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Xenogen ivis

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The Xenogen IVIS is a non-invasive in vivo imaging system designed for real-time monitoring and quantification of bioluminescent and fluorescent reporters in small animal models. The system utilizes a highly sensitive charge-coupled device (CCD) camera to capture high-resolution images of luminescent or fluorescent signals within living animals.

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Lab products found in correlation

Living image 4, by PerkinElmer (4 mentions) B ndg mice, by Biocytogen (4 mentions) D luciferin, by Yeasen (3 mentions) Balb c nude mice, by Charles River Laboratories (2 mentions) Xenolight rediject d luciferin, by PerkinElmer (1 mentions) D luciferin, by PerkinElmer (1 mentions) C57bl 6 recipients, by Jackson ImmunoResearch (1 mentions) Matrigel, by Thermo Fisher Scientific (1 mentions) Nude mice, by Charles River Laboratories (1 mentions) D luciferin sodium salt, by Abcam (1 mentions) Luciferin, by PerkinElmer (1 mentions) Shc002, by Merck Group (1 mentions)

Close spelling variants of this product

Xenogen IVIS Spectrum (41 citations) Xenogen IVIS Imaging System (34 citations) Xenogen IVIS 200 Imaging System (32 citations) Xenogen IVIS system (18 citations) Xenogen IVIS Lumina (18 citations) Xenogen IVIS-100 imaging system (11 citations) Xenogen IVIS imager (7 citations) Xenogen-IVIS 200 in vivo Imaging System (7 citations) Xenogen IVIS® Spectrum In Vivo Imaging System (6 citations) Xenogen IVIS Lumina imaging system (4 citations)

22 protocols using xenogen ivis

1

In Vivo Bioluminescent Imaging of Bladder Cancer

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T24 bladder cancer cells stably expressing luciferase (1 × 105) were suspended in 200 μL PBS and injected into the lateral tail veins of 5-week-old male B-NDG mice (BIOCYTOGEN, Beijing, China). Four weeks later, mice were anaesthetized with isoflurane, and D-luciferin sodium salt (150 mg/kg) was injected intraperitoneally. Bladder cancer cells were detected with an in vivo imaging system, Xenogen IVIS (PerkinElmer, MA, USA). The total flux in photons per second was calculated for the lung region using Living Image 4.3.1 (PerkinElmer/Caliper).
Zhan Y., Cao C., Li A., Mei H, & Liu Y. (2023). Enhanced RNA knockdown efficiency with engineered fusion guide RNAs that function with both CRISPR-CasRx and hammerhead ribozyme. Genome Biology, 24, 9.
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2

Limiting Dilution Assay for Glioblastoma Stem Cells

Cited 2 times
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All animal procedures were performed in accordance with Cleveland Clinic IACUC approved protocols. For in vivo limiting dilution studies, acutely dissociated GBM xenografts were sorted as TfR high (top 20%) and TfR low (bottom 20%) and recovered for 1 h in a 37°C incubator. Three dilutions (10,000, 1000, or 100 cells; n = 5 mice per group) were intracranially injected into mice 4–6 weeks of age. Brains were removed at the onset of neurological signs. For ferritin shRNA studies, luciferase-labeled CSCs were transduced with lentiviral vectors expressing NT, FTH1, or FTL shRNA. At 2 d post-transduction 10,000 viable cells were intracranially injected into mice as previously described (Flavahan et al., 2013 (link); Yan et al., 2014 (link)). A Xenogen IVIS (Perkin Elmer) was used for in vivo imaging.
Schonberg D.L., Miller T.E., Wu Q., Flavahan W.A., Das N.K., Hale J.S., Hubert C.G., Mack S.C., Jarrar A.M., Karl R.T., Rosager A.M., Nixon A.M., Tesar P.J., Hamerlik P., Kristensen B.W., Horbinski C., Connor J.R., Fox P.L., Lathia J.D, & Rich J.N. (2015). Preferential Iron Trafficking Characterizes Glioblastoma Stem-like Cells. Cancer cell, 28(4), 441-455.
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3

Bioluminescent Lung Cancer Model

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Lung cancer models of NSCLC were created by injecting 5 × 106 A549-luciferase cells in sterile PBS into the tail veins of female SCID beige mice. Cancer development and progression were monitored using the Xenogen IVIS (PerkinElmer) bioluminescence imaging system. 100 μL of 30 mg/mL Xenolight Rediject D-Luciferin (PerkinElmer) was injected intraperitoneally into the mice approximately 10 min before the animals were imaged.
Perepelyuk M., Shoyele O., Birbe R., Thangavel C., Liu Y., Den R.B., Snook A.E., Lu B, & Shoyele S.A. (2016). siRNA-Encapsulated Hybrid Nanoparticles Target Mutant K-ras and Inhibit Metastatic Tumor Burden in a Mouse Model of Lung Cancer. Molecular Therapy. Nucleic Acids, 6, 259-268.
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4

