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C57bl 6 mice

Manufactured by Jackson ImmunoResearch
Sourced in United States, Montenegro, Canada, China, France, United Kingdom, Japan, Germany

C57BL/6 mice are a widely used inbred mouse strain commonly used in biomedical research. They are known for their black coat color and are a popular model organism due to their well-characterized genetic and physiological traits.

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4 025 protocols using c57bl 6 mice

1

Competitive BM Transplantation in Mice

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As recipients, we used 8‐ to 10‐wk‐old CD45.1+ C57BL/6 mice (The Jackson Laboratory). Mice were placed in a restrainer to ensure immobility during γ‐irradiation. We applied a 10.5‐Gy single dose of irradiation. Donor BM from CD45.2 allele‐bearing C57BL/6 mice (The Jackson Laboratory) was harvested by flushing the femur BM under sterile conditions, and lineage‐negative CD45.2+ BM cells were i.v. injected at 400 ×103 cells/recipient density. As competitor cells, we injected an equal amount of lineage‐negative cells from CD45.1+ BM. The amount of CD45.1+ and CD45.2+ leukocytes in BM and peripheral blood and the amount of CD45.1+, F4/80+, and CD45.2+, F4/80+ ATMs was measured by FACS at 20 wk after BM transplantation.
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2

Transgenic Mouse Generation for miR-34a

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For all experiments with wild type (wt) mice, C57BL/6 mice were purchased from Jackson Laboratories. Experiments were performed primarily at VA Ann Arbor Healthcare System, with additional experiments at National Jewish Health; both Animal Care Facilities are fully accredited by the American Association for Accreditation of Laboratory Animal Care. Mice were housed under specific pathogen-free conditions and used for experiments between 8–16 weeks of age. To generate miR-34a+/− mice, miR-34a flox/flox mice on a C57BL/6 background (37 (link)) (Jackson) were crossed with LysM cre mice (Jackson). The F1 generation of miR-34a flox/− LysM cre mice (referred to as miR-34a+/−) was genotyped following Jackson protocols, with non-littermate, age-matched C57BL/6 mice as wt controls in all such experiments. Mice were fed standard animal chow (rodent lab chow 5008; Purina, St. Louis, MO) and chlorinated tap water ad libitum. Animal care and experimentation were conducted in accordance with U.S. Department of Health and Human Services Guide for the Care and Use of Laboratory Animals and were approved by the Animal Use Committee at VA Ann Arbor Healthcare System and National Jewish Health.
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3

Evaluation of Complement Deficient Mice

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BALB/c mice were obtained from Bommice (Ry, Denmark). Mice deficient in FcγRIIB, C.129S4(B6)-Fcgr2btmlTtK/cAnNTac N12 (FcγRIIB KO) were purchased from Taconic Biosciences, Inc. (Hudson, NY, USA), FcRγ KO founders were a gift from Dr J. V. Ravetch [16 (link)] and backcrossed to BALB/c for 10 generations. Wildtype C57BL/6 mice, C57BL/6 mice lacking complement factor C3 (C3 KO) and Ig allotype congenic mice, C.BKa-Ighb/lcrSMnJ (CB17), were obtained from Jackson Laboratories (Bar Harbor, ME, USA). Mice lacking CR1/2 (Cr2 KO) were a gift from Dr H. Molina [17 (link)] and backcrossed for 10 generations to BALB/c background. C57BL/6 C1qA-deficient founder mice (C1q KO), lacking the classical pathway activator C1q, were obtained from Dr M. Botto [18 (link)]. Mice were age and sex matched within each experiment. All animal experiments were approved by the Uppsala Animal Research Ethics Committee. Animals were bred and maintained in the animal facilities at the National Veterinary Institute (Uppsala, Sweden).
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4

Generating TRPV1-Deficient Mice for DRG Isolation

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C57BL6 mice carrying the TRPV1tm1Jul (targeted mutation 1, David Julius) knock-out allele in homozygosity were obtained from The Jackson Laboratory and crossed with wild-type C57BL6 mice to generate TRPV1-/+ animals, and these heterozygotes were bred in timed pregnancies to produce mixed-genotype litters (confirmed by PCR; for primer squences, see Table 1) of wild-type and TRPV1-/- E13.5 embryos for DRG isolation.
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5

