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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
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
data suggest miR (show MLXIP Proteins)-374a is a negative regulator of Fas death receptor which is able to enhance the cell survival and protect retinal pigment epithelial cells against oxidative conditions.
CD3 (show CD3 Proteins)(+) CD8 (show CD8A Proteins)(+) NKG2D (show KLRK1 Proteins)(+) T Lymphocytes Induce Apoptosis and Necroptosis in HLA-Negative Cells via FasL (show FASL Proteins)-Fas Interaction
High-grade gliomas (HGG) showed significantly lower FAS but higher FAS ligand (FAS-L (show FASL Proteins)) expression than high-grade gliomas (HGG).
Peripheral CD95 expression higher than 30% could be used among the exclusion criteria in a multicomponent score for mycosis fungoides diagnosis.
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).
Knockout (KO) or knockdown of caspase-8 (show CASP8 Proteins), CD95 or FADD (show FADD Proteins) prevents activation of Plk3 (show PLK3 Proteins) upon CD95 stimulation, suggesting a requirement of a functional death-inducing signaling complex for Plk3 (show PLK3 Proteins) activation.
STAT1 (show STAT1 Proteins) is a key regulator of the cancer stem cell-inducing activity of CD95.
Two unrelated patients with severe recessive autoimmune lymphoproliferative syndrome had rare splicing defects in exon 6 of FAS.
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
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.
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
accelerating effects of Tlr9 (show TLR9 Proteins) deficiency
K8/K18 (show KRT18 Proteins)-dependent PKCdelta (show PKCd Proteins)- and ASMase (show SMPD1 Proteins)-mediated modulation of lipid raft size can explain the more prominent FasR-mediated signaling resulting from K8/K18 (show KRT18 Proteins) loss.
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