-Jamayran A, & Jiang H. (2019). Control of Hematopoietic Stem and Progenitor Cell Function through Epigenetic Regulation of Energy Metabolism and Genome Integrity. Stem Cell Reports, 13(1), 61-75.
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5

Mouse Strain Characterization for Immunological Studies

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WT C57BL/6J (stock no. 000664), CMV-cre (stock no. 006054), Itgax-cre (stock no. 008068) and Vav-cre (stock no. 008610) mice were obtained from the Jackson Laboratory. B6-Ly5.1/Cr mice (strain code 564) were obtained from Charles River. Irf8 +32−/− mice (stock no. 032744; The Jackson Laboratory) were generated in house and described previously6 (link). Mice harbouring floxed alleles of Nfil3 (Nfil3fl/fl mice) and Cebpb (Cebpbf/fl mice) were described previously46 (link),47 (link). Nfil3−/− mice were provided by A. Look and T. Mak48 (link). All mice were maintained on the C57BL/6J background in our specific-pathogen free facility following institutional guidelines and with protocols approved by the AAALAC-accredited Animal Studies Committee at Washington University in St Louis. All animals were maintained on 12-h light cycles and housed at 21 °C and 50% humidity. Experiments were performed with mice at 6–12 weeks of age, with sex-matched littermates whenever possible.
Liu T.T., Kim S., Desai P., Kim D.H., Huang X., Ferris S.T., Wu R., Ou F., Egawa T., Van Dyken S.J., Diamond M.S., Johnson P.F., Kubo M., Murphy T.L, & Murphy K.M. (2022). Ablation of cDC2 development by triple mutations within the Zeb2 enhancer. Nature, 607(7917), 142-148.
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6

Conditional Knockout Mice for SATB1 and TFAM

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SATB1-floxed mice and transgenic mice expressing mitochondrial transcription factor A (TFAM) were previously described (Ikeuchi et al, 2005 (link); Kondo et al, 2016 (link)). Vav-Cre and TFAM-floxed mice were purchased from The Jackson Laboratory. Lck-Cre mice were obtained from the Laboratory Animal Resource Bank at NIBIOHN. SATB1 or TFAM conditional knockout mice were generated by crossing floxed, Vav-Cre, and Lck-Cre mice. All mice were maintained on a C57BL/6 background under specific pathogen-free conditions at the Toho University School of Medicine animal facility (Kuwabara et al, 2009 (link)). All mouse experiments were approved by the Toho University Animal Care and User Committee (No. 20-51-435) and Toho University Safety Committee for Recombinant DNA Experiments (No. 20-51-440). Experiments were performed on 8- to 12-wk-old mice.
Kuwabara T., Ishikawa F., Ikeda M., Ide T., Kohwi-Shigematsu T., Tanaka Y, & Kondo M. (2021). SATB1-dependent mitochondrial ROS production controls TCR signaling in CD4 T cells. Life Science Alliance, 4(11), e202101093.
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7

Conditional Deletion of A20 in Mice

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All mice were bred, housed and handled in the Association for Assessment and Accreditation of Laboratory Animal Care-accredited animal facility of Cincinnati Children’s Hospital Medical Center (CCHMC). Animal care was in strict compliance with the institutional guidelines established by CCHMC, the Guide for the Care and Use of Animals (National Academy of Sciences 1996), and the Association for Assessment and Accreditation of Laboratory Animal Care International. A20fl/fl mice were kindly provided by AM (University of California San Francisco) and described elsewhere (29 (link)). A20fl/fl mice were crossed with Vav-Cre mice (Jackson Laboratory, 008610) or RosaCreER mice (Jackson Laboratory, 008463) for conditional deletion of A20 (A20fl/fl;Vav-Cre, A20fl/fl;RosaCreER). Both male and female mice were included in all experiments. BM cells were obtained by crushing the femur, tibia, and pelvic bone, and maintained in Iscove’s MDM (Cellgro, Cat No. 10-016-CV) with 10% fetal bovine serum.
Smith M.A., Culver-Cochran A.E., Adelman E.R., Rhyasen G.W., Ma A., Figueroa M.E, & Starczynowski D.T. (2020). TNFAIP3 Plays a Role in Aging of the Hematopoietic System. Frontiers in Immunology, 11, 536442.
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8

