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However, human patients and mouse mutants often do not display identical phenotypes.
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14, 22, 74 The development of functional teeth in mouse mutants also often arrests at the bud stage.
In addition, precise reference intervals for biochemical and hematological parameters will allow a more detailed characterization of mouse mutants harboring mutations that often do not induce striking phenotypes, such as micro-RNAs depletion.
Furthermore, Scn8a Clth /Scn8a Clth mice displayed a greater frequency of trunk curling and limb grasping, which are often displayed by mouse mutants with neurological defects including Scn8a med − TgA 4 Bs / Scn8a med − TgA 4 Bs mice (Kohrman et al. 1995).
Seibler, J. et al. Rapid generation of inducible mouse mutants.
Yoon, K. & Gaiano, N. Notch signaling in the mammalian central nervous system: insights from mouse mutants.
Mouse mutants will be informative to reveal the general importance of Krm1/2 for Dkk action.
Herrmann, S., Hofmann, F., Stieber, J. & Ludwig, A. HCN channels in the heart: lessons from mouse mutants.
Marrella, V. et al. A hypomorphic R229Q Rag2 mouse mutant recapitulates human Omenn syndrome.
Neuroscientists studying these mutant mice often use balance beams or other challenging tasks to compare their coordination with typical mice.
Spatial learning requires intact PKA signaling in the hippocampus [46] and deficits in hippocampal LTP and LTD in mutant mice often correlate with deficits in spatial learning and memory tasks [47].
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