C57bl 6 gt rosa 26sortm1 hbegf awai j

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The C57BL/6-Gt(ROSA)26Sortm1(HBEGF)Awai/J is a genetically modified mouse strain. It contains a targeted mutation in the Rosa26 locus, which allows for the expression of the human HBEGF gene in a controlled manner.

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C57BL/6 (2462 citations) C57BL/6-Gt (2 citations)

28 protocols using c57bl 6 gt rosa 26sortm1 hbegf awai j

Mice Strains for Immunological Research

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C57BL/6J mice, WBB6F₁-Kit^W/W-v (Kit^W/W-v) mice [and the corresponding control WBB6F₁-Kit^+/+ (Kit^+/+) mice], IL-1R1^−/− (B6.129S7-Il1r1^tm1Imx/J), IL-18^−/− (B6.129P2-Il18^tm1Aki/J) and iDTR^fl/fl mice (C57BL/6-Gt(ROSA)26Sor^{tm1(HBEGF)Awai}/J) were purchased from Jackson Laboratories (Bar Harbor, Me). C57BL/6J (WT) mice were obtained from Jackson Laboratories and either bred at the Stanford University Research Animal Facility or used for experiments after maintaining the mice for at least two weeks in our animal facility. C57BL/6-Kit^W-sh/W-sh mice were originally provided by Peter Besmer (Molecular Biology Program, Memorial Sloan-Kettering Cancer Center, New York, NY, USA); we then backcrossed these mice to C57BL/6J mice for more than 11 generations (7 (link)). Mcpt8^DTR/+ (and the corresponding control Mcpt8^+/+) mice (8 (link)), IL-1α^−/− (9 (link)), IL-1β^−/− (9 (link)), TNF^−/− (10 (link)) and Cpa3-Cre; Mcl-1^fl/fl mice (and the corresponding control Cpa3-Cre; Mcl-1^+/+ mice) (11 (link)) were all on the C57BL/6 background and bred and maintained at the Stanford University Research Animal Facility. We used age-matched male mice for all experiments. All animal care and experimentation were conducted in compliance with the guidelines of the National Institutes of Health and with the specific approval of the Institutional Animal Care and Use Committee of Stanford University.

Reber L.L., Marichal T., Sokolove J., Starkl P., Gaudenzio N., Iwakura Y., Karasuyama H., Schwartz L.B., Robinson W.H., Tsai M, & Galli S.J. (2014). Mast cell-derived IL-1β contributes to uric acid crystal-induced acute arthritis in mice. Arthritis & rheumatology (Hoboken, N.J.), 66(10), 2881-2891.

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Genetic Manipulation of Microglia Lineage

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Six to twelve weeks old male mice were used for all experiments in accordance with institutional guidelines as approved by the Mayo Clinic Institutional Animal Care and Use Committee. CX3CR1^CreER/+:R26^iDTA/+ and CX3CR1^CreER/+:R26^iDTR/+ mice were generated by crossing CX3CR1^CreER/CreER mice [B6.129P2(Cg)-CX3CR1^{tm2.1(cre/ERT2)Litt}/WganJ; Jackson Labs, Bar Harbor, ME] with either R26^iDTA/+ [B6.129P2-Gt(ROSA)26Sortm1(DTA)Lky/J; Jackson Labs] or R26^iDTR/+ [C57BL/6-Gt(ROSA)26Sor^{tm1(HBEGF)Awai}/J; Jackson Labs]. CX3CR1^CreER/+: Csf1r^Flox/Flox mice were generated by crossing CX3CR1^CreER/+: Csf1r^Flox/Flox mice with Csf1r^Flox/Flox mice (B6.Cg-Csf1rtm1.2Jwp/J; Jackson Labs). Littermate, CX3CR1^CreER/+ mice or Csf1r^Flox/Flox mice treated with tamoxifen were used as respective controls. Experimenters were blind to genotypes.

Wu W., Li Y., Wei Y., Bosco D.B., Xie M., Zhao M.G., Richardson J.R, & Wu L.J. (2020). Microglia depletion aggravates the severity of acute and chronic seizures in mice. Brain, behavior, and immunity, 89, 245-255.

