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We established previously that inactivation of one Bmp4 allele in Grem1-deficient mouse embryos also restores ureteric bud outgrowth and branching morphogenesis [5].
A more recent study of preimplantation mouse embryos also reported CRGs immediately after fertilization both in-vitro and in-vivo, especially clock and bmal1 (probably of maternal origin initially), but rhythms were not seen over the first four days up to the blastocyst stage [40].
Similarly to zebrafish, intercellular coupling in chick and mouse embryos also involves Notch signaling).
Animal totipotent cells like oocytes and two-cell mouse embryos also exhibit high levels of TE transcription [ 48].
Because loss of Brca1 in mouse embryos also leads to induction of p21WAF1 [ 29**], however, the role of BRCA1 in p21WAF1 regulation is not clear.
Absence of Nr2e1 in mouse embryos also results in premature neurogenesis, which contributes to the defects in the upper cortical layers [ 9].
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Nestin-expressing fetal stem cells in post-implantation development, and stem cell-rich tissues including adult bone marrow and nasal epithelium of the late development mouse embryo also exhibit high 5-hmC levels, whereas the actively proliferating unipotent cells of adult mammalian skin or liver do not.
Beclin1 deficient mice embryos also die as early as embryonic day 7.546.
CLEVER-seq of mouse early embryos also reveals the highly patterned genomic distribution and parental-specific dynamics of 5fC during mouse early pre-implantation development.
A reduction of cyclin-D1-expressing cells in the developing CNS of Notch signaling-deficient mouse embryos was also observed.
OET of mouse embryos has also been demonstrated for the purposes of embryo sorting prior implantation [ 15].
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