Fas/Apo [Apoptosis]-1 and Associated Proteins in the Differentiating Cerebral Cortex: Induction of Caspase-Dependent Cell Death and Activation of NF-κB

Fas ligand FADD Neuroblast Caspase 8
DOI: 10.1523/jneurosci.19-05-01754.1999 Publication Date: 2018-04-03T11:50:19Z
ABSTRACT
The developing cerebral cortex undergoes a period of substantial cell death. present studies examine the role suicide receptor Fas/Apo[apoptosis]-1 in cortical development. Fas mRNA and protein are transiently expressed subsets cells within rat during peak apoptosis. Fas-immunoreactive were localized close proximity to ligand (FasL)-expressing cells. Fas-associated signaling interacting (RIP) was by some Fas-expressing cells, whereas death domain (FADD) undetectable early postnatal cortex. FLICE-inhibitory (FLIP), an inhibitor activation, also expression more ubiquitous embryonic neuroblasts dissociated culture compared situ brain, suggesting that environmental milieu partly suppresses at this developmental stage. Furthermore, FADD, RIP, FLIP culture. activation (FasL) or anti-Fas antibody induced caspase-dependent primary neuroblast cultures. accompanied rapid downregulation expression, non-cell cycle-related incorporation nucleic acids nuclear translocation RelA/p65 subunit transcription factor NF-κB. Together, these data suggest adult number may be established, part, active process receptor-mediated suicide, initiated killer (FasL-expressing) have functions addition brain.
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