Tamoxifen mice

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  1. Karim-7-7 User

    Tamoxifen mice


    Tamoxifen induction regimens should be determined empirically for the specific mouse lines and experimental setup involved. However, the following protocol provides a starting point for the induction of Cre in adult (P56) mice. The following procedure has been used with success to induce robust Cre activity in all major organ systems (validated in ubiquitous Cre /ER expressers, such as B6. The tamoxifen-inducible Cre-lox P system is widely used to overcome gene targeting pre-adult lethality, to modify a specific cell population at desired time-points, and to visualize and trace cells in fate-mapping studies. In this study we focused on tamoxifen degradation kinetics, because for all genetic fate-mapping studies, the period during which tamoxifen or its metabolites remain active in the CNS, is essential. Additionally, we aimed to define the tamoxifen administration scheme, enabling the maximal recombination rate together with minimal animal mortality. The time window between tamoxifen injection and the beginning of experiments should be large enough to allow complete degradation of tamoxifen and its metabolites. Otherwise, these substances could promote an undesired recombination, leading to data misinterpretation. We defined the optimal time window, allowing the complete degradation of tamoxifen and its metabolites, such as 4-hydroxytamoxifen, N-desmethyltamoxifen, endoxifen and norendoxifen, in the mouse brain after intraperitoneal tamoxifen injection. We determined the biological activity of these substances in vitro, as well as a minimal effective concentration of the most potent metabolite 4-hydroxytamoxifen causing recombination in vivo.

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    Refined protocols of tamoxifen injection for inducible DNA. 4-hydroxytamoxifen and endoxifen in brain and serum of mice by liquid. Tamoxifen administration to mice. Whitfield J1, Littlewood T2, Soucek L1. Author information 1Vall d'Hebron Institute of Oncology VHIO, Barcelona 08035, Spain; Universitat Autònoma de Barcelona, 08193 Bellaterra Cerdanyola del Vallès, Spain; 2Department of Biochemistry, University of Cambridge, Cambridge CB2 1GA, United Kingdom. Cold Spring Harb Protoc. 2015 Mar 2;20153269-71. doi 10.1101/pdb. prot077966. Tamoxifen administration to mice. Whitfield J1, Littlewood T2, Soucek.

    We use cookies to make interactions with our website easy and meaningful, to better understand the use of our services, and to tailor advertising. For further information, including about cookie settings, please read our Cookie Policy . By continuing to use this site, you consent to the use of cookies. Tamoxifen is an estrogen analogue that binds with higher affinity than estrogen to altered estrogen binding domains. There are several ways to administer tamoxifen to mice each with advantages and disadvantages. If precise dosage is not paramount, administration via food is the gentlest to the animal. Keep in mind that induction varies depending on Cre and target genes.

    Tamoxifen mice

    Tamoxifen-Induced Cre-loxP Recombination Is Prolonged in. - PLOS, Tamoxifen administration to mice.

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  4. I want to induce a conditional knockout in pancreatic beta cells. I fed my mice on Tamoxifen containing diet starting from 4 weeks of age for 1 month as this.

    • Tamoxifen in chow versus tamoxifen intraperitoneal injection for..
    • Tamoxifen administration to mice. - NCBI.
    • Tamoxifen - Wikipedia.

    Heat to 37°C before administration. Verify that tamoxifen is properly dissolved. feed orally to mice with a feeding needle. Fix the mice at their neck and ridge so that the belly is directed to the floor. Hold the mouse tightly so that it can not move the head, but not too tight to avoid choking. Carefully introduce the feeding needle in the mouth behind the tongue max. 1 cm. It is helpful to mark 1 cm on the needle Effects of oral tamoxifen treatments on food and drug intake. Mtm1 −/y mice and wild type WT littermates were weaned on post-natal day 23 ± 1, slightly after disease onset, at which time they. Abstract. The strategy of fusing a protein of interest to a hormone-binding domain HBD of a steroid hormone receptor allows fine control of the activity of the fused protein.

     
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