C57bl 6 ins2akita j mice

Manufactured by Jackson ImmunoResearch

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The C57BL/6-Ins2Akita/J mice are a strain of laboratory mice. These mice have a genetic mutation in the insulin 2 (Ins2) gene, which leads to the development of type 1 diabetes.

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C57bl 6j mice, by Jackson ImmunoResearch (2 mentions) Wild type c57bl 6j male mice, by Jackson ImmunoResearch (1 mentions) C57bl 6j, by Jackson ImmunoResearch (1 mentions)

5 protocols using c57bl 6 ins2akita j mice

Diabetic Akita Mouse Model Study

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Male wild-type C57BL/6J mice (stock no. 000664) and diabetic C57BL/6-Ins2^Akita/J mice (stock no. 003548) of 10–14 weeks old were obtained from the Jackson Laboratory (Bar Harbor, ME). Mice were fed standard mouse chow and water ad libitum, and were maintained under a 12:12 h light–dark cycle. All animal experiments were carried out in accordance with the institutional animal care and use committee-approved protocols (approval no. 20683, dated 2 December 2020) of the University of Louisville School of Medicine and conformed to the Guide for the Care and Use of Laboratory Animals of the National Institutes of Health (NIH Publication, 2011), U.S.A. Wild-type and diabetic Akita mice were treated either with normal saline or with GYY (0.25 mgKg⁻¹ d⁻¹, I.P.) for 8 weeks [13 (link),58 (link),59 (link)]. At the end of the experiment, mice were euthanized by using 2X tribromoethanol (TBE), and both blood and kidney samples were collected.

Juin S.K., Pushpakumar S, & Sen U. (2021). GYY4137 Regulates Extracellular Matrix Turnover in the Diabetic Kidney by Modulating Retinoid X Receptor Signaling. Biomolecules, 11(10), 1477.

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Femur Fracture Healing in Diabetic Mice

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All protocols and experiments described were approved by the Washington University IACUC. Male heterozygous C57BL/6-Ins2^Akita/J mice (Akita, stock No. 003548) and female C57Bl/6J mice (wildtype, stock No. 000664) purchased from Jackson Laboratory were set up as breeders at 8-weeks age. Mice were genotyped using qPCR (Transnetyx, Ins2-1 MUT probe). Experimental mice were littermate males heterozygous for the mutation (Ins2-1 MUT probe present, Akita) and males without the mutation (wildtype, WT). Akita and WT mice were housed together under standard conditions. A total of 167 mice were used (69 Akita, 98 WT), with serum glucose measured on all mice. Unilateral (right) femur fractures were created at 18 weeks, and mice were euthanized 3 to 21 days later. Bilateral femora were harvested at post-fracture days 3 (D3, n = 13 Akita, n = 16 WT), 7 (D7, n = 14 Akita, n = 18 WT), 14 (D14, n = 15 Akita, n = 24 WT) and 21 (D21, n = 20 Akita, n= 29 WT), with euthanasia performed by CO₂ asphyxiation (except where otherwise noted). Group sample sizes are indicated for each outcome below. A subset of Akita and WT mice were not fractured (Non-Fx; n = 6/group) and used for baseline serum measurements at 18 weeks. All other data presented are from mice subjected to fracture.

Hu P., McKenzie J.A., Buettmann E.G., Migotsky N., Gardner M.J, & Silva M.J. (2021). Type 1 diabetic Akita mice have low bone mass and impaired fracture healing. Bone, 147, 115906.

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Circadian Rhythm and Diabetes Mouse Models

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Male WT C57BL6J mice and C57BL/6-Ins2^Akita/J mice were purchased from the Jackson Laboratory (Bar Harbor, ME). PdxCre;Bmal1^flx/flx and Cry1^-/-;Cry2^-/- mice were produced and maintained on C57BL6J background at the Northwestern University Center for Comparative Medicine (Protocols IS00000466, IS00003253, IS00008732, IS0005838) (Peek et al., 2013 (link); Vitaterna et al., 1999 (link)). Unless otherwise stated, animals were maintained on a 12:12 light:dark cycle and allowed free access to water and regular chow. All animal care and use procedures were conducted in accordance with regulation of the Institutional Animal Care and Use Committee at Northwestern University.

Marcheva B., Weidemann B.J., Taguchi A., Perelis M., Ramsey K.M., Newman M.V., Kobayashi Y., Omura C., Manning Fox J.E., Lin H., Macdonald P.E, & Bass J. (2022). P2Y1 purinergic receptor identified as a diabetes target in a small-molecule screen to reverse circadian β-cell failure. eLife, 11, e75132.

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Transgenic Mouse Models Overexpressing BMF and hnRNP F

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Tg mice specifically overexpressing human myc-BMF in their RPTCs were generated using a similar strategy to that described previously^{20 (link),28 (link),49 (link)}. In brief, full-length human BMF cDNA fused with Myc-tag was inserted into pKAP2 plasmid at the NotI site. The plasmid pKAP2 containing the KAP promoter that is responsive to androgen was a gift from Dr. Curt D. Sigmund (University of Iowa, Iowa City, IA)^{50 (link)}.
Akita hnRNP F-Tg mice were generated by cross-breeding hnRNP F-Tg mice with heterozygous Akita (C57BL/6-Ins2 Akita/J) mice (Jackson Laboratory, Ann Harbor, ME) as previously described^{28 (link)}.

Ghosh A., Zhao S., Lo C.S., Maachi H., Chenier I., Lateef M.A., Abdo S., Filep J.G., Ingelfinger J.R., Zhang S.L, & Chan J.S. (2019). Heterogeneous Nuclear Ribonucleoprotein F Mediates Insulin Inhibition of Bcl2-Modifying Factor Expression and Tubulopathy in Diabetic Kidney. Scientific Reports, 9, 6687.

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Investigating Diabetic Neuroinflammation in Mice

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All animal procedures were conducted at the University of Louisville Health Sciences Center, were in compliance with guidelines established by the National Institutes of Health Guide for the Care and Use of Laboratory Animals, and were approved by the University of Louisville Institutional Animal Care and Use Committee. Male wild-type (WT; C57BL/6J) and Akita (genetic T1D mice, C57BL/6-Ins2^Akita/J) mice (8–10 weeks old) were obtained from The Jackson Laboratory (Bar Harbor, ME). The experimental mice groups were 1) sham, 2) IR, 3) sham^Akita, and 4) IR^Akita. Akita mice with a glucose level >400 mg/dL were used in the study. We assessed inflammatory (tumor necrosis factor-α [TNF-α], interleukin-6 [IL-6]) and anti-inflammatory (IL-10) cytokines and glial markers (glial fibrillary acidic protein [GFAP]), integrin-α M [CD11b]) using real-time quantitative (q)-PCR. Neuronal (neuronal nuclei [NeuN], neuronal-specific enolase [NSE], nNOS), vascular (zona occluden-1 [ZO-1], claudin-5, eNOS), and epigenetic (DNMT-1 and DNMT-3a) markers were determined using Western blot. MMP-9, vascular (vascular endothelial [VE]-cadherin, occludin), glial (connexin-43 [Cx-43], GFAP), and neuronal (NeuN) markers were quantified using immunohistochemistry (IHC) analysis.

Kalani A., Kamat P.K, & Tyagi N. (2015). Diabetic Stroke Severity: Epigenetic Remodeling and Neuronal, Glial, and Vascular Dysfunction. Diabetes, 64(12), 4260-4271.

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