About 50% of spinal motoneurons undergo programmed cell death (PCD) after target contact, but little is known about how this process is initiated. Embryonic motoneurons coexpress the death receptor Fas and its ligand FasL at the stage at which PCD is about to begin. In the absence of trophic factors, many motoneurons die in culture within 2 d. Most (75%) of these were saved by Fas-Fc receptor body, which blocks interactions between Fas and FasL, or by the caspase-8 inhibitor tetrapeptide IETD. Therefore, activation of Fas by endogenous FasL underlies cell death induced by trophic deprivation. In the presence of neurotrophic factors, exogenous Fas activators such as soluble FasL or anti-Fas antibodies triggered PCD of 40-50% of purified motoneurons over the following 3-5 d; this treatment led to activation of caspase-3, and was blocked by IETD. Sensitivity to Fas activation is regulated: motoneurons cultured for 3 d with neurotrophic factors became completely resistant. Levels of Fas expressed by motoneurons varied little, but FasL was upregulated in the absence of neurotrophic factors. Motoneurons resistant to Fas activation expressed high levels of FLICE-inhibitory protein (FLIP), an endogenous inhibitor of caspase-8 activatio...Continue Reading
Cell death of motoneurons in the chick embryo spinal cord. II. A quantitative and qualitative analysis of degeneration in the ventral root, including evidence for axon outgrowth and limb innervation prior to cell death
Cell death of motoneurons in the chick embryo spinal cord. I. A light and electron microscopic study of naturally occurring and induced cell loss during development
Molecular cloning and expression of the Fas ligand, a novel member of the tumor necrosis factor family
Cell-autonomous Fas (CD95)/Fas-ligand interaction mediates activation-induced apoptosis in T-cell hybridomas
FADD, a novel death domain-containing protein, interacts with the death domain of Fas and initiates apoptosis
Peptide inhibitors of the ICE protease family arrest programmed cell death of motoneurons in vivo and in vitro
FMRFamide-like and allatostatin-like immunoreactivity in the lateral heart nerve of Periplaneta americana: colocalization at the electron-microscopic level
Fas and Fas ligand in embryos and adult mice: ligand expression in several immune-privileged tissues and coexpression in adult tissues characterized by apoptotic cell turnover
FLICE, a novel FADD-homologous ICE/CED-3-like protease, is recruited to the CD95 (Fas/APO-1) death--inducing signaling complex
Cardiotrophin-1, a cytokine present in embryonic muscle, supports long-term survival of spinal motoneurons
Programmed cell death in neurons: focus on the pathway of nerve growth factor deprivation-induced death of sympathetic neurons
Bcl-xL functions downstream of caspase-8 to inhibit Fas- and tumor necrosis factor receptor 1-induced apoptosis of MCF7 breast carcinoma cells.
Delayed selective motor neuron death and fas antigen induction after spinal cord ischemia in rabbits
Survival motor neuron (SMN) protein in rat is expressed as different molecular forms and is developmentally regulated
Low concentrations of 1-methyl-4-phenylpyridinium ion induce caspase-mediated apoptosis in human SH-SY5Y neuroblastoma cells
Rheumatoid arthritis synovial macrophages express the Fas-associated death domain-like interleukin-1beta-converting enzyme-inhibitory protein and are refractory to Fas-mediated apoptosis
H(2)O(2) induces upregulation of Fas and Fas ligand expression in NGF-differentiated PC12 cells: modulation by cAMP
Expression patterns of erythropoietin and its receptor in the developing spinal cord and dorsal root ganglia
Interactions of PACAP and ceramides in the control of granule cell apoptosis during cerebellar development.
Effects of tumour necrosis factor-alpha on developing cerebellar granule and Purkinje neurons in vitro.
Protective effect of memantine against Doxorubicin toxicity in primary neuronal cell cultures: influence a development stage.
Role of spin trapping and P2Y receptor antagonism in the neuroprotective effects of 2,2'-pyridylisatogen tosylate and related compounds
In vitro induction of neuronal apoptosis by anti-Fas antibody-containing sera from amyotrophic lateral sclerosis patients
Transcription-dependent and -independent control of neuronal survival by the PI3K-Akt signaling pathway
Sedimentation field flow fractionation purification of immature neural cells from a human tumor neuroblastoma cell line
Direct inhibition of c-Jun N-terminal kinase in sympathetic neurones prevents c-jun promoter activation and NGF withdrawal-induced death
Cu,Zn-superoxide dismutase increases toxicity of mutant and zinc-deficient superoxide dismutase by enhancing protein stability.
Inhibition of Fas-mediated apoptosis through administration of soluble Fas receptor improves functional outcome and reduces posttraumatic axonal degeneration after acute spinal cord injury
Disruption of Bax protein prevents neuronal cell death but produces cognitive impairment in mice following traumatic brain injury.
Elevated levels of IFNγ and LIGHT in the spinal cord of patients with sporadic amyotrophic lateral sclerosis
Suppression of Fas-FasL coexpression by erythropoietin mediates erythroblast expansion during the erythropoietic stress response in vivo
The extracellular matrix, p53 and estrogen compete to regulate cell-surface Fas/Apo-1 suicide receptor expression in proliferating embryonic cerebral cortical precursors, and reciprocally, Fas-ligand modifies estrogen control of cell-cycle proteins
Inhibition of apoptosis blocks human motor neuron cell death in a stem cell model of spinal muscular atrophy.
Chronic activation in presymptomatic amyotrophic lateral sclerosis (ALS) mice of a feedback loop involving Fas, Daxx, and FasL
Apoptotic caspases belong to the protease enzyme family and are known to play an essential role in inflammation and programmed cell death. Here is the latest research.
Apoptosis is a specific process that leads to programmed cell death through the activation of an evolutionary conserved intracellular pathway leading to pathognomic cellular changes distinct from cellular necrosis