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Furthermore, implications drawn from these models for gene therapy in retinal diseases are discussed.
The system may be useful in monitoring FVIII in cultured supernatants and in mouse models for gene therapy experiments.
The most well understood genetic models for gene interactions are described in terms of qualitative (Mendelian) rather than quantitative traits [37].
On the other hand, systems biologists have built numerous mathematical models for gene and protein networks that cells utilize to control themselves [1].
Omholt et al. [12] introduced simple differential equation models for gene regulatory networks with one and two loci to better understand the regulatory conditions underlying dominance and additivity.
In contrast, primary cultures retain many of phenotypic characteristics of the original tissue, including normal physiological functions, and, therefore, can be highly relevant models for gene discovery, target validation, drug testing, and development of biomarkers.
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Table 2 shows the 2- to 7-order risk association models for gene-gene interaction.
There are several putative models for gene-environment interactions, including synergy, modification of effects and redundancy.
Although constitutive overexpression of genes in transgenic rats has been successfully applied to generate relevant models for gene-related diseases [ 55- 57], only limited attempts have been made in the past to establish transgenic rat models with inducible and tissue-specific gene expression and no one has successfully addressed the brain [ 58].
The limited mouse models for CL/P include KO models for genes regulating signaling and transcription (Juriloff and Harris, 2008).
We present models for genes causing inherited cardiac conditions, though the framework is transferable to other genes and syndromes.
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