C57bl 6j ticam1lps2 j

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C57BL/6J-Ticam1Lps2/J is a laboratory mouse strain that carries a mutation in the Ticam1 gene, which is also known as Trif. This gene is involved in the Toll-like receptor signaling pathway. The Lps2 allele in this strain refers to a mutation in the Lps gene, which is associated with the immune response to lipopolysaccharide.

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C57BL/6J (4187 citations)

17 protocols using c57bl 6j ticam1lps2 j

Enteroid and Colonoid Cultivation

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All studies using mice were approved by and performed according to the University of Miami Institutional Animal Care and Use Committees’ (IACUC) guidelines (Protocol number 14–041). Animal sacrifice was performed using isoflurane anesthesia followed by cervical dislocation. Wild-type (C57BL/6J) were originally purchased from Jackson Laboratories (Bar Harbor ME) and bred in-house. Ticam1^Lps2 (C57BL/6J-Ticam1^Lps2/J, Jackson laboratories, Bar Harbor ME) tissue was a generous gift from Dr. Masayuki Fukata, University of California Los Angeles. Enteroids were grown from mice between 5–12 weeks old. Colonoids were grown from mice 5–8 weeks old.

Davies J.M., Santaolalla R., von Furstenberg R.J., Henning S.J, & Abreu M.T. (2015). The Viral Mimetic Polyinosinic:Polycytidylic Acid Alters the Growth Characteristics of Small Intestinal and Colonic Crypt Cultures. PLoS ONE, 10(9), e0138531.

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Genetically Modified Mice for LPS Study

Cited 1 time

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Female Balb/c mice at 6–8 weeks of age were used for LPS experiments (Charles River Labs). Ripk3^−/− (on C57BL/6 background) and matched controls were previously described (Newton et al., 2004) and provided to us by Dr. Vishva Dixit (Genentech). Sting^−/− mice were a gift from Dr. Alexander Poltorak. TRIF^−/−(Ticam1^−/−) (C57BL/6J-Ticam1Lps2/J) mice and corresponding control mice (C57BL/6J, B6.129P2) were purchased from Jackson labs. D138N RIPK1, K45A RIPK1, K51A RIPK3, and Mlkl^−/− mice were previously described (30 (link), 32 –34 ).
All use of animals was approved by the Tufts University, UMASS, and Fox Chase Cancer Center Institutional Animal Care and Use Committees. Mice were maintained in Tufts animal facility in cages with light/dark cycle and experiments performed according to the protocol with all efforts to minimize the number and suffering of the animals.

Saleh D., Najjar M., Zelic M., Shah S., Nogusa S., Polykratis A., Paczosa M.K., Gough P.J., Bertin J., Whalen M., Fitzgerald K., Slavov N., Pasparakis M., Balachandran S., Kelliher M., Mecsas J, & Degterev A. (2017). Kinase activities of RIPK1 and RIPK3 can direct IFNβ synthesis induced by lipopolysaccharide. Journal of immunology (Baltimore, Md. : 1950), 198(11), 4435-4447.

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Mouse Strain Breeding and Experimental Use

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Six to eight week old male and female C57BL/6J (wild type (WT)) and TRIF^−/− (C57BL/6J-Ticam1^Lps2/J) mice were purchased from the Jackson Laboratories (Bar Harbor, ME) and used for adult breeders and adult experiments. MyD88^−/− mice (B6.129P2-Myd88^tm1Defr) were obtained from S Akira, initially maintained at Rhode Island Hospital and Brown University, and transferred to UF for breeding and colony maintenance. Interferon type 1 receptor null mice (B6.129S2-Ifnar1^tm1Agt/J; IFNAR^−/−) breeders were purchased from Jackson Laboratories. These mice had been backcrossed onto a B6 background for six generations, and inbred on the B6 background for an additional 12 generations. Adult mice were mated in a harem schema with one male to two females. Neonatal mice were studied between four and seven days of age. All experiments were approved by the Institutional Animal Care and Use Committee at the University of Florida, College of Medicine.

Cuenca A.G., Joiner D.N., Gentile L.F., Cuenca A.L., Wynn J.L., Kelly-Scumpia K.M., Scumpia P.O., Behrns K.E., Efron P.A., Nacionales D., Lui C., Wallet S.M., Reeves W.H., Mathews C.E, & Moldawer L.L. (2014). TRIF dependent innate immune activation is critical for survival to neonatal gram negative sepsis. Journal of immunology (Baltimore, Md. : 1950), 194(3), 1169-1177.