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Xenograft Mouse Models for Cancer

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All animal experiments were in compliance with Institutional Animal Care and Use Committee of Baylor College of Medicine. Nude mice [Athymic Nude-Foxn1^nu] and SCID/Beige mice [C.B-17/IcrHsd-Prkdc scid Lyst bg-J] were purchased from Envigo. Osx1-GFP-cre/iDTR was generated from Osx1-GFP-cre [B6.Cg-Tg(Sp7-tTA,tetO-EGFP/cre)1Amc/J] and STP-iDTR mice [C57BL/6-Gt(ROSA)26Sortm1(HBEGF) Awai/J] originally obtained from Jackson Laboratory. For all in vivo experiment, 4- to 7-week-old female mice were used.

Bado I.L., Zhang W., Hu J., Xu Z., Wang H., Sarkar P., Li L., Wan Y.W., Liu J., Wu W., Lo H.C., Kim I.S., Singh S., Janghorban M., Muscarella A.M., Goldstein A., Singh P., Jeong H.H., Liu C., Schiff R., Huang S., Ellis M.J., Gaber M.W., Gugala Z., Liu Z, & Zhang X.H. (2021). The bone microenvironment increases phenotypic plasticity of ER+ breast cancer cells. Developmental cell, 56(8), 1100-1117.e9.

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Conditional Deletion of GSK3β in Neutrophils

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Wild type (WT) C57Bl/6NTac mice were purchased from Taconic Biosciences, Inc. (Germantown, NY). ROSA26iDTR mice (C57BL/6-Gt(ROSA)26Sor^{tm1(HBEGF)Awai}/J) (stock no. 007900) and MRP8-Cre⁺ mice (B6.Cg-Tg(S100A8-cre,-EGFP)1Ilw/J) (stock no. 021614) were purchased from The Jackson Laboratory. MRP8-Cre⁺ mice were crossed with ROSA26iDTR mice to generate PMN^DTR (MRP8-Cre⁺; ROSA26iDTR) and PMN^WT littermate controls (MRP8-Cre⁻; ROSA26iDTR). To generate mice with conditional deletion of GSK3β in neutrophils, we crossed the Gsk3β^fl/fl mouse (obtained from Dr. Franca Cambi, University of Pittsburgh, Pittsburgh, PA) with MRP8-Cre⁺. All mice were housed under specific pathogen-free conditions under the supervision of Division of laboratory animal resources (DLAR). All animal experiments were conducted following National Institute of Health (NIH) guidelines under protocols approved by the University of Pittsburgh IACUC.

Jawale C.V., Ramani K., Li D.D., Coleman B.M., Oberoi R.S., Kupul S., Lin L., Prokopienko A.J., Desai J.V., Delgoffe G.M., Lionakis M.S., Bender F.H., Nolin T.D., Gaffen S.L, & Biswas P.S. (2020). Restoring glucose uptake rescues neutrophil dysfunction and protects against fatal bloodstream fungal infections in kidney disease. Science translational medicine, 12(548), eaay5691.

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Transgenic Mouse Models in Immunological Research

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Seven- to 8-week-old WT C57BL/6J (stock 00064), BALB/cByJ (stock 001026), B6.Cg-Tg(Chst4-EGFP)23Nrud/J (referred to as HEV-GFP mice; stock 022787), C57BL/6-Gt (ROSA)26Sortm1 (HBEGF)Awai/J (C57BL/6 iDTR, referred to as DTR mice; stock 007900), B6.FVB-1700016L21RikTg (ItgaxDTR/EGFP)57Lan/J (CD11c-DTR/GFP, referred to as CD11c/DTR or CD11c-GFP mice; stock 004509), and C57BL/6-Tg (UBC-GFP)30Scha/J (referred to as UBC-GFP mice; stock 004353) were purchased from The Jackson Laboratory. CCL19^Cre mice were a gift from Shannon Turley at Genentech (South San Francisco, California, USA). LTβR-KO mice were obtained from Alexei Tumanov (The University of Texas Health Science Center, San Antonio, Texas, USA). CCL19^Cre mice were backcrossed with DTR mice to generate CCL19/DTR mice. Offspring were genotyped by PCR, according to the protocol from The Jackson Laboratory.
All male and female mice were housed in a specific pathogen–free animal facility. All experiments were performed with age- and sex-matched, 8- to 12-week-old mice.

