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There are two NHEJ pathways characterized by different sets of factors contributing to DNA repair.
The M1 phenotype is associated with proinflammatory pathways characterized by the release of proinflammatory cytokines and increased microbial killing [ 19].
The signaling pathways characterized by the MAPKs p38, ERK, and JNK are known to play a potential role in the regulation of inflammatory response [ 26, 54].
Here, two major growth forms, papillary non-invasive and flat-invasive, have been identified, underlying two separate molecular pathways characterized by distinct mutations [ 4].
In mammals, T cells develop along two discrete pathways characterized by expression of either the αβ or the γδ T cell receptors.
Pathway sizes are highly heterogeneous, there are pathways characterized by complex structures, and, then, composed by more than fifty gene products, and other composed by less than ten gene products.
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Dear Editor, Autophagy is a lysosome-based degradation pathway, characterized by formation of a double-membrane vesicle named the autophagosome.
The mitochondria-mediated caspase activation pathway is a major apoptotic pathway characterized by mitochondrial outer membrane permeabilization (MOMP) and subsequent release of cytochrome c into the cytoplasm to activate caspases.
The apoptotic pathway typically attributed to this delayed death is the intrinsic/mitochondrial-mediated pathway characterized by a loss of mitochondrial potential, release of cytochrome c, and activation of caspase-9.
One is the intrinsic pathway (also called the mitochondria pathway) characterized by the occurrence of mitochondrial swelling, increase in mitochondrial membrane permeability, and the leakage of apoptotic effectors, such as Cyto-c, mitochondrial apoptosis-induced channel (MAC), apoptotic protease activating factor-1 (Apaf-1), pro-caspase-9, caspase-9, caspase-3, Bcl-2, and Bax.
CTM focus on the metabolic disease related phenotype, then explores particular signaling pathway characterized by molecular targets or transcriptional events through biochemical or cellular readouts of cellular profiling assays, further to identify their susceptibility genes and enable patients to achieve a personalized medicines treatment.
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