B6.129s2 alox15tm1fun j

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B6.129S2-Alox15tm1Fun/J is a laboratory mouse strain with a targeted mutation in the Alox15 gene. The Alox15 gene encodes the 12/15-lipoxygenase enzyme, which is involved in the metabolism of arachidonic acid. This mouse strain is used in research to study the role of 12/15-lipoxygenase in various biological processes.

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5 protocols using b6.129s2 alox15tm1fun j

Age-matched C57BL/6 and Alox15-/- Mice

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Male and female, age-matched C57BL/6 mice, 6 to 8 wk of age, were obtained from The Jackson Laboratory (Bangor, ME). Male and female, age-matched Alox15^−/− mice were obtained from The Jackson Laboratory (B6.129S2-Alox15^tm1Fun/J, Stock No: 002778) and bred at Tulane University. All animals were housed in a specific pathogen-free, Association for Assessment and Accreditation of Laboratory Animal Care-certified facility and handled according to Public Health Service Office of Laboratory Animal Welfare policies after review and approval by the Tulane Institutional Animal Care and Use Committee.

Makullah M., Ellis D.A., Jones M, & Steele C. (2023). Hematopoietic 12/15-lipoxygenase activity negatively contributes to fungal-associated allergic asthma. American Journal of Physiology - Lung Cellular and Molecular Physiology, 325(2), L104-L113.

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Evaluation of Nicotinic and Lipoxygenase Deficiency

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Male (age 10 to 16 wk) C57BL/6 (wild-type; Charles River Laboratories), α7-nicotinic receptor–deficient (C57BL/6 background, B6.129S7-Chrna7tm1Bay/J, stock no. 003232 from The Jackson Laboratory), and 12/15-lipoxgenase (Alox15)–deficient (C57BL/6 background, B6.129S2-Alox15tm1Fun/J, stock no. 002778 from The Jackson Laboratory) mice were used. Mice were housed under a 12-h light/dark cycle with ad libitum access to food and water.

Caravaca A.S., Gallina A.L., Tarnawski L., Shavva V.S., Colas R.A., Dalli J., Malin S.G., Hult H., Arnardottir H, & Olofsson P.S. (2022). Vagus nerve stimulation promotes resolution of inflammation by a mechanism that involves Alox15 and requires the α7nAChR subunit. Proceedings of the National Academy of Sciences of the United States of America, 119(22), e2023285119.

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Diabetic Retinopathy and Oxidative Stress

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Animals were used in accordance with the Association for Research in Vision and Ophthalmology (ARVO) Statement for the Use of Animals in Ophthalmic and Vision Research and all procedures were approved by the Institutional Animal Care and Use Committee (IACUC) of Augusta University. We used 8-week-old male wild-type (WT), 12/15-Lo knockout mice (12/15-Lo^−/−; B6.129S2-Alox15tm1Fun/^J; stock no: 002778, Jackson Laboratories, Bar Harbor, ME, USA), or Nox2-deficient mice (Nox2^−/−; B6.129S-Cybb^tm1Din/J; stock No: 002365, Jackson Laboratories) on C57BL/6J background. Diabetes was induced by intraperitoneal injection of streptozotocin (STZ) (Sigma, St Louis, MO, USA) at 50 mg/kg for 3–5 days until the mice developed diabetes (random blood glucose ≥ 13.9 mmol/l). Intravitreal injections were performed in non-diabetic mice as previously described using 12-HETE (Cayman Chemical, Ann Arbor, MI, USA) [25 (link), 26 (link)].

Elmasry K., Ibrahim A.S., Saleh H., Elsherbiny N., Elshafey S., Hussein K.A, & Al-Shabrawey M. (2018). Role of endoplasmic reticulum stress in 12/15-lipoxygenase-induced retinal microvascular dysfunction in a mouse model of diabetic retinopathy. Diabetologia, 61(5), 1220-1232.

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Generation and Characterization of Murine Cd19-Expressing B Cell Reporter Model

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Male and female 7–12-wk-old C57BL/6, B6.129P2(C)-Cd19^{tm1(cre)Cgn/J}, B6.Cg-Gt(ROSA)26Sor^tm6^{(CAG-ZsGreen1)Hze/J}, and B6.129S2-Ighm^tm1Cgn/J mice were obtained from The Jackson Laboratory and were provided access to food and water ad libitum. The Cd19^ZsGreen1 mouse model was generated by crossing homozygous B6.129P2(C)-Cd19^{tm1(cre)Cgn/J} mice with homozygous B6.Cg-Gt(ROSA)26Sor^tm6^{(CAG-ZsGreen1)Hze/J} mice, resulting in fluorescent B cell reporter Cd19^ZsGreen1 mice. LXA₄-deficient mice, termed “Alox15^−/−” (B6.129S2-Alox15^tm1Fun/J) were purchased from The Jackson Laboratory. All mice were housed in the environmentally controlled specific-pathogen-free facility at the University of Calgary. Sibling mice were housed together by sex and used between 6 and 12 wk of age. Male and female mice were used equally among experiments. All animal protocols were approved by the University of Calgary Animal Care Committee (protocol no. AC18-0071).

Podstawka J., Sinha S., Hiroki C.H., Sarden N., Granton E., Labit E., Kim J.H., Andonegui G., Lou Y., Snarr B.D., Sheppard D.C., Rosin N.L., Biernaskie J, & Yipp B.G. (2021). Marginating transitional B cells modulate neutrophils in the lung during inflammation and pneumonia. The Journal of Experimental Medicine, 218(9), e20210409.

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Genetic Mouse Models for Immune Research

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C57BL/6 mice, Alox15^−/− mice (B6.129S2-Alox15^tm1Fun/J), Alox5^−/− mice (B6.129S2-Alox5^tm1Fun/J), CD45.1 mice (B6.SJL-Ptprc^aPepc^b/BoyJ), Mrp8^cre mice (B6.Cg-Tg(S100A8-cre,-EGFP)1Ilw/J), Csf2rb^−/− mice (B6.129S1-Csf2rb^tm1Cgb/J) and K18-hACE2 (B6.Cg-Tg(K18-ACE2)2Prlmn/J) mice were purchased from Jackson Laboratories. Alox15^−/− K18-hACE2 mice were generated by crossing K18-hACE2 mice with Alox15^−/− animals. Alox15^lox/lox mice on a C57BL/6 background were a gift from S. Tersey (University of Chicago, USA) and were crossed with Mrp8^cre mice to generate specific deletion of the ALOX15 pathway in neutrophils. Ltb4r2^−/− mice on a C3HeJ background were a gift from C. Brown (University of Missouri, USA). All animals were housed and inbred at the animal facility of the Research Institute of McGill University under specific pathogen-free conditions with ad libitum access to food and water, a temperature of 21 °C (±1 °C), relative humidity of 40–60% (±5%) and light cycle of 12 h on, 12 h off (daily cycle). Mice were randomly allocated to experimental groups, and experiments were performed using both female and male age- and sex-matched mice.

Pernet E., Sun S., Sarden N., Gona S., Nguyen A., Khan N., Mawhinney M., Tran K.A., Chronopoulos J., Amberkar D., Sadeghi M., Grant A., Wali S., Prevel R., Ding J., Martin J.G., Thanabalasuriar A., Yipp B.G., Barreiro L.B, & Divangahi M. (2023). Neonatal imprinting of alveolar macrophages via neutrophil-derived 12-HETE. Nature, 614(7948), 530-538.

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