Immune-deficient Mouse Models for Leukemia

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In all, 8–12 weeks male immune-deficient NSG (NOD/SCID/IL-2Rgc-null) mice: NSG (Stock No: 005557) (The Jackson Laboratory, Bar-Harbor, ME, USA). NOD.Cg-PrkdcscidIl2rgtm1Wjl Tg(PGK1-KITLG*220)441Daw/SzJ mice (stock No: 017830) (The Jackson Laboratory, Bar-Harbor, ME, USA). NOD.Cg-PrkdcscidIl2rgtm1Wjl Tg(CMV-IL-3,CSF2,KITLG)1Eav/MloySzJ mice (Stock No.: 013062) NSG-SGM3(The Jackson Laboratory, Bar-Harbor, ME, USA) DNMT3AR882H KI mice, constitutively express the human DNMT3A mutation. SRSF2P95H floxed mice possess loxP sites flanking the endogenous coding region of the serine/arginine-rich splicing factor 2 (SRSF2) gene (Stock No: 028376) (The Jackson Laboratory, Bar-Harbor, ME, USA). DNMT3AR882H or SRSF2P95H were crossed with VAV Cre (Stock No: 008610) (The Jackson Laboratory, Bar-Harbor, ME, USA). All experiments were performed in accordance with institutional guidelines approved by the Weizmann Institute of Science Animal Care Committee (02630418-4).
Zioni N., Bercovich A.A., Chapal-Ilani N., Bacharach T., Rappoport N., Solomon A., Avraham R., Kopitman E., Porat Z., Sacma M., Hartmut G., Scheller M., Muller-Tidow C., Lipka D., Shlush E., Minden M., Kaushansky N, & Shlush L.I. (2023). Inflammatory signals from fatty bone marrow support DNMT3A driven clonal hematopoiesis. Nature Communications, 14, 2070.
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9

Genetically Modified Mouse Strains

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Shp-2 floxed mice, FcRγ-deficient (Fcer1g−/−) mice (obtained from J.V. Ravetch, The Rockefeller University), dectin-1-deficient (Clec7a−/−) mice (obtained from Y. Iwakura, The University of Tokyo) and Mincle-deficient (Clec4e−/−) mice (obtained from S. Yamasaki, Kyushu University, Japan) were constructed as previously described47 (link),49 (link),50 (link). Cd11c-cre, Vav-cre and LysM-cre mice were purchased from Jackson Laboratories (Bar Harbor, ME). These mice were bred and maintained in a pathogen-free animal facility at Institut Pasteur of Shanghai. All the procedures were conducted in compliance with a protocol approved by the Institutional Animal Care and Use Committee at Institut Pasteur of Shanghai.
Deng Z., Ma S., Zhou H., Zang A., Fang Y., Li T., Shi H., Liu M., Du M., Taylor P.R., Zhu H.H., Chen J., Meng G., Li F., Chen C., Zhang Y., Jia X.M., Lin X., Zhang X., Pearlman E., Li X., Feng G.S, & Xiao H. (2015). SHP-2 Mediates C-type Lectin Receptors-induced Syk Activation and Anti-fungal TH17 Responses. Nature immunology, 16(6), 642-652.
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10

Conditional Deletion of hnRNP L in Mice

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hnRNP L floxed mice were described previously26 (link). MxCre, VavCre, H2kBcl2 and Trp53−/− mice were obtained from Jackson laboratories or from a colony maintained at the IRCM. The animal ethics committee of the IRCM approved all animal experiments. MxCre+hnRNP Lfl/fl or hnRNP Lfl/fl mice were injected intraperitoneally with 500 μg of polyinosinic-polycytidylic acid (pIpC; Sigma-Aldrich) every other day for a total of 5 times and were analyzed 14 days after the first injection. All mice were aged between 8–16 weeks for BM analysis.
Gaudreau M.C., Grapton D., Helness A., Vadnais C., Fraszczak J., Shooshtarizadeh P., Wilhelm B., Robert F., Heyd F, & Möröy T. (2016). Heterogeneous Nuclear Ribonucleoprotein L is required for the survival and functional integrity of murine hematopoietic stem cells. Scientific Reports, 6, 27379.
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