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B6.129 hif1atm3rsjo j mice

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B6.129-Hif1atm3Rsjo/J mice are a genetically modified mouse strain with a targeted mutation in the Hif1a gene. This gene encodes the hypoxia-inducible factor 1-alpha (HIF-1α) subunit, a transcription factor that plays a key role in the cellular response to hypoxia. The specific mutation in these mice has been designed to allow for conditional and tissue-specific deletion of the Hif1a gene.

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Lab products found in correlation

Wild type b6 mice c57 blncr1, by Charles River Laboratories (2 mentions) B6 cg tg itgax cre 1 1reiz j mice, by Jackson ImmunoResearch (1 mentions) C57bl 6j, by Jackson ImmunoResearch (1 mentions) B6.129p2 b2mtm1unc j, by Jackson ImmunoResearch (1 mentions) C 129s vhltm1jae j, by Jackson ImmunoResearch (1 mentions) Epas1tm1mcs j mice, by Jackson ImmunoResearch (1 mentions) B6 cg ndor1tg ubc cre ert2 1ejb 1j, by Jackson ImmunoResearch (1 mentions) Ubc cre ert2 mice, by Jackson ImmunoResearch (1 mentions) B6.129p2 nos2tm1lau j mice, by Jackson ImmunoResearch (1 mentions)

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B6.129-Hif1atm3Rsjo/J (7 citations)

5 protocols using b6.129 hif1atm3rsjo j mice

1

Genetically Modified Mice for EAE

Cited 2 times
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Adult female mice were used on a C57Bl/6J background (The Jackson Laboratory, 000664), except for HIF-1α reporter FVB.129S6-Gt(ROSA)26Sortm2(HIF1A/luc)Kael/J mice (The Jackson Laboratory, 006206). B6.Cg-Tg(Itgax-cre)1–1Reiz/J mice (The Jackson Laboratory, 008068) were bred with B6.129-Hif1atm3Rsjo/J mice (The Jackson Laboratory, 007561) to generate ItgaxCreHIF-1αfl mice. ItgaxCreXBP1fl mice26 (link) were a gift from J. R. Cubillos Ruiz and L. Glimcher. C57BL/6-Tg(Tcra2D2, Tcrb2D2)1Kuch/J mice51 (link) (The Jackson Laboratory, 006912) were used for co-co-culture with DCs. All mice were housed in sterile autoclaved cages with irradiated food and acidified, autoclaved water. Mouse handling and weekly cage changes were performed by staff wearing sterile gowns, masks and gloves in a sterile biosafety hood. All mice were kept in a specific-pathogen-free facility at the Hale Building of Transformative Medicine at the Brigham and Women’s Hospital. All mice were 8–10 weeks old at the time of EAE induction. All procedures were reviewed and approved under the guidelines of the Institutional Animal Care and Use Committee (IACUC) at Brigham and Women’s Hospital.
Zhu Y., Traub L.M, & Kornfeld S. (1999). High-Affinity Binding Of The AP-1 Adaptor Complex to Trans-Golgi Network Membranes Devoid Of Mannose 6-Phosphate Receptors. Molecular Biology of the Cell, 10(3), 537-549.
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2

HIF1α Knockout in NK Cells

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Wild-type B6 mice (C57/BLNCR1) were purchased through Charles River Laboratories (Wilmington, MA). HIF1α-specific deletion in NK cells was achieved through crossing B6.129-Hif1a<tm3Rsjo>/J mice from The Jackson Laboratory (Bar Harbor, ME) with Ncr1iCre mice from Eric Vivier. Control β2m knockout mice (B6.129P2-B2m<tm1Unc>/J) were obtained from The Jackson Laboratory.
Victorino F., Bigley T.M., Park E., Yao C.H., Benoit J., Yang L.P., Piersma S.J., Lauron E.J., Davidson R.M., Patti G.J, & Yokoyama W.M. (2021). HIF1α is required for NK cell metabolic adaptation during virus infection. eLife, 10, e68484.
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3

