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Moreover, mouse studies revealed abnormalities of NMJs lacking DGC components [10]-[15 [10]-[15ing a role for a defective neurotransmission in some dystrophies [16], [17].
Two recent mouse studies revealed an indispensable role of Rnd3 in mouse neuron development.
Mouse studies revealed a similar result when animals expressing the polyQ expanded exon 1 of huntingtin (Htt) showed a progressive neurological phenotype recapitulating characteristics of HD.
Since our mouse studies revealed aggressive social behavior as a central phenotype modulated by subtle Mecp2 overexpression, we started a hypothesis-driven analysis on subjects of the GRAS Göttingen Research Association for Schizophreniaa) data collection (Ribbe et al, 2010).
More recently, mouse studies revealed that hypothalamus-specific IKK β/NF- κB activation led to depletion and impaired neuronal differentiation of htNSC and ultimately to obesity and prediabetes development [ 99].
The best characterized functions of RND3 are its inhibitory effect on Rho kinase-mediated biological functions including actin cytoskeleton formation, phosphorylation of myosin light chain phosphatase, and apoptosis 6– 8. Two recent mouse studies revealed an indispensable role of RND3 in mouse neuron development 9, 10.
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Mouse studies reveal structural and functional deficiencies in CA1 place cells that might represent the neural correlate of the spatial impairment.
The validity of this suggestion was thoroughly proven in human and mouse studies revealing that PPARs are indeed master regulators of metabolism [7].
TYROBP knockout mouse studies reveal deficits in cognitive functions and prepulse inhibition [ 49], symptoms that have been manifested in many schizophrenia patients.
Mouse studies reveal that memory T cells are only able to mediate GvL and not GvHD, whereas naive T cells mediate both (Dutt et al., 2011).
47 This mouse study revealed that adding selumetinib was beneficial for mice with Kras or Kras / p53 mutant lung cancer, but not with Kras and Lkb1 mutations.
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