Zhao J., Jung S., Li X., Li L., Kasinath V., Zhang H., Movahedi S.N., Mardini A., Sabiu G., Hwang Y., Saxena V., Song Y., Ma B., Acton S.E., Kim P., Madsen J.C., Sage P.T., Tullius S.G., Tsokos G.C., Bromberg J.S, & Abdi R. (2022). Delivery of costimulatory blockade to lymph nodes promotes transplant acceptance in mice. The Journal of Clinical Investigation, 132(24), e159672.

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Mouse Strain Utilization for Bone Research

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C57BL/6, B6.129-Leprtm2(cre)Rck/J (Lepr-cre), B6.Cg-Gt(ROSA)26Sortm14(CAG-tdTomato)Hze/J, and C57BL/6-Gt(ROSA)26 Sortm1 (HBEGF) Awai/J mice were purchased from Jackson Laboratory. Osx-cre^ERT2 mice (Maes et al., 2010 (link)) were provided by author H.M.K. and backcrossed with C57BL/6 for 5 generations. Nes-Gfp mice (Mignone et al., 2004 (link)) were bred in our facilities. Col1(2.3)-Gfp mice (Kalajzic et al., 2002 (link)) were provided from D. Rowe, J. Butler, and S. Rafii. All mice were maintained in pathogen-free conditions, and the Animal Care and Use Committees of Albert Einstein College of Medicine approved all experimental procedures.

Mizoguchi T., Pinho S., Ahmed J., Kunisaki Y., Hanoun M., Mendelson A., Ono N., Kronenberg H.M, & Frenette P.S. (2014). Osterix marks distinct waves of primitive and definitive stromal progenitors during bone marrow development. Developmental cell, 29(3), 340-349.

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Genetically-Modified Mouse Model for Influenza

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C57BL/6J and C57BL/6-Gt(ROSA)26Sor^{tm1(HBEGF)Awai}/J mice were purchased from Jackson Laboratories via Charles River (Tranent, UK). C57BL/6-NKp46:iCre^+/+ mice were kindly provided by Professor Eric Vivier (Centre d'Immunologie de Marseille-Luminy, Institut Universitaire de France, France). C57BL/6-Rosa26iDTR^+/+ and C57BL/6-NKp46:iCre^+/+ mice were crossed to generate F1 NKp46-iCre/Rosa26iDTR^+/− (referred to as NKp46-DTR). Groups of NKp46-DTR mice were age- and sex-matched for all experiments, with influenza challenge occurring between 8 and 10 weeks of age. Both sexes of the F1 generation were used in this study, with 68 female and 106 male NKp46-DTR mice being used in total. The sexes of mice used in each experiment are shown in the figure panels ({M} male, {F} female) and figure legends. All mice were maintained in individually ventilated cages in a specified pathogen free facility.

Mooney J.P., Qendro T., Keith M., Philbey A.W., Groves H.T., Tregoning J.S., Goodier M.R, & Riley E.M. (2020). Natural Killer Cells Dampen the Pathogenic Features of Recall Responses to Influenza Infection. Frontiers in Immunology, 11, 135.

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Adoptive Transfer of Immune Cells in Mice

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Eight-week-old C57BL/6 mice were purchased from Charles River Laboratories. CIRP^–/– mice were originally obtained from Jun Fujita (Kyoto University, Kyoto, Japan); TLR4^–/– mice were obtained from Kevin Tracey (Feinstein Institutes for Medical Research); and OT-II transgenic mice [B6.Cg-Tg(TcraTcrb)425Cbn/J] were obtained from Yong-Rui Zou (Feinstein Institutes for Medical Research). ROSA-iDTR^KI mice [C57BL/6-Gt(ROSA)26Sor^{tm1(HBEGF)Awai}/J] and MRP8-Cre⁺ mice [B6.Cg-Tg(S100A8-cre,-EGFP)1Ilw/J] were purchased from The Jackson Laboratory. MRP8-Cre⁺ mice were crossed with ROSA-iDTR^KI mice to generate PMN^DTR mice (MRP8-Cre⁺; ROSA-iDTR^KI). Mice were housed at approximately 23°C with 12-hour light cycles and provided standard laboratory food and water ad libitum. Only male mice were used in this study. Animals were randomly assigned to the sham, vehicle, or adoptive transfer groups.

