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We previously have shown that genetic deletion of Erk3 in mice results in growth restriction, cyanosis, and early neonatal lethality because of pulmonary immaturity and respiratory distress.
Deletion of α-pv in mice leads to embryonic lethality because of cardiovascular defects.
Its loss leads to late fetal/neonatal lethality because of placental malfunction.
Consistent with these fundamental functions, deletion of β1 integrins in ECs leads to early embryonic lethality because of angiogenic defects.
Lung cancer remains a major cause of cancer-related lethality because of high incidence and recurrence in spite of significant advances in staging and therapies.
According to Smyth et al. [ 29], null mutation of LAMC1 causes embryonic lethality because of the absence of the basement membrane and failure to differentiate the endoderm.
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Unfortunately, traditional transgenic procedures have only limited use in analyzing alleles that cause lethality because lines of founder mice cannot be established.
Hematotoxicity could be the direct toxicity of these compounds followed by sinusoidal congestion and hepatoxicity such as, necrosis, inflammation, toxicities to other organs and even lethality because the delivery of oxygen to tissues is impaired.
These survivors do not appear to have acquired linked genetic suppressors of lethality because they continue to transmit the R11 insertion to homozygous progeny at reduced frequency.
A dosage compensation defect does not appear to be the direct cause of hybrid lethality because X chromosome transcripts are not preferentially affected in lethal hybrids (Wei et al. 2014).
We showed here that mel-Hmr is insufficient to explain the X-linked portion of hybrid male lethality, because a mel-Hmr-HA transgene does not induce lethality of X sim hybrid males (Table 6).
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