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Immunodeficient Mouse Models in CRCHUM

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This study was carried out in accordance with Canadian Council on Animal Care guidelines. The protocol was approved by the institutional Animal Care Committee of the CRCHUM.
C57BL/6 (B6) wild-type (Wt) and Trif-deficient mice (C57BL/6JTicam1^Lps2/J or Trif^LPS2/LPS2, B6 background), were purchased from Jackson Laboratories (Bar Harbor, ME). MyD88^−/− mice in the B6 genetic background were kindly provided by Dr. Shizuo Akira (Research Institute for Microbial Diseases, Osaka University, and Japan Science and Technology Agency, Tokyo, Japan) and were maintained as described previously (Adachi et al., 1998 (link)). Mice were maintained under standard 12:12 h light/dark conditions at the Centre de recherche du CHUM (CRCHUM). The animals used in the experiments were female and were permanently housed under specific pathogen-free conditions.

Layoun A., Samba-Mondonga M., Fragoso G., Calvé A, & Santos M.M. (2018). MyD88 Adaptor Protein Is Required for Appropriate Hepcidin Induction in Response to Dietary Iron Overload in Mice. Frontiers in Physiology, 9, 159.

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Mouse Strains for Immunological Studies

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B10.A and B10.A.SJL-Rag2^−/− -Ptprc^a-5C.C7(TcRa, TcRb) were obtained from Taconic Farms (Germantown, NY). C57BL/6, C57BL/6 OT-II (B6.Cg- Tg (TcraTcrb) 425Cbn/J, Tram^−/− C57BL/6J- Ticam1Lps2/J, TLR3^−/− B6;129S1- Tlr3tm1Flv/J, MyD88^−/− CBy.129P2(B6) - MyD88tm1Defr/J, IFNAR^−/− B6.129S2- Ifnar1tm1Agt/Mmjax, IL-1R^−/− B6.129S7-Il1r1tm1Imx/J were purchased from Jackson Laboratories (Bar Harbor, ME). All mice were housed under specific pathogen-free animal conditions at the National institute of Allergy and Infectious Diseases (NIAID), and used between 6 and 12 weeks of age in accordance with guidelines provided by the Institutional Animal Care and Use Committee of the NIAID.

Caucheteux S.M., Hu-Li J., Mohammed R., Ager A, & Paul W.E. (2016). Cytokine Regulation of Lung Th17 Response to Airway Immunization using LPS Adjuvant. Mucosal immunology, 10(2), 361-372.

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Mouse Models for Immune Signaling Study

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Six- to twelve-week-old C57BL6/J mice (B6 mice), B6.Cg-Tg(HLA-A/H2-D)^2Enge/J transgenic breeder mice expressing a human HLA-A2 gene (AAD mice), and B6.129P2(SJL)-Myd88^tm1.1defr/J (Myd88^−/−), B6.129S2-Ifnar1^tm1Agt/Mmjax (IFNAR^−/−), C57BL/6J-Tmem173^gt/J (STING^−/−), C57BL/6J-Ticam1Lps2/J (Trif^−/−), and C57BL/6-Tg(TcraTcrb)1100Mjb (OT1) breeder mice were obtained from The Jackson Laboratory (Bar Harbor, ME). All animals were housed and bred under specific pathogen–free conditions at the Division of Laboratory Animal Resources, University of Kentucky (UK) Medical Center, and all animal protocols were reviewed and approved by the UK Institutional Animal Care and Use Committee following the National Institutes of Health animal care guidelines.

Gandhapudi S.K., Ward M., Bush J.P., Bedu-Addo F., Conn G, & Woodward J.G. (2019). Antigen Priming with Enantiospecific Cationic Lipid Nanoparticles Induces Potent Antitumor CTL Responses through Novel Induction of a Type I IFN Response. Journal of immunology (Baltimore, Md. : 1950), 202(12), 3524-3536.

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Murine BMDM Preparation Using Knockout Mice

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C57BL/6J (Jackson Laboratories strain #000664), BALB/c (Jackson Laboratories strain #000651), Sting-/- (C57BL/6J-Sting^gt/J, Jackson Laboratories strain # 017537), Tlr4-/- (Jackson Laboratories strain #007227) Tlr2-/- (B6.129-tlr2^tm1Kir/J, Jackson Laboratories strain #004650), Myd88-/- (B6.129P2(SJL)-Myd88^tm1.1Defr/J, Jackson Laboratories strain #009088), TNFAR-/- (B6.129S-Tnfrsf1a^tm1Imx Tnfrsf1b^tm1Imx/J, Jackson Laboratories strain #003243), and Trif-/- (C57BL/6J-Ticam1^Lps2/J, Jackson Laboratories strain #005037) mice were used for the preparation of BMDM.

Hinman A.E., Jani C., Pringle S.C., Zhang W.R., Jain N., Martinot A.J, & Barczak A.K. (2021). Mycobacterium tuberculosis canonical virulence factors interfere with a late component of the TLR2 response. eLife, 10, e73984.