Preclinical Evaluation of Therapeutic Combinations for Pancreatic Cancer

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All mouse studies were approved by the University of Cincinnati Institutional Animal Care and Use Committee (IACUC) (protocol: 07-01-11-01, approval date: 17 September 2018) that maintains an American Association of Assessment and Accreditation of Laboratory Animal Care (AAALAC) facility. C57BL/6 mice purchased from Jackson Laboratories were orthotopically transplanted with 500,000 7940B cells derived from a primary spontaneous PDAC tumor arising in the body of the pancreas (C57BL/6) of a male transgenic KrasLSL-G12D/+, Trp53LSL-R172H/+, Pdx1-Cre (KPC) mouse [39 (link),40 (link)] (kindly donated by Dr. Gregory Beatty, University of Pennsylvania). Nod scid gamma mice were orthotopically transplanted with 500–1000 pancreatic cancer organoids derived from PDAC patients.
In a separate series of experiments, 7 days post-orthotopic transplantation, C57BL/6 mice (Jackson Laboratories) were treated with gemcitabine (Selleckchem, S1149) (325 μg/mouse, i.p.) every 2 weekdays and Epothilone A (abaraxane, Selleckchem, S1297) (13 μg/mouse, i.v.) every 5 days, InVivoPlus anti-mouse PD-1 (BioXCell, BP0146) (200 μg/mouse, i.p.) every 5 days, Cabozantinib (cabo, Selleckchem, S1119) (780 μg/mouse, oral gavage) every weekday or a combination of 3 or 4 drugs for 7 days. The mice were sacrificed, tumors were removed and weighed.
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6

Transgenic Mouse Models for Neurotrauma

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All experiments were performed according to NIH guidelines for the care and use of animals in research and under protocol approved by IACUC at the University of Maryland, Baltimore. All experiments were performed on young adult male mice (9–12 weeks old, 21–27 g). Sham and CCI surgeries were performed on the following mice: Cx3cr1-GFP mice (The Jackson Laboratory, 005582), Ccr2-RFP mice (The Jackson Laboratory, 017586), C57Bl/6 mice (The Jackson Laboratory, 00064), transgenic C57Bl/6 mice expressing GFP-LC3 [64 (link)], ROSAtdTomato mice (The Jackson Laboratory, 007914), Lyz2/LyzM-Cre mice (The Jackson Laboratory, 004781) and Becn1/Beclinflox/flox mice (The Jackson Laboratory, 028794). Lyz2/LyzM-Cre mice and Becn1/Beclinflox/flox mice were crossed with each other for two generations to produce Becn1flox/flox; Lyz2Cre/Cre knockout mice, all mice genotyped for flox and Cre alleles according to the The Jackson Laboratory genotyping protocol. All mice were housed on sterilized bedding in a specific pathogen- free facility (12 h light/dark cycle).
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7

Hemorrhagic Shock and Rescue in Aging Mice

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Young (5-6-week-old) and mature (3-4-month-old) male C57BL/6 mice used were obtained from Jackson laboratories and aged (23-26-month-old) C57BL/6 mice were from the National Institute of Aging rodent colony. Animal studies were conducted as per the protocol approved by the Institutional Animal Use and Care committee at the Augusta University. Hemorrhagic shock was induced as described before [25 (link)]. Briefly 60% blood volume was removed in 45 minutes through femoral artery, to induce hypovolemic shock (Mean arterial pressure: 30-35 mm Hg) and this MAP was maintained for another 45 minutes (shock period). Sham animals were not subjected to bleeding or fluid resuscitation, but they were subjected to laparotomy and groin incisions. For survival studies, EVs or vehicle was given immediately after the shock period (Fig. 1A). Each group for this study had 5-6 animals. For organ function studies, the animals were resuscitated following shock period for 1 hour, with Ringers Lactate (twice the shed blood volume), observed for another two hours and sacrificed to remove tissues for mitochondrial function assessment (Fig. 2A). Each group for this study had 6 animals. In this latter group, EVs or vehicle was administered as a single dose (50 µl; 2 mg/Kg body weight) at 10 minutes after the start of fluid resuscitation.
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8

