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Molf ei

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The MOLF/Ei is a laboratory equipment product used for research purposes. It serves as a core tool for conducting various experiments and analyses. The MOLF/Ei is designed to perform its intended functions without further interpretation or extrapolation.

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Lab products found in correlation

Ifnar b6.129s2 ifnar1tm1agt mmjax, by Jackson ImmunoResearch (2 mentions) C57bl 6j, by Jackson ImmunoResearch (2 mentions) C57bl 6, by Jackson ImmunoResearch (1 mentions)

4 protocols using molf ei

1

Characterizing Tippy Mice: A Neurological Model

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Heterozygous tippy mice (Jackson Laboratory stock #001055; maintained on C57BL/6;C3HeB/Fe genetic background) were originally obtained from the Jackson Laboratory and interbred in-house. Homozygous mutant mice were distinguished from their heterozygous tippy and homozygous control littermates by ataxic gait and small body size. Analysis was conducted with interbred mice from generations 1–5. No evidence was seen of the phenotype changing across generations. A few homozygous tippy mice were nursed beyond P20. Unaffected littermates and wild-type mice were used in the experiments as controls. Control C3HeB/Fe (stock #000658) and Molf/Ei (stock #000550) strains were also purchased from Jackson Laboratory. Mice between the ages of P10–P35 were deeply anesthetized with i.p. sodium pentobarbital (60mg/kg body weight) and transcardially perfused with appropriate fixatives. This study was carried out on mice in strict accordance with the recommendations in the Guide for the Care and Use of Laboratory Animals of the National Institutes of Health. All chemicals were purchased from Sigma-Aldrich unless otherwise stated.
Shih E.K., Sekerková G., Ohtsuki G., Aldinger K.A., Chizhikov V.V., Hansel C., Mugnaini E, & Millen K.J. (2015). The spontaneous ataxic mouse mutant tippy is characterized by a novel Purkinje cell morphogenesis and degeneration phenotype. Cerebellum (London, England), 14(3), 292-307.
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2

Generation of Knockout Mouse Strains

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C57BL/6J, MOLF/Ei, and Ifnar−/−(B6.129S2-Ifnar1tm1Agt/Mmjax) (Müller et al., 1994 (link)) mouse strains were obtained from The Jackson Laboratory. Ifnb−/− mice (Deonarain et al., 2003 (link)) were a gift from Dr. S. Vogel (University of Maryland). Mlkl−/− (Murphy et al., 2013 (link)) mice were generated by Dr. W. Alexander (Walter and Eliza Hall Institute) and were a gift from Dr. M. Kelliher (University of Massachusetts). Ifnb−/−Mlkl−/− double knockout mice were generated by crossing Ifnb−/− and Mlkl−/− mice to homozygosity. Similarly, RIP1 Ki Ifnb−/− mice were generated by crossing Ifnb−/− and Ripk1K45A/K45A mice to homozygosity. Akt1−/−, Akt3−/− and wild-type littermate controls (Easton et al., 2005 (link); Mao et al., 2007 (link)) were a gift from Dr. P. Hinds (Tufts University). 4E-BP triple knockout mice were a gift from Dr. N. Sonenberg (McGill University). RIP1/3 kinase inactive mice (Ripk1K45A/K45ARipk3K51A/K51A, RIPKi) (Berger et al., 2014 (link); Mandal et al., 2014 (link)) were gifts from Dr. A. Degterev. All genetically modified mice were fully backcrossed to the C57BL/6J background. All mice were housed in a pathogen-free facility at the Tufts University School of Medicine and experiments were performed in accordance with regulations and approval of the Tufts University Institutional Animal Care and Use Committee.
Muendlein H.I., Sarhan J., Liu B.C., Connolly W.M., Schworer S.A., Smirnova I., Tang A.Y., Ilyukha V., Pietruska J., Tahmasebi S., Sonenberg N., Degterev A, & Poltorak A. (2020). Constitutive Interferon Attenuates RIPK1/3-Mediated Cytokine Translation. Cell reports, 30(3), 699-713.e4.
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3

