This type of cell death is termed caspase-independent cell death (CICD) that occurs in response to mitochondrial outer membrane permeabilisation and disruption of mitochondrial morphology.
The inner zone cells showed increased cell proliferation in response to 5%and10%0% serum, while outer zone cells were only stimulated by 10% serum.
In response to death stimuli, mitochondrial outer membrane becomes permeabilized to release cytochrome c that could bind its cytoplasmic receptor Apaf1 to form the apoptosome and to activate caspase cascades for apoptosis, a form of programmed cell death.
In contrast with the TOC proteins, components of the translocon at the inner envelope membrane of chloroplasts (TIC) did not change in abundance in response to stress, nor did an outer membrane protein uninvolved in the protein import mechanism, outer envelope protein 80 (OEP80) [ 3, 4, 20].
The micelles showed reversible dispersion/aggregation in response to temperature cycles through an outer polymer shell lower critical solution temperature (LCST) for PNIPAAm at around 34 °C, observed by optical absorbance measurements.
Rapid tissue evolutionary rates could be therefore related to a specific mode of duplication (SSD genes) and faster molecular evolution (high ω values) in response to this exposure to the outer environment.
In Escherichia coli, the σE regulon is induced specifically in response to the unbalanced synthesis of outer membrane proteins [ 17] and to the misfolding of polypeptides that have been translocated across the cytoplasmic membrane [ 19].
In the absence of Kif3A, varr is unable to reach the outer segment in response to light [49], suggesting that Kif3A is responsible for its transport through the connecting cilium.
In response to cell stress, YfiB in the outer membrane can sequester the periplasmic protein YfiR, releasing its inhibition of YfiN on the inner membrane and thus provoking the diguanylate cyclase activity of YfiN to induce c-di-GMP production.
