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Human FAS Protein expressed in Synthetic - ABIN2691045
Liles, Kiener, Ledbetter, Aruffo, Klebanoff: Differential expression of Fas (CD95) and Fas ligand on normal human phagocytes: implications for the regulation of apoptosis in neutrophils. in The Journal of experimental medicine 1996
Show all 6 Pubmed References
Human FAS Protein expressed in Insect Cells - ABIN967460
Cheng, Zhou, Liu, Shapiro, Brauer, Kiefer, Barr, Mountz: Protection from Fas-mediated apoptosis by a soluble form of the Fas molecule. in Science (New York, N.Y.) 1994
Show all 3 Pubmed References
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.
the analysis of mRNA level showed that disease progression is associated with significantly increased expression of FasR and/or FasL (show FASL Proteins). In conclusion, our observation seems to confirm that spherical model of cancer lines is more reliable for some sophisticated analysis because of their greater resemblance to the CSCs from human CRC (show CALR Proteins) samples in comparison to commonly used adherent cells
study indicates FAS-FASL (show FASL Proteins) promoter SNPs may promote the production of cross-reactive anti-ganglioside antibodies in GBS (show GNB5 Proteins)
In primary hyperparathyroidism, hyperplasias demonstrated the highest expression of TRAIL and Fas, whereas in adenomas it was increased compared to normal tissue, but lower than in hyperplasias.
Data suggest that Fas and TNFR1 (show TNFRSF1A Proteins) are involved in glaucoma mechanisms in cornea; pro-apoptotic effect of anti-glaucoma medication clonidine on corneal epithelial cells triggers Fas/TNFR1 (show TNFRSF1A Proteins)-mediated, mitochondria-dependent signaling pathway. (Fas = Fas cell surface death receptor ; TNFR1 (show TNFRSF1A Proteins) = TNF (show TNF Proteins) receptor superfamily member 1A)
These data suggested that YY1 (show YY1 Proteins) may be important for apoptosis induction via the regulation of Fas during sepsis. Therefore, Fas may be a potential therapeutic target to prevent MOD through regulation of YY1 (show YY1 Proteins) expression. Furthermore, YY1 (show YY1 Proteins) and Fas expression in PBMCs may be used to as prognostic markers.
Fas activation rapidly changes the interconversion of PC and PI, which then drives enhanced endocytosis, thus likely propagating death signaling from the cell surface to mitochondria and other organelles
using pifithrin alpha we observed a decrease in apoptosis induced by MG132, and by APO-1 plus MG132, suggesting that restoration of APO-1 sensitivity occurs in part through an increase in both the levels and the activity of p53 (show TP53 Proteins). The use of small molecules to inhibit the proteasome pathway might permit the activation of cell death, providing new opportunities for CC treatment.
Fas - 670A/G genotypes or alleles were not significantly different between controls and transplant recipients and among transplant recipients with and without acute rejection following pediatric renal transplantation
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.
This study demonstrated that Ischemic neurons release sFasL (show FASL Proteins), which contributes to M1-microglial polarization.
results indicate that IL-1beta (show IL1B Proteins), produced by the inflammasome and Fas-dependent mechanisms, contributes cooperatively to the Th17/Th1 (show HAND1 Proteins) induction during bacterial infection. This study provides a deeper understanding of the molecular mechanisms underlying Th17/Th1 (show HAND1 Proteins) induction during pathogenic microbial infections in vivo.
this study shows that CD95-mediated calcium signaling promotes Th17 cell trafficking to inflamed organs in lupus-prone mice
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
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
, 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