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Complete local landscape for a defined molecular function-the alternative splicing of an exon (FAS/CD95 exon 6). The extensive epistasis in the landscape predicts that exonic regulatory sequences may diverge between species even when exon inclusion levels are functionally important and conserved by selection.
Paper analyses results of serum cytokines and lymphocyte apoptosis study in nodular goiter against the background of autoimmune thyroiditis and thyroid adenoma based on the cell preparedness to apoptosis, the number of apoptotic lymphocytes and the content of proapoptotic tumor necrosis factor-alpha, interleukins in serum, considering the polymorphism of BCL-2, CTLA-4 and APO-1 genes.
These results demonstrated that overexpression of ING4 (show ING4 Proteins) can induce the apoptosis of melanoma cells and CD3 (show CD3 Proteins)+ T cells through signaling pathways such as the Fas/FasL (show FASL Proteins) pathway, and that ING4 (show ING4 Proteins) gene therapy for melanoma treatment is a novel approach.
Tag7 (show PGLYRP1 Proteins) activates lymphocytes capable of Fasl (show FASL Proteins)-Fas-dependent contact killing of virus-infected cells.
These results indicated that cMyc (show MYC Proteins) and Fas regulated the sensitivity of A549 cells to irradiation by regulating caspase8-mediated Bid (show BID Proteins) activation and the subsequent association with the mitochondrial pathway of apoptosis.
this study characterized in juvenile systemic lupus erythematosus a distinct profile from adult SLE that comprises increased sFas, sTRAIL, and reduced sFasL (show FASL Proteins), notably in patients with active disease and with nephritis.
results from the current study showed that the association of FAS-670A/G SNP with idiopathic azoospermia was not found in a population of men with idiopathic infertility.
The Btk (show BTK Proteins)-dependent PIP5K1gamma lipid kinase activation by Fas counteracts FasL (show FASL Proteins)-induced cell death.
Study identify genes highly expressed in Kras knockout lung cancer cells, including the Fas receptor gene. Antibodies that activate Fas receptor selectively induced apoptosis in Kras-independent lung cancer cells suggesting that FAS is involved in KRAS-related drug resistance.
The authors observed differential expression of CD95(Fas) in CD27 (show CD27 Proteins)(+) B-cells from cirrhotic patients that was inversely correlated with peripheral CD27 (show CD27 Proteins)(+) B-cell frequency. They conclude that peripheral CD27 (show CD27 Proteins)(+) memory B-cells in cirrhosis exhibit increased sensitivity to Fas-induced apoptosis in an activation-dependent manner to which endotoxin contributes, associated with reduced frequency of circulating memory B-cells.
Messenger RNA and protein levels of prostaglandin (PG) E synthase (PGES (show PTGES Proteins)), PGF2alpha receptor (PGFR), tumor necrosis factor-alpha (TNF (show TNF Proteins)) and Fas were found to be higher in the corpus luteum of pregnancy than in corpus luteum of the cycle.
Results did not support that K8/K18 (show KRT18 Proteins) filaments influence the expression of Fas on the surface of luteal cells.
activation of the Fas pathway and presence of FSH (show BRD2 Proteins) during in vitro maturation increased the incidence of apoptosis in cumulus cells
demonstrated for the first time that normal ejaculated spermatozoa express Fas antigen (show FASL Proteins); data showed that a large percentage of normal ejaculated spermatozoa of fertile bulls are immunocytochemically positive for Fas
identification of 14-3-3zeta (show YWHAZ Proteins) as a novel phosphocofilin binding protein involved in the maintenance of the cellular phosphocofilin pool
Findings indicate that induction of apoptosis through Fas is dependent on receptor palmitoylation in primary immune cells, and Fas may prevent autoimmunity by mechanisms other than inducing apoptosis.
Both Sharpin/Fas and Sharpin/Fasl (show FASL Proteins) compound mutant mice developed an auto-inflammatory phenotype similar to that seen in Sharpin null mice, indicating that initiation of apoptosis by FAS signalling is likely not involved in the pathogenesis of this disease.
leucine deprivation induces the expression of miR (show MLXIP Proteins)-212-5p in a GCN2 (show EIF2AK4 Proteins)/ATF4 (show ATF4 Proteins)-dependent manner. miR (show MLXIP Proteins)-212-5p suppresses lipid accumulation in liver by targeting FAS and SCD1 (show SCD Proteins) under both normal diet and high-fat diet conditions.