Jin H., Aziz M., Murao A., Kobritz M., Shih A.J., Adelson R.P., Brenner M, & Wang P. (2023). Antigen-presenting aged neutrophils induce CD4+ T cells to exacerbate inflammation in sepsis. The Journal of Clinical Investigation, 133(14), e164585.

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Genetic Mouse Models for Somatosensory Research

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C57BL/6J wild-type (Stock#: 000664), B6;129S6-Gt(Rosa)26Sor^{tm14(CAG-tdTomato)Hze}/J (Rosa26^tdTomato; Stock#:007908), C57BL/6-Gt(Rosa)26Sor^{tm1(HBEGF)Awai}/J (Rosa26^HBEGF; Stock#:007900), B6N.Cg-Sst^{tm2.1(cre)Zjh}/J (Stock#: 018973) and B6N(Cg)-Nmb^{tm1.1(KOMP)Vlcg/J} mice (Stock#:025862) were ordered form the Jackson Laboratory (Bar Harbor, ME). Mrgpra3^gfp-Cre, Pirt^GCaMP3/+ and MRGPRX1;Mrgpr-clusterΔ^-/- mice were generous gifts from Dr. Xinzhong Dong of Johns Hopkins University. Mrgprd^egfp/+ mice were from Dr. David J. Anderson of the California Institute of Technology. Trpm8^gfp/+ mice were from Dr. Gina Story. Nav1.8^Cre, Nmb^-/-, Nmbr^-/-, and Nmbr^gfp transgenic mice were from Dr. Zhou-Feng Chen of Washington University in St. Louis. Slc17a8^Cre/+ tissues were from Dr. Qiufu Ma of Dana-Farber Cancer Institute. Animals used for behavioral tests were backcrossed to the C57BL/6J background for at least 10 generations and maintained in the congenic background. Male mice (two to three months old) were used for behavioral tests. All animal experiments were performed under protocols approved by Institutional Animal Care and Use of Washington University School of Medicine.

Huang C.C., Yang W., Guo C., Jiang H., Li F., Xiao M., Davidson S., Yu G., Duan B., Huang T., Huang A.J, & Liu Q. (2018). Anatomical and Functional Dichotomy of Ocular Itch and Pain. Nature medicine, 24(8), 1268-1276.

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Generation of F1 CD4iDTR Mice

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C57BL/6J, and the breeding pairs of B6.Cg-Tg(Cd4-are)1Cwi/BfluJ and C57BL/6-Gt(Rosa)26Sor^{tm1(HBEGF)Awai}/J were purchased from the Jackson Laboratory (Bar Harbor, ME, USA). F1 CD4iDTR mice were generated by crossing B6.Cg-Tg(Cd4-are)1Cwi/BfluJ and C57BL/6-Gt(Rosa)26Sor^{tm1(HBEGF)Awai}/J as described previously [58 (link)]. The DNA for genotyping was prepared from ear punching. Genotyping was confirmed by PCR using the following primer pairs: for CD4-cre (336 bp product), 5′-gttctttgtatatattgaatgttagcc-3′ (Common Forward), 5′-tatgctctaaggacaagaattgaca-3′ (Wild-type Reverse), and 5′-ctttgcagagggctaacagc-3′ (Mutant Reverse); and for iDTR (340 bp product), 5′-gcgaagagtttgtcctcaacc-3′ (Mutant Reverse), 5′-aaagtcgctctgagttgttat-3′ (Common Forward), and 5′-ggagcgggagaaatggatatg-3′ (Reverse). All mice in this study were maintained in accordance with the guidelines of Ohio State University (OSU). All animal experiments were conducted with the protocol approved by the OSU Animal Care and Use Committee.

Kim S., Shukla R.K., Kim E., Cressman S.G., Yu H., Baek A., Choi H., Kim A., Sharma A., Wang Z., Huang C.A., Reneau J.C., Boyaka P.N., Liyanage N.P, & Kim S. (2022). Comparison of CD3e Antibody and CD3e-sZAP Immunotoxin Treatment in Mice Identifies sZAP as the Main Driver of Vascular Leakage. Biomedicines, 10(6), 1221.

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