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Most apoptotic stimuli converge on Caspase 3, a cysteine protease and the main effecter caspase during Fas mediated apoptosis.
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Among the caspases characterized in humans, caspase-3 is the main downstream effecter caspase that play essential roles in degrading the majority of key cellular components in apoptotic cells [ 28].
Caspase 3 is the main effector caspase that is involved in both external and internal apoptosis pathway and it is the most abundant caspase in the brain [22].
Caspase-3 has been recognized as a main effector caspase in the apoptotic cascade.
Activated caspase-3 is generally considered the main effector caspase during the execution phase of apoptotic cell death (Koester and Bolton, 1999; Herngartner, 2000; Vaux, 2002).
However, the main effector caspase-3 appeared as largely arrested at a premature 20-kDa cleavage product; and caspase-9 was not cleaved.
In C. elegans, DAF-16 was the main effecter of the well-characterized IIS signaling pathway [22, 25].
The γTuRC (γ-tubulin ring complex) is the main effecter of this process and consists of γ-tubulin, GCPs (γ-tubulin complex proteins) and NEDD1 (neural precursor cell expressed developmentally down-regulated gene-1) [4], [5], [5].
As mentioned previously, under the effect of a Delta signal from a neighbouring cell, the upregulation of the main effecter of the Delta/Notch pathway, hes1, results in the overall repression of the neuronal differentiation inducing genes (mash1, hes6).
Caspase-3 is believed to be the major effecter caspase in neuronal apoptosis.
Caspase 3 participates in caspase-dependent apoptotic pathway and is the major effecter caspase in apoptotic cell death [ 33].
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