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the multiplication of viruses after it enters the blood(passive) is caused byactive viremia
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the release of apoptogenic factors such as cytochrome c from isolated mitochondria in a cell - free assaycausedthe release of apoptogenic factors such as cytochrome c from isolated mitochondria in a cell - free assay
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the nuclear accumulation of transcription factors governing ribosomal components while inhibiting nuclear localization of transcription factors for autophagy - promoting genessimultaneously triggersthe nuclear accumulation of transcription factors governing ribosomal components while inhibiting nuclear localization of transcription factors for autophagy - promoting genes
a plethora of signalling cascades , including the mitogen - activated protein kinase ( MAPK ) , Janus kinase / signal transducer and activator of transcription ( JAK / STAT ) and phosphoinositol-3-kinase ( PI3K)/Akt / mammalian target of rapamycin ( mTOR ) pathways ( Figure 1triggera plethora of signalling cascades , including the mitogen - activated protein kinase ( MAPK ) , Janus kinase / signal transducer and activator of transcription ( JAK / STAT ) and phosphoinositol-3-kinase ( PI3K)/Akt / mammalian target of rapamycin ( mTOR ) pathways ( Figure 1
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to continued activation of higher concentrations of c - Jun built up in this period that overcomes the affinity barrier to form active AP-1 homodimersleadsto continued activation of higher concentrations of c - Jun built up in this period that overcomes the affinity barrier to form active AP-1 homodimers
from changes in the level of Ca2 + activation or the Ca2 + sensitivity of the contractile systemcould resultfrom changes in the level of Ca2 + activation or the Ca2 + sensitivity of the contractile system
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catabolic metabolism , which prevents the synthesis of glycogen , lipids , and most proteins while activating glycogen breakdown , oxidative phosphorylation , and mitochondrial biogenesistriggerscatabolic metabolism , which prevents the synthesis of glycogen , lipids , and most proteins while activating glycogen breakdown , oxidative phosphorylation , and mitochondrial biogenesis
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to apoptosis by quercetin , which was supported by results showing that blockade of JNK activity using DN - JNK1-expressing plasmid vector suppressed quercetin - induced PARP proteolysis and inhibited the reduction of DNA synthesis by quercetincontributedto apoptosis by quercetin , which was supported by results showing that blockade of JNK activity using DN - JNK1-expressing plasmid vector suppressed quercetin - induced PARP proteolysis and inhibited the reduction of DNA synthesis by quercetin
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