Nog mice

Manufactured by Taconic Biosciences

Sourced in Denmark

The NOG mouse is a genetically engineered strain of laboratory mouse developed by Taconic Biosciences. The NOG mouse is characterized by the absence of mature T cells, B cells, and natural killer (NK) cells, making it a useful model for immunological research and the study of human disease.

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Lab products found in correlation

Matrigel, by BD (3 mentions) Hil2 nog mice, by Taconic Biosciences (2 mentions) Trametinib, by Selleck Chemicals (2 mentions) 17β estradiol, by Merck Group (1 mentions) N hexane, by Merck Group (1 mentions) Matrigel, by Corning (1 mentions) Ivis imaging system, by PerkinElmer (1 mentions) Gentamycin, by Thermo Fisher Scientific (1 mentions) Nude mice, by Jackson ImmunoResearch (1 mentions) X rad 320, by Precision X-Ray (1 mentions) Mouse tumor dissociation kit, by Miltenyi Biotec (1 mentions) Aldhefluor assay kit, by STEMCELL (1 mentions) Anti human epcam pe, by Miltenyi Biotec (1 mentions) C57bl 6 mice, by Charles River Laboratories (1 mentions) Vemurafenib, by Roche (1 mentions) Deoxyribonuclease 1, by Merck Group (1 mentions) D4263, by Merck Group (1 mentions) Collagenase type 1 c0130, by Merck Group (1 mentions) R26 tdtomato, by Jackson ImmunoResearch (1 mentions) Bmi1creer, by Jackson ImmunoResearch (1 mentions)

Close spelling variants of this product

NOD.Cg-Prkdcscid Il2rgtm1Sug/JicTac (NOG) mice (8 citations) CIEA-NOG mice (7 citations) NOD/Shi-scid/IL-2Rγnull (NOG) mice (5 citations) IL-2 NOG mice (2 citations) NOG-EXL mice (2 citations) CIEA NOG immunodeficient mice (2 citations) HIL2-NOG) mice (2 citations)

17 protocols using nog mice

Xenograft Model of Mammary Progenitor Cells

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From primary co-culture with iHBFC^CD105 or iHBFC^CD26, approximately 500,000 myoepithelial cells, with or without removal of co-cultured CD271^low fibroblasts by FACS, representing two biopsies, were admixed with 125,000 or 500,000 irradiated (~ 20 Gy) iHBFC^CD105 or iHBFC^CD26 cells and suspended in cold 1:1 collagen gel to growth factor reduced Matrigel (BD Biosciences) for transplantation. Cells were orthotopically injected into the 4th left and right mammary fat pad of 7–10-week-old female NOD.Cg-Prkdc^SCIDIl2rg^tm1sug mice (NOG mice, Taconic) (iHBFC^CD105: 10 transplants, 5 mice; iHBFC^CD26: 8 transplants, 4 mice). Mice were supplemented with 0.67 μg/mL 17β-estradiol (Sigma-Aldrich) in the drinking water throughout the experimental period. After 8 weeks, the mice were sacrificed and the mammary glands excised and snap frozen in − 80 °C n-Hexane (Sigma) before mounting for cryostat sectioning.

Morsing M., Kim J., Villadsen R., Goldhammer N., Jafari A., Kassem M., Petersen O.W, & Rønnov-Jessen L. (2020). Fibroblasts direct differentiation of human breast epithelial progenitors. Breast Cancer Research : BCR, 22, 102.

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Establishing Patient-Derived Xenograft Models

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All animal experiments were performed in accordance with EU directive 2010/63 (regional animal ethics committee of Gothenburg #36-2014). The PDXs were obtained by injecting 2 × 10⁵ cells mixed with equal volume of Matrigel (Corning, NY, USA) subcutaneously at the flank of immunocompromised, non-obese severe combined immune-deficient interleukin-2 chain receptor γ knockout mice (NOG mice; Taconic, Ry, Denmark) as described previously.^{30 (link)} Tumors were measured with caliper at regular time points and tumor volume calculated using the formula: tumor volume (mm³)=(length(mm)) × (width(mm))²/2. B16F10-luciferase cells were transplanted by subcutaneous injection. Seven days after transplantation, mice were injected with 100 μl of 30 mg/ml d-luciferin. Mice were sedated in an isofluran administrating chamber and then placed in an IVIS Lumina III XR machine (Perkin-Elmer, Norwalk, CT, USA).

Muralidharan S.V., Einarsdottir B.O., Bhadury J., Lindberg M.F., Wu J., Campeau E., Bagge R.O., Stierner U., Ny L., Nilsson L.M, & Nilsson J.A. (2017). BET bromodomain inhibitors synergize with ATR inhibitors in melanoma. Cell Death & Disease, 8(8), e2982-.