Our data show that loss of Fas activity strongly affects the early development of atopic dermatitis (AD) by leading to Th2-dominant inflammation characterized by dermal infiltration of CD4 (show CD4 Proteins)+ T cells, neutrophils and increased skin expression of Th2 cytokines.However, Fas/FasL (show FASL Proteins)-apoptotic pathway is also involved in restricting tissue remodelling and dermal fibrosis during AD.
Hrd1 (show SYVN1 Proteins)-null B cells exhibited high Fas expression during activation and rapidly underwent Fas-mediated apoptosis, which could be largely inhibited by FasL (show FASL Proteins) neutralization. Fas mutation in Hrd1 (show SYVN1 Proteins) KO mice abrogated the increase in B-cell AICD. We identified Hrd1 (show SYVN1 Proteins) as the first E3 ubiquitin ligase (show MUL1 Proteins) of the death receptor Fas and Hrd1 (show SYVN1 Proteins)-mediated Fas destruction as a molecular mechanism in regulating B-cell immunity.
FAS contributes to mitochondrial dysfunction, steatosis development, and insulin (show INS Proteins) resistance under high fat diet.
anti-apoptotic molecules BclxL (show BCL2L1 Proteins) and Bcl-2 (show BCL2 Proteins) and the pro-apoptotic factors BAD and BID (show BID Proteins) cooperate to promote migration of triple-negative breast cancer cells stimulated with cl-CD95L (show FASL Proteins).
These findings reveal a role for MOAP-1 (show MOAP1 Proteins) in Fas signaling in the liver by promoting MTCH2 (show MTCH2 Proteins)-mediated tBid recruitment to mitochondria.
The in vivo delivery of CRISPR/Cas9 could maintain liver homeostasis and protect hepatocytes from Fas-mediated cell apoptosis in the fulminant hepatic failure model.
Fas was expressed on fetal pig pancreatic cells, both beta and non-beta cells, and the level of expression could be upregulated by exposure to interleukin 1beta
The expression of FAS and FAS ligand (show FASL Proteins) in splenic macrophages co-infected with porcine circovirus 2 and porcine reproductive and respiratory syndrome virus is reported
The present results may provide some insights to understand the role of Fas/FasL (show FASL Proteins) in the spinal cord but not motor cortex with neuronal apoptosis and neuroplasticity in monkeys subjected to hemisection spinal cord injury.
Ligustrazine has notable protective effects on pulmonary ischemia/reperfusion injury inhibiting Fas/FasL (show FASL Proteins) mRNA express in lung tissue and decreasing apoptosis.
The protein encoded by this gene is a member of the TNF-receptor superfamily. This receptor contains a death domain. It has been shown to play a central role in the physiological regulation of programmed cell death, and has been implicated in the pathogenesis of various malignancies and diseases of the immune system. The interaction of this receptor with its ligand allows the formation of a death-inducing signaling complex that includes Fas-associated death domain protein (FADD), caspase 8, and caspase 10. The autoproteolytic processing of the caspases in the complex triggers a downstream caspase cascade, and leads to apoptosis. This receptor has been also shown to activate NF-kappaB, MAPK3/ERK1, and MAPK8/JNK, and is found to be involved in transducing the proliferating signals in normal diploid fibroblast and T cells. Several alternatively spliced transcript variants have been described, some of which are candidates for nonsense-mediated mRNA decay (NMD). The isoforms lacking the transmembrane domain may negatively regulate the apoptosis mediated by the full length isoform.
APO-1 cell surface antigen
, CD95 antigen
, Delta Fas/APO-1/CD95
, FAS 827dupA
, FASLG receptor
, Fas (TNF receptor superfamily, member 6)
, Fas AMA
, TNF receptor superfamily member 6
, apoptosis antigen 1
, apoptosis-mediating surface antigen FAS
, tumor necrosis factor receptor superfamily member 6
, tumor necrosis factor receptor superfamily, member 6
, Fas antigen
, 14-3-3 protein zeta/delta
, factor activating exoenzyme S
, protein kinase C inhibitor protein 1
, Fas (TNF receptor superfamily member)
, apo-1 antigen
, Fas antigen (ATP1)
, Fas receptor
, Tumor necrosis factor receptor superfamily, member 6
, apoptosis (APO-1) antigen 1 ( FAS ), member 6
, Fas receptor CD95