Murine BCR-ABL+ B-ALL Xenograft Model

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Mouse BCR-ABL+Arf−/−Luciferase+ B-ALL cells were injected (2×105) into non-conditioned, 6–8 week-old, female C57BL/6 recipients (Jackson Laboratory). Five days after the transfer, recipients were treated with DHA and ABT-263 by oral gavage. ABT-263 was formulated in a mixture of 60% Phosal 50 PG, 30% PEG 400, and 10% EtOH and dosed at 100 mg/kg/day as previously described (28 (link)). DHA was formulated in 0.5% carboxymethylcellulose, 0.5% Tween-80, and 0.5% benzyl alcohol and dosed at 200 mg/kg/day. Treatment was given daily for 15 days (days 5–20) during and after which the mice were monitored. Mice were bred and utilized in accordance with SJCRHACUC. Bioluminescence imaging was assessed by Xenogen IVIS (Perkin Elmer, MA) after mice were injected with D-luciferin (Perkin Elmer) at 150 mg/kg. Images (photons/second) were quantified through application of a contour drawn around the target region and normalized to maximum luminescence activity. For ex vivo analysis of MCL-1 expression, recipient mice 10 days after transplant of 2×105 mouse BCR-ABL+ B-ALL cells were treated with vehicle or DHA (200 mg/kg) by gavage. Four or 8 hours after treatment, splenic blast cells were isolated and subjected to immunoblotting.
Budhraja A., Turnis M.E., Churchman M.L., Kothari A., Yang X., Xu H., Kaminska E., Panetta J.C., Finkelstein D., Mullighan C.G, & Opferman J.T. (2017). Modulation of Navitoclax Sensitivity by Dihydroartemisinin-Mediated MCL-1 Repression in BCR-ABL+ B-Lineage Acute Lymphoblastic Leukemia. Clinical cancer research : an official journal of the American Association for Cancer Research, 23(24), 7558-7568.
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5

Establishing Lung Cancer Xenograft Model

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T24 bladder cancer cells stably expressing luciferase (1 × 105 cells) were suspended in 200 μL of phosphate-buffered saline and injected into the lateral tail vein of 5-week-old male B-NDG mice (Biocytogen, Beijing, China). Four weeks later, the mice were anaesthetized with isoflurane, and D-luciferin sodium salt (150 mg/kg) was injected intraperitoneally. Bladder cancer cells were counted with an in vivo imaging system, Xenogen IVIS (PerkinElmer, Boston, MA, USA). The total flux of photons per second was calculated for the lung region using Living Image 4.3.1 software (PerkinElmer/Caliper).
Zhan Y., Li A., Cao C, & Liu Y. (2022). CRISPR signal conductor 2.0 for redirecting cellular information flow. Cell Discovery, 8, 26.
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6

Xenograft and Metastasis Model Protocols

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All animal experiments were approved by the Institutional Animal Care and Use Committee (IACUC) of Peking University First Hospital (Beijing, China) and conducted in accordance with its recommendations and ethical regulations. For the tumour xenograft implantation experiment, 1 × 105 SW780 cells were injected subcutaneously into 5-week-old male BALB/c nude mice (Vital River, Beijing, China), which were subsequently sacrificed 8 weeks later. For the metastasis experiment, 1 × 105 5637-Luc cells were suspended in 200 μL PBS and injected into the lateral tail veins of 5-week-old male B-NDG mice (BIOCYTOGEN, Beijing, China). Four weeks after the injection, mice were anaesthetized with isoflurane (YIPIN Pharmaceutical CO., LTD., Hebei, China). Ten minutes after D-luciferin was injected, sodium salt (150 mg/kg) was injected intraperitoneally, and cancer cells were detected with an in vivo imaging system, Xenogen IVIS (PerkinElmer, MA, USA). The total flux in photons per second was calculated and reported for each mouse’s lung and liver region using Living Image 4.3.1 (PerkinElmer/Caliper).
Zhan Y., Chen Z., He S., Gong Y., He A., Li Y., Zhang L., Zhang X., Fang D., Li X, & Zhou L. (2020). Long non-coding RNA SOX2OT promotes the stemness phenotype of bladder cancer cells by modulating SOX2. Molecular Cancer, 19, 25.
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7