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PDX Model-Based Tumor Immunotherapy Evaluation

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The design and performance of animal experiments in the current study were in accordance with EU Directive 2010/63. PDX mice (PDXv.2 model, [23 (link)]), and were established as follows: small tumor pieces were placed under the skin on the flank of 6–15-week-old NOG mice (non-obese severe combined immune-deficient interleukin-2 chain receptor γ knockout mice, Taconic, Denmark). Tumors were measured weekly with calipers, and tumor volumes were calculated as width × width × length/2. For further transplantations or treatments, tumors were extracted, and tumor suspensions were serially passaged via subcutaneous injections to NOG mice or human IL-2 transgenic NOG (hIL2-NOG) mice (Taconic). For TIL treatments, 10 × 10⁶ RepTILs were transferred intravenously to hIL-2 NOG mice with actively growing tumors, as confirmed by caliper measurements. Trametinib was mixed into the chow at 2.5 mg/kg, resulting in an approximate dose of 0.5 mg/kg mouse per day. Trametinib treatment started around 3 weeks after RepTIL transfer.

Liang F., Nilsson L.M., Byvald F., Rezapour A., Taflin H., Nilsson J.A, & Yrlid U. (2022). A Fraction of CD8+ T Cells from Colorectal Liver Metastases Preferentially Repopulate Autologous Patient-Derived Xenograft Tumors as Tissue-Resident Memory T Cells. Cancers, 14(12), 2882.

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Engraftment and Immunotherapy of Human Tumors

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All mouse experiments were performed in accordance with EU Directive 2010/63 (Regional Animal Ethics Committee of Gothenburg #2014-36, #2016-100, and #2018-1183). Non-obese diabetic-severe combined immune-deficient interleukin-2 chain receptor γ chain knockout mice (NOG mice, Taconic, Ry, Denmark) and human IL-2 transgenic NOG (hIL2-NOG) mice (Taconic) were used for the engraftment of tumor samples. Tumor size was monitored by caliper measurements, alternatively bioluminescent signals, using the IVIS imaging system (Perkin-Elmer). When tumor growth was confirmed by two consecutive measurements, hIL2-NOG mice were treated with autologous human tumor-infiltrating lymphocytes (TILs; 20 million cells per mouse) by intravenous injection into the tail vein. NOG mice served as untreated controls.

Forsberg E.M., Riise R., Saellström S., Karlsson J., Alsén S., Bucher V., Hemminki A.E., Olofsson Bagge R., Ny L., Nilsson L.M., Rönnberg H, & Nilsson J.A. (2023). Treatment with Anti-HER2 Chimeric Antigen Receptor Tumor-Infiltrating Lymphocytes (CAR-TILs) Is Safe and Associated with Antitumor Efficacy in Mice and Companion Dogs. Cancers, 15(3), 648.

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Rectal Cancer Patient-Derived Xenografts

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Patient-derived xenografts were created from biopsies from consented patients with rectal cancer prior to treatment. All animal protocols were performed in accordance with our institutional-approved protocol. Fresh tumor samples were rinsed with PBS and gentamycin (Thermo Fisher Scientific); necrotic tissue was removed, and a 2 mm³-sized tumor piece was implanted into Central Institute for Experimental Animals NOG mice (Taconic). Once tumors were of appropriate size (10 × 20 mm³), mice were sacrificed, and tumors were removed. Tumor pieces of 2 mm³ were implanted in the flank of Nude mice (Jackson Laboratories). Once tumors reached 150 mm³, mice were split into the following treatment groups: vehicle or capecitabine (100 mg/kg) and 2 Gy (Gy) radiation 5 days per week for 2 weeks. Capecitabine (LC Laboratory) was given via oral gavage. Mice were placed in a custom jig for shielding, and radiation was delivered to tumors via X-RAD 320 (Precision X-Ray, Inc) daily. Mice were weighed, and tumors were measured with calipers at least twice weekly. Tumor volumes were calculated based on caliper measurements as previously described (29 (link)). Tumors were harvested 1 week after completion of the 2-week treatment.

Smithson M., Irwin R., Williams G., Alexander K.L., Smythies L.E., Nearing M., McLeod M.C., Al Diffalha S., Bellis S.L, & Hardiman K.M. (2022). Sialyltransferase ST6GAL-1 mediates resistance to chemoradiation in rectal cancer. The Journal of Biological Chemistry, 298(3), 101594.

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Xenograft Tumor Growth Assay

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All animal experiments were performed in accordance with regional/local animal ethics committee approval (approval number 36/2014). C6 or NCH412K cells were injected subcutaneously onto the flanks of immunocompromised, non-obese severe combined immune-deficient interleukin-2 chain receptor γ knockout mice (NOG mice; Taconic, Denmark). Tumours were measured with caliper at regular time points and tumour volumes were calculated using the formula: tumour volume (mm3) = (length(mm)) × (width(mm))2/2. Treatments were started when the tumours were actively growing, judged by increasing volumes on repeated caliper measurements. Trametinib was mixed in the chow at 2.5 mg/kg giving an approximate dose of 0.5 mg/kg mouse per day. HMBA was given in drinking water as 2.5% HMBA, 0.33 g/L bicarbonate, 2% sucrose. Vehicle was given as 0.33 g/L bicarbonate, 2% sucrose. Mice were sacrificed and tumours were harvested before or when tumours reached ethical size limit.

Funck-Brentano E., Vizlin-Hodzic D., Nilsson J.A, & Nilsson L.M. (2020). BET bromodomain inhibitor HMBA synergizes with MEK inhibition in treatment of malignant glioma. Epigenetics, 16(1), 54-63.

