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We propose that the present observations, in additional to their basic cell biological significance, may contribute to mechanistic understanding of complex genetic diseases.
Therefore, as a first step towards the understanding of complex genetic traits involved in the host response to influenza infections, we have studied the susceptibility to infection with H1N1 and H7N7 influenza virus subtypes in different inbred laboratory mouse strains.
Hill cautioned that early successes with Mendelian traits will not translate into rapid understanding of complex genetic interactions.
We believe that this approach will find wide application among evolutionary biologists in the near future and will allow advancements in our understanding of complex genetic regions.
Currently, in human medicine, such gene expression signatures have considerably improved the diagnosis and understanding of complex genetic disorders and infectious diseases [ 12, 15, 16].
Current understanding of complex genetic control of N and P utilisation is being converged towards precision breeding such as marker assisted breeding for nutrient efficient varieties.
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Identification of genetic variants associated with gene expression (eQTLs), methylation (mQTLs) etc is becoming ever more important in understanding the biology of complex genetic disorders.
This is an extremely important development for the following reasons: Identification of genetic variants associated with gene expression (eQTLs), methylation (mQTLs) etc is becoming ever more important in understanding the biology of complex genetic disorders.
Epigenomics not only offers an improved understanding of fundamental biological processes such as cellular differentiation and early embryogenesis, but is also widely recognized to be key in understanding the pathogenesis of complex genetic diseases like cancer (Baylin and Ohm, 2006; Feinberg et al., 2006; Jones and Baylin, 2007).
In summary, our study substantially increases the catalogue of human eQTLs and improves our understanding of the complex genetic regulation of gene expression, pathways and disease-related processes.
In summary, our study substantially increases the catalogue of human eQTLs and improves our understanding of the complex genetic regulation of gene-expression, pathways and disease-related processes hereon.
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