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anti-Human FAS Antikörper:
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Mouse (Murine) Polyclonal FAS Primary Antibody für IHC (fro), IHC (p) - ABIN3044338
Jiang, Li, Zhou, Wang, Zhang, Wang: Colistin-induced apoptosis in PC12 cells: involvement of the mitochondrial apoptotic and death receptor pathways. in International journal of molecular medicine 2014
Show all 19 Pubmed References
Human Polyclonal FAS Primary Antibody für IHC (p), WB - ABIN3042387
Liu, Shan, Dong, Liu, Ma, Liu: Combined early fluid resuscitation and hydrogen inhalation attenuates lung and intestine injury. in World journal of gastroenterology 2013
Show all 19 Pubmed References
Human Monoclonal FAS Primary Antibody für FACS - ABIN5541251
Hata, Matsuzaki, Takeya, Yoshida, Sonoki, Nagasaki, Kuribayashi, Kawano, Takatsuki: Expression of Fas/Apo-1 (CD95) and apoptosis in tumor cells from patients with plasma cell disorders. in Blood 1995
Show all 13 Pubmed References
Human Monoclonal FAS Primary Antibody für FACS - ABIN5541252
Boirivant, Pica, DeMaria, Testi, Pallone, Strober: Stimulated human lamina propria T cells manifest enhanced Fas-mediated apoptosis. in The Journal of clinical investigation 1997
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Human Monoclonal FAS Primary Antibody für IHC (fro), IF - ABIN1106610
Vega, Jazirehi, Huerta-Yepez, Bonavida et al.: Rituximab-induced inhibition of YY1 and Bcl-xL expression in Ramos non-Hodgkin's lymphoma cell line via inhibition of NF-kappa B activity: role of YY1 and Bcl-xL in Fas resistance and ... in Journal of immunology (Baltimore, Md. : 1950) 2005
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Mouse (Murine) Monoclonal FAS Primary Antibody für FACS - ABIN2689463
Enari, Hug, Nagata: Involvement of an ICE-like protease in Fas-mediated apoptosis. in Nature 1995
Show all 9 Pubmed References
Mouse (Murine) Monoclonal FAS Primary Antibody für CyTox, FACS - ABIN1177304
Hiromatsu, Aoki, Makino, Matsumoto, Mizuochi, Gotoh, Nomoto, Ogasawara, Nagata, Yoshikai: Increased Fas antigen expression in murine retrovirus-induced immunodeficiency syndrome, MAIDS. in European journal of immunology 1994
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Mouse (Murine) Monoclonal FAS Primary Antibody für CyTox, FACS - ABIN2689461
Kägi, Vignaux, Ledermann, Bürki, Depraetere, Nagata, Hengartner, Golstein: Fas and perforin pathways as major mechanisms of T cell-mediated cytotoxicity. in Science (New York, N.Y.) 1994
Show all 5 Pubmed References
Human Polyclonal FAS Primary Antibody für WB - ABIN2801888
Oehm, Behrmann, Falk, Pawlita, Maier, Klas, Li-Weber, Richards, Dhein, Trauth: Purification and molecular cloning of the APO-1 cell surface antigen, a member of the tumor necrosis factor/nerve growth factor receptor superfamily. Sequence identity with the Fas antigen. in The Journal of biological chemistry 1992
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Human Polyclonal FAS Primary Antibody für IHC (p), IHC - ABIN266061
Chen, Yan, Chien, Kuo, Chen, Cheng, Su: Sann-Joong-Kuey-Jian-Tang inhibits hepatocellular carcinoma Hep-G2 cell proliferation by increasing TNF-α, Caspase-8, Caspase- 3 and Bax but by decreasing TCTP and Mcl-1 expression in vitro. in Molecular medicine reports 2013
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Results found that Fas mRNA expression in the exposed group were significantly higher than that in the control group. The levels of gene expression were positively correlated with the concentrations of urinaryinorganic arsenic, monomethylarsonic acid and dimethylarsinic acid in all subjects.
The current research reveals a vital role of CRIP1 in colorectal cancer(CRC) progression, which provide a novel target for clinical drug resistance of colorectal cancer and undoubtedly contributing to the therapeutic strategies in CRC.
The initial activation of CD95 occurs locally and is limited to the contact region of the cytotoxic synapse.
Hybridization-based panel sequencing of patients with well-characterized primary cutaneous marginal zone lymphoma identified genetic alterations in the FAS gene which affect the functionally relevant death domain of the apoptosis-regulating FAS/CD95 protein in a dominant-negative manner.
increased SRSF4 expression stimulates Fas exon 6 inclusion, and that reduced SRSF4 expression promotes exon 6 exclusion.
CD39, CD43, CD81, and CD95 expressions appear to be helpful to distinguish CD10(+) BCL.
No significant difference was observed in genotypic or allelic frequencies between control and endometriosis groups for rs13416436 and rs2037815 (CASP8 gene). On the other hand, a significant difference between rs3740286 and rs4064 (FAS gene) was found. Regarding polymorphisms in the FAS gene, a statistically significant difference was found in co-dominant and dominant models.
Fas polymorphism rs1800682 is associated with intervertebral disc degeneration (IVDD), and along with rs2234767, is associated with musculoskeletal degenerative diseases in Chinese population. Fas (rs2234767) correlates with risk of osteoarthritis and rheumatoid arthritis.
