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Exact(24)
SNAP-25, a neuron-specific SNARE protein, has been well-characterized and mouse embryos lacking Snap25 are viable.
In contrast to Bmp4-deficient kidney rudiments (Figure 1A, 1B), no ectopic ureteric buds were observed in mouse embryos lacking Bmp7 (data not shown).
Mouse embryos lacking either the de novo DNA methyltransferases (Dnmt3a and Dnmt3b) or the maintenance DNA methyltransferase (Dnmt1) die shortly after gastrulation [1], [2].
To gain further insight into the interactions of the two BMP ligands during kidney development, we attempted to generate mouse embryos lacking Bmp7 constitutively and Bmp4 conditionally.
Additional ureteric buds form in mouse embryos lacking either Slit2 or Robo2, which are normally required to restrict Gdnf expression to caudal mesenchyme [6].
This is due to the activity of FGF10, as additional inactivation of Fgf10 in mouse embryos lacking both Gdnf and Spry1 completely abolishes ureteric bud formation.
Similar(36)
Mouse oocytes and cells from early mouse embryos lack this reaction to exogenous dsRNA and are therefore a common model system for studying mammalian gene-knockdown effects.
RAB7-deficient mouse embryos lack the large vacuoles, but accumulate smaller vesicles in the VE.
Vangl2 Lp/Lp mouse embryos lack PCP signalling and undergo almost complete failure of neural tube closure.
However, even studies of mouse embryos lack analysis of the earliest stages of cloaca patterning and morphogenesis.
Also, Vegf-c−/− mouse embryos lack lymphatic vessels and Vegf-c+/− mice suffer from lymphatic hypoplasia, demonstrating haploinsufficiency of a single Vegf-c allele for lymphatic development (Karkkainen et al, 2004).
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