Subcutaneous Xenograft and Metastasis Assay

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Five million 786-O cells expressing KLF5 or control vector were subcutaneously injected into 6-week-old female BALB/c nude mice (n=4 for each group). Tumor was measured weekly and volume was calculated according to the following formula: volume= length × width × (width/2). At week 11, mice were euthanized and applied to further histological analysis. For lung metastasis assay, KLF5 or vector expressed 786-O cells were infected with GFP-Luc, then three million cells were injected into retro-orbital venous plexus of nude mice (n=6 for each group). For bioluminescence imaging (BLI), D-luciferin (YEASEN, Shanghai, China) was injected into anesthetized mice and bioluminescence images were captured (Xenogen IVIS, PerkinElmer, Waltham, MA, USA). At week 12, mice were euthanized and applied to further histological analysis. All measurements were performed blindly and all animals were manipulated and housed according to protocols approved by Shanghai Medical Experimental Animal Care Commission.
Fu R.J., He W., Wang X.B., Li L., Zhao H.B., Liu X.Y., Pang Z., Chen G.Q., Huang L, & Zhao K.W. (2017). DNMT1-maintained hypermethylation of Krüppel-like factor 5 involves in the progression of clear cell renal cell carcinoma. Cell Death & Disease, 8(7), e2952-.
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8

Xenograft and Metastasis Tumor Models in Mice

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All animal experiments were approved by the Institutional Animal Care and Use Committee (IACUC) of The First Affiliated Hospital of Zhengzhou University and conducted in accordance with its recommendations and ethical regulations. For the tumour xenograft implantation experiment, 1 × 106 SW780 cells were injected subcutaneously into 5-week-old male BALB/c nude mice (Vital River, Beijing, China), which were subsequently sacrificed 5 weeks later. For the metastasis experiment, 1 × 105 5637-Luc cells were suspended in 200 μL PBS and injected into the lateral tail veins of 5-week-old male B-NDG mice (BIOCYTOGEN, Beijing, China). Four weeks later, mice were anaesthetized with isoflurane and D-luciferin sodium salt (150 mg/kg) was injected intraperitoneally, and cancer cells were detected with an in vivo imaging system, Xenogen IVIS (PerkinElmer, MA, USA). The total flux in photons per second was calculated and reported for each mouse’s lung and liver region using Living Image 4.3.1 (PerkinElmer/Caliper).
Zhan Y., Zhang L., Yu S., Wen J., Liu Y, & Zhang X. (2020). Long non-coding RNA CASC9 promotes tumor growth and metastasis via modulating FZD6/Wnt/β-catenin signaling pathway in bladder cancer. Journal of Experimental & Clinical Cancer Research : CR, 39, 136.
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9

Xenograft Mouse Tumor Imaging

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Nude mice (4–6 weeks old) were obtained from Charles River Laboratory (San Diego, CA, USA) and injected with 300 μl of Matrigel (Invitrogen Waltham, MA, USA) slurry (prepared at a 1:1 ratio with 1X phosphate-buffered saline) containing 10 million cells that constitutively expressed luciferase. Luciferase activity was measured by injecting d-luciferin (50 mg/kg mouse) into anesthetized mice abdominally. We then acquired live images using a Xenogen IVIS (PerkinElmer, New York, NY, USA) as previously described.44 (link)
Han B., Park H.K., Ching T., Panneerselvam J., Wang H., Shen Y., Zhang J., Li L., Che R., Garmire L, & Fei P. (2017). Human DBR1 modulates the recycling of snRNPs to affect alternative RNA splicing and contributes to the suppression of cancer development. Oncogene, 36(38), 5382-5391.
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10

Intracranial Xenograft Tumor Model

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GSCs (1 × 105 viable cells) were grafted intracranially into NSG (NOD scid gamma mouse) mice (InVivos) aged 6 to 8 weeks. Tumor incidence was determined at indicated time points by luciferase imaging of mice using Xenogen IVIS (PerkinElmer) according to the manufacturer’s instructions. Animals were maintained until neurological signs were apparent, at which point they were euthanized. All mouse manipulations were performed with the approval of National University of Singapore Institutional Animal Care and Use Committee.
Yoon J., Grinchuk O.V., Kannan S., Ang M.J., Li Z., Tay E.X., Lok K.Z., Lee B.W., Chuah Y.H., Chia K., Tirado Magallanes R., Liu C., Zhao H., Hor J.H., Lim J.J., Benoukraf T., Toh T.B., Chow E.K., Kovalik J.P., Ching J., Ng S.Y., Koh M.J., Liu X., Verma C.S, & Ong D.S. (2021). A chemical biology approach reveals a dependency of glioblastoma on biotin distribution. Science Advances, 7(36), eabf6033.
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