Generating Tamoxifen-Inducible Knockout Mice

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C;129S-Vhltm1Jae/J (stock no. 4081, Jackson Laboratories, Bar Harbor, ME, USA) were used to generate the UBC-Cre-ERT2 VhlLoxP/LoxP mice. These mice harbor two loxP sites flanking the promoter and exon 1 of the murine Vhl locus [63 (link)]. The C;129S-Vhltm1Jae/J mice were crossed with B6.Cg-Ndor1Tg(UBC-cre/ERT2)1Ejb/1J or UBC-Cre-ERT2 mice (Jackson Laboratories, stock no. 008085) that ubiquitously express a tamoxifen-inducible Cre recombinase (Cre-ERT2) [64 (link)]. UBC-Cre-ERT2 VhlLoxP/LoxP mice were generated through the appropriate crosses, along with the corresponding control mice. Then UBC-Cre-ERT2 VhlLoxP/LoxPHif1aLoxP/LoxP mice were generated using B6.129-Hif1atm3Rsjo/J mice (Jackson Laboratories, stock no. 007561) that harbor two loxP sites flanking exon 2 of the murine Hif1a locus [65 (link)]. These mice were then crossed with B6.Cg-Ndor1Tg(UBC-cre/ERT2)1Ejb/1J mice as described above to generate UBC-Cre-ERT2 Hif1aLoxP/LoxP mice, which were subsequently crossed with C;129S-Vhltm1Jae/J mice to generate UBC-Cre-ERT2 VhlLoxP/LoxPHif1aLoxP/LoxP mice and their corresponding control mice. The UBC-Cre-ERT2 VhlLoxP/LoxPHif2aLoxP/LoxP mice were generated through the appropriate crosses using Epas1tm1Mcs/J mice (Jackson Laboratories, stock no. 008407) [66 (link)].
Bouthelier A., Meléndez-Rodríguez F., Urrutia A.A, & Aragonés J. (2020). Differential Contribution of N- and C-Terminal Regions of HIF1α and HIF2α to Their Target Gene Selectivity. International Journal of Molecular Sciences, 21(24), 9401.
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4

Investigating HIF1α in NK Cells

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Wild type B6 mice (C57/BLNCR1) were purchased through Charles River Laboratories (Wilmington, MA). HIF1α specific deletion in NK cells was achieved through crossing B6.129-Hif1a tm3Rsjo /J mice from The Jackson Laboratory (Bar Harbor, ME) with Ncr1 iCre mice from Eric Vivier. Control β2m knock out mice were obtained from The Jackson Laboratory.
Victorino F., Bigley T.M., Park E., Yao C., Benoit J., Yang L., Piersma S.J., Lauron E.J., Davidson R.M., Patti G.J., & Yokoyama W.M. (2021). NK cell metabolic adaptation to infection promotes survival and viral clearance.
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5

Myeloid-Specific HIF-1α Knockout Mice

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WT mice were C57BL/6 and were obtained from the Jackson Laboratory, Bar Harbor, ME. All knockout mice were backcrossed to C57BL/6. B6.129-Hif1atm3Rsjo/J mice were obtained from the Jackson Laboratory and were crossed with B6.129P2-Lyz2tm1(cre)Ifo/J to generate mice that had Hif1a deletion targeted to the myeloid lineage. B6.129P2-Nos2tm1Lau/J mice were obtained from the Jackson Laboratory and were bred in house. Bone marrow derived macrophages (BMDM) were obtained by flushing cells from the femurs and tibias of mice and culturing in DMEM with 10% FBS and 10% supernatant from 3T3-M-CSF cells (BMDM media) for 6 days with feeding on day 3. After differentiation, BMDM continued to be cultured in BMDM media containing M-CSF.
Braverman J., Sogi K.M., Benjamin D., Nomura D.K, & Stanley S.A. (2016). HIF-1α is an essential mediator of IFN-γ dependent immunity to Mycobacterium tuberculosis. Journal of immunology (Baltimore, Md. : 1950), 197(4), 1287-1297.
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