Congenic Mouse Model for KRAS-driven PDAC

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Survival data and primary cell lines were generated from KrasLSL-G12D/+, Trp53LSL-R172H/+, Pdx1-Cre (KPC) mice (14 (link)) bred in-house, backcrossed more than 10 generations with C57BL/6 mice (Jackson Laboratories), and assessed at the DartMouse Speed Congenic Core Facility at the Geisel School of Medicine at Dartmouth College. The raw SNP data were analyzed using DartMouse’s SNaP-Map and Map-Synth software, allowing the determination for each mouse of the genetic background at each SNP location. Backcrossed KPC mice were found to be congenic based on the DartMouse Illumina GoldenGate Genotyping Assay, which interrogated 1,449 SNPs spread throughout the genome. C57BL/6 OVA transgenic mice (Act-mOVA) (38 (link)) were purchased from Jackson Laboratories. Tumor implant studies were performed using 8- to 10-week-old female C57BL/6 mice purchased from Jackson Laboratories. For induction of oral tolerance to OVA, wild-type mice were treated by oral gavage with 50 mg OVA protein (Sigma-Aldrich) dissolved in 250 μl PBS or with PBS alone weekly for 3 doses, followed 1 week later by tumor challenge with 1.25 × 105 V6.Ova tumor cells subcutaneously.
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9

Murine Models of NAFLD Induction

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Eight-week-old weight-matched male C57BL/6 mice and CD45.1 congenic C57BL/6 mice were purchased from The Jackson Laboratory (Bar Harbor, ME). MCD has short modeling duration, low cost, and easy acquisition, which can effectively induce steatosis and steatohepatitis, and the lipid distribution in liver can simulate human NAFLD well.42 (link), 43 (link), 44 (link) One of the most important disadvantages of the MCD model is that the extrahepatic metabolic performance differs from that of the vast majority of human NAFLD patients, with this model displaying significant loss weight gain and decreased blood glucose levels.44 (link) In addition, CDHFD-fed mice also developed well to mimic human NAFLD and fibrosis disease.44 (link) Because of its long duration, it has a high chance of progressing to liver cancer.45 (link) Thus, we mainly used these 2 diets to induce NAFLD models. After being allowed to adapt for 5 days, the C57BL/6 mice were fed either a NCD or a MCD (10401; Beijing HFK Bioscience, Beijing, China) for 5 weeks or a CDHFD for 18 weeks. The mice were housed in a pathogen-free, comfortable temperature environment with a 12-hour light/dark cycle. All animal studies were performed in compliance with the ethical guidelines for animal studies and approved by the animal ethics committee of Beijing Friendship Hospital, Capital Medical University.
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10

Cisplatin-Induced Acute Kidney Injury in Mice

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The procedure was based on the previously published method68 (link). In detail, C57BL/6 mice (6-week-old male, average weight 16–18 g) were purchased from Jackson Laboratories (Bar Harbor, ME, USA), and Gdf15 KO C57BL/6 mice were kindly provided by Dr. Se-Jin Lee (Johns Hopkins University, Baltimore, MD, USA). All mice of the same age were placed in one cage and randomly transferred to different cages without bias. Mice were randomly assigned to specific treatment groups. The mice were acclimatized for 14 days before experimentation and maintained at 22 ± 2 °C under 45–55% relative humidity, with a 12/12 h light/dark cycle. Three mice were housed per cage and provided sufficient food and water in environmentally protected cages, comprising a transparent polypropylene body and stainless-steel top cover. Chemotherapy-induced AKI was induced by an intraperitoneal injection of cisplatin (20 mg/kg). Eight-week-old wild-type and Gdf15 KO mice were treated with vehicle or CP (20 mg/kg, intraperitoneally) for 72 h (n = 4 − 5). To induce DSS-induced colitis and renal complications, seven-week-old male mice were treated with 3% DSS (molecular weight 36,000–50,000 Da; MP Biomedical, Solon, OH, USA) ad libitum in drinking water for eight days. Two days later, the mice were sacrificed under deep ether anesthesia.
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