Generation of Knockout Mouse Strains

Cited 2 times
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C57BL/6J, MOLF/Ei, and Ifnar−/−(B6.129S2-Ifnar1tm1Agt/Mmjax) (Müller et al., 1994 (link)) mouse strains were obtained from The Jackson Laboratory. Ifnb−/− mice (Deonarain et al., 2003 (link)) were a gift from Dr. S. Vogel (University of Maryland). Mlkl−/− (Murphy et al., 2013 (link)) mice were generated by Dr. W. Alexander (Walter and Eliza Hall Institute) and were a gift from Dr. M. Kelliher (University of Massachusetts). Ifnb−/−Mlkl−/− double knockout mice were generated by crossing Ifnb−/− and Mlkl−/− mice to homozygosity. Similarly, RIP1 Ki Ifnb−/− mice were generated by crossing Ifnb−/− and Ripk1K45A/K45A mice to homozygosity. Akt1−/−, Akt3−/− and wild-type littermate controls (Easton et al., 2005 (link); Mao et al., 2007 (link)) were a gift from Dr. P. Hinds (Tufts University). 4E-BP triple knockout mice were a gift from Dr. N. Sonenberg (McGill University). RIP1/3 kinase inactive mice (Ripk1K45A/K45ARipk3K51A/K51A, RIPKi) (Berger et al., 2014 (link); Mandal et al., 2014 (link)) were gifts from Dr. A. Degterev. All genetically modified mice were fully backcrossed to the C57BL/6J background. All mice were housed in a pathogen-free facility at the Tufts University School of Medicine and experiments were performed in accordance with regulations and approval of the Tufts University Institutional Animal Care and Use Committee.
Muendlein H.I., Sarhan J., Liu B.C., Connolly W.M., Schworer S.A., Smirnova I., Tang A.Y., Ilyukha V., Pietruska J., Tahmasebi S., Sonenberg N., Degterev A, & Poltorak A. (2020). Constitutive Interferon Attenuates RIPK1/3-Mediated Cytokine Translation. Cell reports, 30(3), 699-713.e4.
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4

Genetically Modified Mouse Strains for Immunology Research

Cited 3 times
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C57BL/6, MOLF/Ei, Ifnar−/− (B6.129S2-Ifnar1tm1Agt/Mmjax), Trif-/-(C57BL/6J-Ticam1Lps2/J), MyD88-/-(B6.129P2(SJL)-Myd88tm1.1Defr/J), strains were obtained from the Jackson Laboratory. Tlr7.1 Tg mice [41 (link)] (C57BL/6-Tg(Tlr7)1Boll) were obtained from Dr. B. Huber (Tufts). Ifnb−/− were a gift from Dr. S. Vogel (UMaryland). Trif−/−/MyD88−/−, cGAS−/− and RIP3−/−/Caspase-8−/− animals were a gift from Dr. K. Fitzgerald (UMass). RIP3−/−/Caspase-8−/− animals [46 (link)] were generated by Dr. D. Green (St. Jude). RIP1 kinase inactive (Rip1D138N/D138N) [47 (link)] and Mlkl−/− animals were a gift from Dr. M. Kelliher (UMass). Mlkl−/− [48 (link)] animals were generated by Dr. W. Alexander (Walter and Eliza Hall Institute). Zbp1−/− mice [49 (link)] were a gift from Dr. S. Balachandran. Sting−/− animals were a gift from Dr. G. Barber (UMiami). RIP3 RHIM domain mutant (Ripk3ΔR/ΔR) mice [50 (link)] were a gift from Dr. Francis Chan. All genetically modified mice were fully backcrossed to the C57BL/6 background. B6. MOLF-Tmem173molf (STINGMOLF/MOLF) congenic mice were established by backcrossing 10 generations to C57BL/628. All mice were housed in a pathogen-free facility at the Tufts University School of Medicine and experiments were performed in accordance with regulations and approval of the Tufts University Institutional Animal Care and Use Committee.
Sarhan J., Liu B.C., Muendlein H.I., Weindel C.G., Smirnova I., Tang A.Y., Ilyukha V., Sorokin M., Buzdin A., Fitzgerald K.A, & Poltorak A. (2018). Constitutive interferon signaling maintains critical threshold of MLKL expression to license necroptosis. Cell Death and Differentiation, 26(2), 332-347.
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