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Higher expression of cytoplasmic polyadenylation element-binding protein 1 (CPEB1) in parthenotes compared to normal embryos may increase cell cycle arrest and cellular senescence by inducing p53 translation [35].
These cell wall defects may increase cell permeability.
However, contaminants may increase cell permeability and hence inhibit substrate uptake by a nonspecific action.
Anti-apoptotic signalling was also identified, however, which may increase cell survival and promote tumourigenesis.
Under ER stress, activation of GRP78 may increase cell survival through the unfolded protein response [ 22].
Anti-apoptotic signalling that may increase cell survival and promote tumourigenesis was also evident.
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Improved production media and fed batch supplementation as well as controlled bioreactor processes may further increase cell densities and prolong production time which can further enhance production levels.
A combination of RPE and photoreceptor with anti-angiogenic factors (e.g., anti-vascular endothelial growth factor) may potentially increase cell viability and engraftment.
IGF-1 may therefore mildly increase cell volume without affecting ΔΨp.
These results suggest that B cell stimulation following pathogen exposure may increase B cell sensitivity to environmental AhR ligands through AhR up-regulation.
These results suggest that STAT1 may increase the cell viability in bortezomib-treated ovarian cancer cells by modulating several different molecules involved in the apoptotic cascade.
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