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Exact(20)
IL-17A may trigger apoptosis directly in tubular cells or indirectly by mediating the production of other factors.
Chemical and physical properties such as reactive oxygen species (ROS) and direct damage to plasma membrane may trigger apoptosis and necrosis respectively.
Even micronucleation induced by inhibitors of microtubules may trigger apoptosis of human lymphocytes [40].
It was recently shown that the N-terminus of APP may trigger apoptosis [23].
Thus, entrapment of genes in the micronuclei may have severe phenotypic effects on the cells, which may trigger apoptosis.
As a consequence, the peptides may trigger apoptosis.
Similar(40)
ER stress may act as a defense mechanism against external insults; however, prolonged and/or severe ER stress may ultimately trigger apoptosis.
TLR3 may directly trigger apoptosis in certain cancer cells.
Notably, icaritin may potently trigger apoptosis in Raji cells that had been treated for 48 h.
In addition, TLR3 may directly trigger apoptosis in certain cancer cells [ 21, 22].
The fusion-associated small transmembrane (FAST) proteins are responsible for the induction of syncytia and may also trigger apoptosis [ 28– 30].
More suggestions(15)
may trigger violence
may trigger relief
may inhibit apoptosis
may affect apoptosis
may regulate apoptosis
may be apoptosis
may trigger defense
may stimulate apoptosis
may trigger counter-intervention
may attenuate apoptosis
may undergo apoptosis
may promote apoptosis
may prevent apoptosis
may increase apoptosis
may impair apoptosis
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