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The known nullomers in chimpanzee, cow, dog, and mouse genomes show patterns that are consistent with those seen in humans.
Interestingly, the estimated ages of retroelements in human and mouse genomes show ongoing high activity in the mouse genome but not human genome [ 78].
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Analysis of the human and mouse genomes shows that the HEG and Muc13 genes are organized in the same manner in these animals.
Comparison of human and mouse genomes shows that the serpins of nine of the vertebrate clades show conserved numbers and synteny, with the variations being restricted to clades A and B. In particular, the mouse clade A serpins have expanded, with human α1-antitrypsin being represented by a cluster of 5 genes in the mouse, and human α1-Antitrypsin being represented by a cluster of 14 genes.
This month's publication of a draft of the mouse genome shows that genetically, too, we have much in common: 99percentt of our genes are also in mice.
Analysis of syntenic regions of the mouse genome shows that few noncoding exons are shared between human and mouse, yet human splicing profiles are recapitulated on Hsa21 in mouse cells, indicative of regulation by a deeply conserved splicing code.
The testis-specific gene expression profile along the mouse genome shows that testis-specific genes are distributed on all the chromosomes with different gene density.
An important question that arises each time when a modification of the mouse genome shows a phenotype is whether the insertion site contributes to the observed phenotype.
Other recent work on the structure of the mouse genome shows that there are regions of the genome which appear to have undergone selection in the tortuous history toward laboratory domestication of mice, first as pets and then as research subjects (Yang et al. 2007).
The abundance of SDs was often considered as specific to human or hominoids (Bailey and Eichler 2006; Marques-Bonet et al. 2009) because early analyses based on the whole genome shotgun (WGS) assemblies of mammalian genomes, such as the mouse genome, showed a paucity of SDs (e.g., Cheung et al. 2003).
Our sequence analysis of Pkm2 retropseudogenes with upstream start codons in the mouse genome shows partial agreement with the previously identified five-amino-acid extension, but does not clearly elucidate the start codon responsible for the larger protein product detected in sperm (Additional file 6).
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