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Mouse Strain Characterization for Immunology Research

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C57BL/6 and B6D2F1/J mice were purchased from Charles River Laboratories at the age of seven weeks and housed in our facility for at least one week before being used in experiments. B6.129S(C)-Batf3^tm1Kmm/J, B6(Cg)-Irf8^tm1.1Hm/J, B6.129S4-Pten^tm1Hwu/J, B6.129P2(C)-Ccr7^tm1Rfer/J, B6.129S7-Ifng^tm1Ts/J, B6.129S7-Ifngr1^tm1Agt/J, B6(Cg)-Ifnar1^tm1.2Ees/J, B6.129S7-Il1r1^tm1lmx/J, B6.129P2(SJL)-Myd88^tm1.1Befr/J, B6.129S7-Rag1^tm1Mom/J and C57BL/6J-Ticam1^Lps2/J mice were purchased from Jackson Laboratories and bred in our facility or used for experiments after at least one week of housing in our facility. Cd207-Cre mice were provided by B. Clausen^{21 (link)}. JEDI mice were provided by B. Brown. Axl^−/− and Axl^−/−Mertk^−/− bone marrow were provided by C. Rothlin and S. Ghosh. Asc^−/− mice were provided by Millenium.
Floxed mice were crossed to Cd207-Cre mice in our facility. Mice were maintained at specified pathogen-free (SPF) health status in individually ventilated cages at 21–22 °C and 39–50% humidity. Male mice at the age of 8–12 weeks were used for experiments. All animal procedures were approved by the Institutional Animal Care and Use Committees (IACUCs) of the respective institutions.

Maier B., Leader A.M., Chen S.T., Tung N., Chang C., LeBerichel J., Chudnovskiy A., Maskey S., Walker L., Finnigan J.P., Kirkling M.E., Reizis B., Ghosh S., D’Amore N.R., Bhardwaj N., Rothlin C.V., Wolf A., Flores R., Marron T., Rahman A.H., Kenigsberg E., Brown B.D, & Merad M. (2020). A conserved dendritic-cell regulatory program limits antitumour immunity. Nature, 580(7802), 257-262.

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Genetically Modified Mouse Models

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Male C57BL/6 WT, STING^–/– (B6[Cg]-Sting1^tm1.2Camb/J), TLR4^–/– ([B6(Cg)-Tlr4^tm1.2Karp/J]), MyD88^–/– (B6.129P2-Myd88^tm1Hlz/J), and TRIF^–/– (C57BL/6J-Ticam1^Lps2/J) mice aged 8–10 weeks (20–25 g) were purchased from The Jackson Laboratory. The mice were housed under standard conditions (room temperature at 22°C, 12/12-hour light/dark cycle) with regular access to standard Purina mouse chow and water ad libitum. The animals were allowed at least 7 days to acclimate under these conditions before being used for experiments.

Chen K., Cagliani J., Aziz M., Tan C., Brenner M, & Wang P. (2021). Extracellular CIRP activates STING to exacerbate hemorrhagic shock. JCI Insight, 6(14), e143715.

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Murine Models for Immunological Studies

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C57BL/6 (WT), B6.SJL-Ptprc^aPepc^b/BoyJ, C57BL/6-Tg(UBC-GFP)30Scha/J (GFP⁺), B6.129P2(SJL)-Myd88^tm1.1Defr/J, B6.129-Tlr2^tm1Kir/J, B6(Cg)-Tlr4^tm1.2Karp/J, B6.129S1-Tlr7^tm1Flv/J, C57BL/6J-Tlr9^M7Btlr/Mmjax, B6.129S7-Il1r1^tm1/mx/J, C57BL/6J-Ticam1^Lps2/J, B6.Cg-Ccl2^tm1.1Pame/J, and B6.129S4-Ccr2^tm1lfc/J (The Jackson Laboratory) were used in this study. Csf2^−/− and Csf2rb^−/− mice on C57BL/6 background (10 generations) were bred in-house (Rauch et al., 2012 (link); Hilgendorf et al., 2014b (link); Weber et al., 2014 (link)). All experiments were conducted with male mice aged 8–16 wk at the time of death. All protocols were approved by the Animal Review Committee at Massachusetts General Hospital.

Anzai A., Choi J.L., He S., Fenn A.M., Nairz M., Rattik S., McAlpine C.S., Mindur J.E., Chan C.T., Iwamoto Y., Tricot B., Wojtkiewicz G.R., Weissleder R., Libby P., Nahrendorf M., Stone J.R., Becher B, & Swirski F.K. (2017). The infarcted myocardium solicits GM-CSF for the detrimental oversupply of inflammatory leukocytes. The Journal of Experimental Medicine, 214(11), 3293-3310.

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