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Ultimately the incorporation of multiple effector genes, expressed into combinations of midgut, haemocoel and salivary glands will become feasible.
Recent work has revealed that multiple effector genes reside in regions of the wilt genome that undergo regular chromosomal reshuffling.
These data emphasize the complexity of the Myc phenotype, even within the relative restrictions of our model system, and support the concept that the coordinated regulation of multiple effector genes is required to recapitulate Myc functions [ 52].
In particular, resistance gene stacks seek to overcome limitations of single major gene resistance by challenging pathogen populations to accumulate mutations in multiple effector genes (Dangl et al. 2013).
While Twist and other transcription factors that can promote EMT have multiple effector genes, also several senescence players, including CDKN2A, harbor E-boxes in their promoters [ 78], suggesting that the EMT-associated transcription factors can also regulate the cell cycle without direct regulation of E-cadherin.
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STAT3-mediated oncogenesis can be attributed by the transcriptional upregulation of multiple downstream effector genes in cancer cells such as Mcl-1, which can promote cell growth, survival, and angiogenesis [ 20, 21].
At sites of reduced oxygen tension, therefore, reduced PHD and factor inhibiting HIF hydroxylase activity permits stabilization and transcriptional activation of HIF, resulting in the modulation of multiple HIF effector genes, which contain hypoxia response elements [ 22], to facilitate the cellular adaptive responses to hypoxia.
The results indicate that multiple, near-identical copies of RXLR effector genes are prevalent in oomycete genomes.
Our analysis demonstrates that multiple, nearly identical copies of RXLR effector genes represent a feature of oomycete genomes that has not previously been recognized.
Terminal selectors work combinatorially, with multiple transcription factors cooperating to regulate sets of terminal effector genes that are necessary for each neuron's mature identity, such as neurotransmitters, channels, and synaptic adhesion molecules (Hobert, 2011).
A systematic characterization of S. sclerotiorum transcriptome on multiple hosts and the functional analysis of differentially regulated effector genes should prove useful to decipher the molecular determinants of quantitative disease resistance and host range in this fungal pathogen.
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