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A super-additive harvest increases total mortality beyond the effect of direct killing itself, through social disruption or the loss of dependent offspring.
Females engaging in inter-group encounters therefore risk the loss of dependent pups, in addition to personal injury or death.
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In this light, we hypothesized that the KRIT1 loss-of-function-dependent upregulation of c-Jun expression and phosphorylation observed in cellular models could also occur in vivo.
Mutagenesis of HRE2 provoked complete loss of Sima dependent induction of the [−1170 +1] luciferase reporter, while mutation or deletion of any of the other 6 HREs had no effect on reporter induction (Fig. 3D).
The possibility of cytokinesis in the absence of complete DNA replication due to increased cross-links and loss of Chk1 dependent checkpoint could account for the observed micronuclei.
In this study we show that loss of Dgcr8 dependent miRNAs in the kidney epithelium leads to severe hydronephrosis, kidney cysts and rapid kidney failure.
Loss of hypoxia-dependent inhibition of mTORC1 sensitizes ATM-deficient cells to p53-dependent apoptosis [42].
The loss of light-dependent inhibition of PTP1B activity in Grb14-/ mice demonstrates that Grb14 regulates light-dependent PTP1B activity.
Thus, loss of MPF-dependent Cdc20 phosphorylation helps APC/CCdc20 activation [4], [5].
We reasoned that this reporter might be especially sensitive to a loss of NELF-dependent repression.
Loss of estrogen-dependent cardiovascular protection diminishes endothelial function, and may involve activation of the renin-angiotensin system (RAS).
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