These data indicate that the Fas/FasL system increases pulmonary protein permeability by a direct effect on the alveolar epithelium that involves the alteration of its TJ proteins and permeability properties.
predisposition to multiple sclerosis as well as to high progression rate are associated with the FAS/APO-1*G/capital A, Cyrillic gene in Russians living in the Altai Territory.
The proportion of CD8(+)T lymphocytes in peripheral blood of patients with HCC [hepatocellular carcinoma ] is higher than that of healthy controls, but the proportion of CD8(+)T lymphocyte apoptosis based on Fas/FasL pathway increased, which may be an important mechanism for tumor cell immune escape.
Fas pathway role in the myelodysplastic syndrome.
Luteolin induced apoptosis of HL-60 cells, and this was associated with c-Jun activation and histone H3 acetylation-mediated Fas/FasL expressions.
Study provides evidence that Fas is targeted and regulated by miR-98 with cardiomyocytes. mir-98 directly binds the 3'UTR of Fas gene.
The Fas/FasL-dependent aberrant iNKT cell responses.
our data suggest that si- and/or shRNAs with certain seed sequences present in CD95 and CD95L and the entire CD95L ORF are toxic to cancer cells.
CD95 engagement evokes nonapoptotic signals that promote inflammation and carcinogenesis. cD95, a death receptor, can trigger both apoptotic and nonapoptotic signaling pathways. Review.
that FAS death domain or TP53 DNA-binding domain mutations, down-regulation of FAS receptor expression
CD95-mediated apoptosis induces Pim-1 down-regulation in Burkitt's lymphoma (BL) B-cells, but Pim-1 down-regulation cannot fully eradicate BL and leukaemia.
Fas single-nucleotide polymorphisms rs2234767 and rs1800682 are involved in the pathogenesis of Idiopathic Aplastic Anemia
Messenger RNA and protein levels of prostaglandin (PG) E synthase (PGES), PGF2alpha receptor (PGFR), tumor necrosis factor-alpha (TNF) 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 filaments influence the expression of Fas on the surface of luteal cells.
activation of the Fas pathway and presence of FSH during in vitro maturation increased the incidence of apoptosis in cumulus cells
demonstrated for the first time that normal ejaculated spermatozoa express Fas antigen; data showed that a large percentage of normal ejaculated spermatozoa of fertile bulls are immunocytochemically positive for Fas
identification of 14-3-3zeta as a novel phosphocofilin binding protein involved in the maintenance of the cellular phosphocofilin pool
These results suggest that the proinflammatory effects of CD8 T cells during mouse adenovirus type 1 infection are mediated in part by Fas activation and are distinct from CD8 T cell antiviral functions.
Fas/FasL signaling is critical for the survival of exhausted CD8(+) T cells during the tumor immune response.
This study investigated the interaction between Fas and MMP-9 in the setting of induction of experimental autoimmune encephalomyelitis (EAE) and compared short- and long-term effects. faslpr mice were resistant against EAE induction, whereas MMP-9 single knockout mice were not.
Data suggest that miR-20a regulates FAS expression through the modulation of the FAS promoter.
Many Th subsets have cytotoxic potential that is enhanced by cognate induction of Fas on target cells.
our computational and experimental approach identified Fas as a regulator of the Th17-to-Th1 cell balance by controlling the availability of opposing STAT1 and STAT3 to have a direct impact on autoimmunity.
FGF21 alleviated atherosclerosis by ameliorating Fas-mediated apoptosis in apoE-/- mice.
TPD7 altered the extrinsic apoptosis pathway by upregulating Fas expression.
In conclusion, these data demonstrate that murine herpesvirus 68-immortalized SL-1 cells can be recognized and controlled by specific cytotoxic T cells through CD95/CD95L-mediated apoptosis.
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 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.
Tag7 activates lymphocytes capable of Fasl-Fas-dependent contact killing of virus-infected cells.
leucine deprivation induces the expression of miR-212-5p in a GCN2/ATF4-dependent manner. miR-212-5p suppresses lipid accumulation in liver by targeting FAS and SCD1 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+ T cells, neutrophils and increased skin expression of Th2 cytokines.However, Fas/FasL-apoptotic pathway is also involved in restricting tissue remodelling and dermal fibrosis during AD.
Hrd1-null B cells exhibited high Fas expression during activation and rapidly underwent Fas-mediated apoptosis, which could be largely inhibited by FasL neutralization. Fas mutation in Hrd1 KO mice abrogated the increase in B-cell AICD. We identified Hrd1 as the first E3 ubiquitin ligase of the death receptor Fas and Hrd1-mediated Fas destruction as a molecular mechanism in regulating B-cell immunity.
FAS contributes to mitochondrial dysfunction, steatosis development, and insulin resistance under high fat diet.
anti-apoptotic molecules BclxL and Bcl-2 and the pro-apoptotic factors BAD and BID cooperate to promote migration of triple-negative breast cancer cells stimulated with cl-CD95L.
These findings reveal a role for MOAP-1 in Fas signaling in the liver by promoting MTCH2-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 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 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 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 ligand
, tumor necrosis factor (ligand) superfamily, member 6
, tumor necrosis factor ligand 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