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The results suggested that (1) MPF induced ooplasmic protrusion by increasing MAPK activities and (2) OA activated MPF by way of MAPK.
This suggested that (1) MPF activated MAPK by way of RhoA during ooplasmic protrusion and (2) OA activated while U0126 inactivated MAPK downstream of RhoA.
Since both MPF and ROCK inactivated MYPT in somatic cells and that MPF activated RhoA in this study, our hypothesis to explain the dependence of MPF on MAPK and ROCK for myosin recruitment is that (1) MPF inactivates MYPT via RhoA and (2) only when MYPT is inactivated can the elevated MAPK activity activate MLCK and thereby myosin II.
To understand how PNMS affects the MPF axis, three hypothetical models will be studied: Model 1: MPF neuroendocrine systems.
Larvae at 3, 5, 7 dpf and 1 mpf were photographed live using a NIKON C2 H600L confocal microscope with 20× and 40× water dipping objectives.
The EGFP was exclusively and steadily expressed in oligodendrocytes at 1 mpf (Fig. 1K) and 3 mpf (Fig. 1L N), showing that this line was still working until adulthood.
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When mouse sperm heads were injected into enucleated oocytes, however, protrusion was observed only after MG132 (Figure 4D) but not demecolcine treatment (Figure 4E .The MPF and MAPK activities increased significantly in intact but not in enucleated oocytes after sperm head injection and demecolcine treatment (Figure 4F).
Model 2: MPF immune systems and metabolic outcome.
20 mpf embryos were cross-linked in formaldehyde, and lysed.
Intense SA-βgal signals were observed only in HL at 3 mpf, whereas little signal was detected in HCC at 9 mpf (Fig. 6A).
By 9 mpf, malignant HCC appeared in 11/42 (26%) transgenics (Fig. 2J L).
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