Sentence examples for mouse mutants revealed from inspiring English sources
In addition to structural abnormalities of cilia, functional defects were noted in Invs[26] and Cys1[27], and both mouse mutants revealed ARPKD phenotype.
However, previous studies with Gli1−/− mouse mutants revealed no detectable deficits in cortical development [ 37].
Analysis of the transcriptional programs in mouse mutants revealed rather distinct transcriptional targets regulated by these transcription factors in the dorsal and ventral telencephalon (Gohlke et al., 2008).
More recent compound DLX1/2 and ASCL1 LOF mouse mutants have revealed unique and overlapping genetic pathways regulated by these factors in the ganglionic eminences [ 25,26].
The appearance of the mouse and rat dumbo ears are quite similar, but at the cellular level the phenotypes of the mouse and rat mutants reveal other striking differences.
In a FHM2 KI mouse model carrying the human W887R mutation in the Atp1a2 orthologous gene, in vivo analysis of CSD in heterozygous F Atp1a2 (+/R887) mutants revealed a decreased induction threshold and an increased velocity of propagation.
Investigation of Creb/Atf1 subfamily mouse mutants has also revealed that Creb/Atf1 subfamily members may compensate for one another.
Interestingly, studying the spontaneous mouse mutant nee has revealed that those mice also exhibited runted growth, craniofacial and skeletal abnormalities, ocular anterior segment dysgenesis, and hearing impairment, similar to SH3PXD2B null mice [ 12].
The preliminary characterization of Ptrh2 mutant mice revealed homozygous Ptrh2 mutants develop a "runting" (dystrophy) syndrome postnatally and die within the first 2 weeks of life.
RT-PCR analysis of the mutant mouse tissue revealed that the mutant allele is expressed in the knock-in mice.
Systemically analysis of over 100 mutant mice revealed new and unexpected phenotypes in 96% of these mutants, approximately one-third of these mouse lines had no previously described phenotype, suggesting that phenotypes have been overlooked even in mouse models that have been studied extensively (Beckers et al., 2009).