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Isolation of HNSCC Cancer Cell Subpopulations

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The use of human HNSCC tissues for this study was approved by the UCLA Institutional Review Board. The human HNSCC primary tissues were obtained from the UCLA Translational Pathological Core and subcutaneously inoculated into flank of 6-week-old NOG mice (Taconic) to generate the PDXs. The murine HNSCC primary tissues from 4NQO-induced Bmi1^CreER;Rosa^tdTomato mouse were transplanted to the flank of 6-week-old NOG mice to generate murine HNSCC xenografts. Human and murine HNSCC xenografted tumors were chopped and then digested into single cell suspensions by using a human tumor cell dissociation kit (Miltenyi Biotec, Cat#130095929) or a mouse tumor dissociation kit (Miltenyi Biotec, Cat# 130096730). To isolate CD276^high and CD276^low cancer cells from tumor tissues, the single cell suspension was incubated with anti-human EpCAM-PE (Miltenyi Biotec, Cat#130110999; 1:50), anti-human CD276-APC (Miltenyi Biotec, Cat#130095522; 1:100) or anti-mouse EpCAM-FITC (Miltenyi Biotec, Cat# 130102214; 1:50) and anti-mouse CD276-APC (BioLegend, Cat#135608; 1:50) for 30 min on ice and then sorted by a FACSVantage SE (Beckton Dickson). The results were analyzed with FlowJo software (https://www.flowjo.com). For ALDH^bright and ALDH^dim cell sorting, cancer cells were stained with an ALDHEFLUOR assay kit (STEMCELL Technologies, Cat#01700).

Wang C., Li Y., Jia L., Kim J.K., Li J., Deng P., Zhang W., Krebsbach P.H, & Wang C.Y. (2021). CD276 expression enables squamous cell carcinoma stem cells to evade immune surveillance. Cell stem cell, 28(9), 1597-1613.e7.

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Xenograft Mouse Model for Rhabdomyosarcoma

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Animal procedures were performed in accordance with IACUC-approved protocol as previously described [48 (link)]. A total of 5 × 10⁶ Rh30 cells were suspended in 100 μL PBS and injected into each flank of six 6-10 week old athymic female NOG mice (Taconic). Mice were monitored until tumors were approximately 50 mm³, and split into treatment and control groups. Mice were administered either CPT-11 (10 mg/kg) or PBS via tail vein injection weekly, and tumor growth was measured weekly by digital caliper. At the end-point of the experiment (when a single tumor reached ~1000 mm³ in volume), the mice were sacrificed and the tumors harvested for immunohistochemistry (IHC) staining, which was carried out using Ki-67 or MyHC (MF20) antibodies as previously described by the Pathology Network Shared Resource at Roswell Park [48 (link)].

Wolff D.W., Lee M.H., Jothi M., Mal M., Li F, & Mal A.K. (2018). Camptothecin exhibits topoisomerase1-independent KMT1A suppression and myogenic differentiation in alveolar rhabdomyosarcoma cells. Oncotarget, 9(40), 25796-25807.

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Orthotopic Xenograft Model for Breast Cancer

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Animal experiments were approved by DFCI IACUC under protocol #11–023. SUM149 or SUM159 cells (1 × 10⁶) expressing TET-inducible Luciferase or EN1-targeting shRNAs were resuspended in 50% Matrigel (BD Biosciences) and injected orthotopically into the mammary fat pads of 6-week old female NOG mice (Taconic). When the tumors became palpable, shRNAs were induced in the treatment group by administering a doxycycline diet (625ppm). Animals were euthanized and tumors were harvested when tumors in the control group reached ~ 1.5 cm size. For histological analyses, 5μm sections of formalin-fixed paraffin-embedded (FFPE) tissue slides were stained with hematoxylin and eosin using standard protocols.

Peluffo G., Subedee A., Harper N.W., Kingston N., Jovanović B., Flores F., Stevens L.E., Beca F., Trinh A., Chilamakuri C.S., Papachristou E.K., Murphy K., Su Y., Marusyk A., D’Santos C.S., Rueda O.M., Beck A.H., Caldas C., Carroll J.S, & Polyak K. (2019). EN1 is a transcriptional dependency in triple-negative breast cancer associated with brain metastasis. Cancer research, 79(16), 4173-4183.

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Comparison of C57BL/6 and NOG Mice

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C57BL/6 mice were obtained from Charles River Laboratories. NOG mice were obtained from Taconic and housed in a specific pathogen-free environment. All mice weighing between 25 and 35 g were used in this study. Free access to sterilized food and water was provided. This experiment was reviewed by the Institutional Animal Care and Use Committee at the Cedars-Sinai Medical Center.

Do A.S., Amano T., Edwards L.A., Zhang L., De Peralta-Venturina M, & Yu J.S. (2020). CD133 mRNA-Loaded Dendritic Cell Vaccination Abrogates Glioma Stem Cell Propagation in Humanized Glioblastoma Mouse Model. Molecular Therapy Oncolytics, 18, 295-303.

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