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Second, epistatic interactions between FCGR3A CNVs and other genes may be required for development of the RA phenotype.
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Some of them may be required for development and differentiation of a sex-specific neural circuit.
A second, more likely explanation is that CD4+ T cells may be required for the development of cHL.
Even though some of these conditions have been described as possible contributors, additional factors may be required for the development of IA [ 5, 16, 26].
A delay between giving the two drugs may be required for the development of a cell body response to paclitaxel-induced axonal damage.
Similarly, a gene may be required for human development but not the development of mice or other animals.
Single oncogene transgenic MM mouse models may have long disease latency until the development of disease, as additional genetic lesions and/or epigenetic dysregulations in tumor-initiating cells may be required for tumor development.
CD98hc may be essential for early post-implantation development by regulating integrin-dependent signaling, while the other function of CD98hc as a component of amino acid transporters may be required for embryonic development at later stages.
Given that TET2 somatic mutations occur in 5.6% of elderly females with skewed X-inactivation without hematological malignancies, additional mutations may be required for lymphoma development.
A distinct VEGF gradient is required for development of the airway tubular structures and lung endothelium, while VEGF overexpression may lead to dysmorphogenesis of the lung [ 9].
ERK phosphorylation is required for development of the lymphatic system33,34,35,55; therefore, reduced ERK phosphorylation induced by tmem33 knockdown may contribute to defective lymphatic sprouting.
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