HUGO ID Detailed Result 11920


HUGO ID 11920
Symbol FAS
Name Fas (TNF receptor superfamily, member 6)
#Occurrence 29
#Paper 7

 


PMID Match String Actual String Score Flanking text Edited by Edit
12843244FASFas0.3(Raoul Raoul et al. 2002 although the critical role of Fas pathway in mediating motor neuron degeneration has not been evaluated 
14960605FASFas0.6et al. 1998 cytoskeletal abnormalities (Wong Wong et al. 1995 Fas ligand (FasL)-mediated FasL -mediated death (Raoul Raoul et al. 2002 
15572176FASFas-ligand0.6pro-apoptotic mediators such as nerve growth factor (NGF) NGF or Fas-ligand a mechanism that may serve to eliminate vulnerable motor neurons 
15572176FASFas0.6by motor neurons in response to trophic factor deprivation 35 Fas pathway activation 101 or loading with zinc-deficient SOD-1 36 
15572176FASFas0.6makes the cells vulnerable to undergo apoptosis in response to Fas ligand (FasL) FasL 39 
15572176FASFas0.6Motor neurons co-express Fas and FasL during the embryonic period of naturally occurring cell 
15572176FASFas0.6in motoneuron survival were observed in mutant mice deficient for Fas signaling 133 
15572176FASFas0.6In contrast Fas signaling has been implicated in motor neuron death induced by 
15572176FASFas0.6mutations G37R G85R or G93A display an increased susceptibility to Fas signaling 99 and 101 
15572176FASFas0.6The apoptotic pathway activated by Fas seems to be specific for motor neurons requiring co-activation of 
15572176FASFas0.6neuron A which upregulates the expression of nNOS p75 NTR Fas cytokines and trophic factors 
16510725FASFas2.1to the events that take place when FasL binds to Fas then death-inducing signaling complex (DISC) DISC will form and caspase-8 
16510725FASFas-associated2.1receptors was also present A study using RPAs showed increased Fas-associated death domain (FADD) FADD and TNF-alpha receptor p55 at 80 
16510725FASFas2.1Fas triggers cell death in embryonic motoneurons by a pathway requiring 
16510725FASFas2.1FasL works in a similar way by binding to Fas/CD95 Fas CD95 receptor and activate it to cause FADD ligation and 
16510725CD95CD952.1works in a similar way by binding to Fas/CD95 Fas CD95 receptor and activate it to cause FADD ligation and DISC 
16624536FASFas0.6motor neuron death via TNF--mediated apoptotic mechanisms 35 and by Fas ligand or NO-induced apoptotic pathways 36 
16624536FASFas-triggered0.6transgenic mice exhibit an increased susceptibility to activation of a Fas-triggered cell death pathway that is unique to motor neurons and 
16624536FASFas0.6explanation for the sensitivity of motor neurons in particular to Fas ligand and NO-triggered cell death mediated at least in part 
16624536FASFas0.6phosphatidylinositol-3 kinase/protein kinase protein kinase B pathway fractalkine will inhibit Fas ligand-induced microglial apoptosis through down-regulation of the pro-apoptotic function of 
16624536FASFas-associated0.6death domain (TRADD) TRADD that can then interact with the Fas-associated death domain to activate caspase 8 leading to downstream activation 
16624536FASFas0.6Fas ligand and TNF-produced by reactive astrocytes can also activate death 
16624536FASFas0.6Raoul et al. ALS motor neurons are particularly susceptible to Fas signaling and the apoptotic pathway implicated is motor neuron-specific 36 
17015226FASFas-ligand0.3Microglial cells could therefore be an important player in a Fas-ligand (FasL)-induced FasL -induced apoptosis pathway within motor neurons that is 
17015226FASFas0.3been proposed as a motor-neuron-specific cell-death pathway downstream of the Fas death receptor 
17015226FASFas0.3Increased susceptibility to death triggered by the Fas receptor requires nitric oxide the Fas death domain-associated protein Daxx 
17015226FASFas0.3death triggered by the Fas receptor requires nitric oxide the Fas death domain-associated protein Daxx and p38 kinase activation which subsequently 
17555556FASFas0.6Other studies have shown that nitric oxide can induce Fas signaling in mutant SOD1 motoneurons which resulted in mutant SOD1 
17555556FASFas-triggered0.6Additionally up-regulation of nNOS was required in this Fas-triggered motoneuron death ( Raoul et al 2002 2006