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Validated All-in-One™ qPCR Primer for FAS(NM_000043.3) Search again
Product ID:
HQP009651
(click here to view gene annotation page)
Powered by BiozSpecies:
Human
Symbol:
Alias:
ALPS1A, APO-1, APT1, CD95, FAS1, FASTM, TNFRSF6
Gene Description:
Fas cell surface death receptor
Target Gene Accession:
NM_000043.3(click here to view gene page)
Estimated Delivery:
Approximately 1-3 weeks, but may vary. Please email sales@genecopoeia.com or call 301-762-0888 to confirm ETA.
Important Note:
By default, qPCR primer pairs are designed to measure the expression level of the splice variant (accession number) you selected for this gene WITHOUT consideration of other possible variants of this gene. If this gene has multiple variants, and you would like to measure the expression levels of one particular variant, multiple variants, or all variants, please contact us for a custom service project at inquiry@genecopoeia.com.
Validated result:
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| A | B |
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Each All-in-One™ qPCR Primer is experimentally validated to yield a single dissociation curve peak and to generate a single amplification of the correct size for the targeted gene. A cDNA Pool, containing reverse transcript products of 8 different human tissue total RNA(Liver, Testis,Muscle,Thyroid,Brain,Spleen,Stomach,Small Intestine)),was used as the qPCR validation template. qPCR was performed using 0.2 µM primer with 2XAll-in-One™ qPCR Mix (Catalog#: QP001,QP002,QP004,QP005). Reactions were incubated for 10min. at 95°C, followed by 40 cycles of 95°C for 10 sec.; 60°C, 20 sec. and 72°C, 15sec. using Bio-Rad iQ5™ Instrument. At the end of the last cycle, temperature was increased from 72 to 95°C to produce a melting curve. Panel A: Validated Result for Amplification Curve; Panel B: Validated Result for Melting Curve. |
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Summary
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. At least eight alternatively spliced transcript variants encoding seven distinct isoforms have been described. The isoforms lacking the transmembrane domain may negatively regulate the apoptosis mediated by the full length isoform. [provided by RefSeq].
Gene References into function
- A review of alternative spliced APO-1 variants and their possible biological roles.
- These results suggest that irradiation induces direct apoptosis of T cells by a Fas-independent mechanism.
- A significant correlation with differentiation status of the tumor was found for the p53 aberration but not for CD95 expression.
- Regulation of Fas expression by STAT3 and c-Jun is mediated by phosphatidylinositol 3-kinase-AKT signaling
- its polymorphism may contributes to the pathogenesis of spondyloarthropathy
- induction of gene expression by doxorubicin in endothelial cells through a p53-dependent mechanism
- Soluble Fas antigen (sFAS) in the serum from patients with adrenal tumors.
- Butyrate induced apoptosis via the Fas/Fas L system and potentiated Fas-triggered apoptosis in MCF-7 cells.
- Expression of Fas and Fas ligand in esophageal tissue mucosa and carcinomas
- Cytochrome c release upon Fas receptor activation
- expression was significantly increased in neonates with pontosubicular neuron necrosis
- FAS germline mutations have been associated with the development of autoimmune lymphoproliferative syndrome (ALPS).
- Participation of Fas-mediated apoptotic pathway in KB, a human head and neck squamous cell carcinoma cell line, after irradiation
- expression associated with apoptosis in sun-exposed keratinocytes
- myelodysplastic syndrome CD34(+)-derived erythroid progenitors underwent abnormal Fas-dependent apoptosis during differentiation that could be responsible for the impaired erythropoiesis.
- Met sequesters Fas, preventing apoptosis.
- Overexpression of the mouse Fas gene in human Hep3B hepatoma cells overcomes their resistance to Fas-mediated apoptosis.
- Latent sensitivity to Fas-mediated apoptosis after CD40 ligation may explain activity of CD154 gene therapy in chronic lymphocytic leukemia
- upregulation of Fas by IFN-gamma in SNU-638 may accelerate the apoptosis pathway through the Fas and FasL interaction between gastric cancer cells and immune cells
- Decreased function of Fas in patients displaying delayed progression of HIV-induced immune deficiency
- Mature dendritic cells are protected from Fas/CD95-mediated apoptosis by upregulation of Bcl-X(L).
- Fas engagement increases expression of interleukin-6 in human glioma cells.
- Differential expressions of Fas and Fas ligand in human placenta
- Genetic polymorphisms of Fas (CD95) in human longevity
- HLA class II signals sensitize B lymphocytes to apoptosis via CD95
- Endotoxin-induced lymphopenia was constituted by cells with the highest rates of disappearance were characterized by an activated phenotype (CD45RA(-) CD45RO(+)) as well as a phenotype linked to apoptosis (CD95(+) CD28(-))
- Our results indicate that Fas-mediated apoptosis is important for endometrial cycling and suggest that dysregulation of the Fas/FasL interactions may have an important role in the development of endometrial cancer.
- "trophoblast-cytokine-Fas/FasL triad" determines the ability of the Fas/FasL system to regulate trophoblast viability
- data suggest that disruption of the cytoskeleton causes apoptosis via activation of CD95 and enhances UV-induced apoptosis, possibly via aiding receptor clustering
- Recipient gene polymorphism and acute renal allograft rejection
- alteration associated with nodal metastasis in non-small cell lung cancer
- Data indicate that the apoptosis program in T cells includes the shedding/secretion of different forms of Fas to spread a death signal.
- Fas defects may play a role in the pathogenesis of mycosis fungoides
- FLIP switches Fas-mediated glucose signaling in human pancreatic beta cells from apoptosis to cell replication.
- Fas promoter -670A/G polymorphism was significantly associated with systemic lupus erythematosus (SLE), suggesting a possibility that Fas promoter contributes, at least in part, to the pathogenesis of SLE
- These results suggest that Fas is involved in neuronal apoptosis in the developing human brain.
- Frequent mutations of Fas gene in nasal NK/T cell lymphoma
- Interferon-gamma increases its expression in B-leukemia cells.
- the death effector domain of FADD is involved in interaction with Fas.
- CCR5 mediates Fas- and caspase-8 dependent apoptosis of both uninfected and HIV infected primary human CD4 T cells
- the role of Fas/Fas ligand (FasL) in tum orgenesis, immune escape, counterattack in colonic cancer
- two novel mutations in the Fas receptor gene TNFRSF6 in autoimmune lymphoproliferative syndrome
- 7 of the 13 melanoma cell lines were found to have impaired Fas signalling. Taken together, our results indicate that downregulation of Fas expression and resistance to Fas-mediated apoptosis are frequent in melanoma.
- suppression of fas-induced apoptotic signal transduction by thymidine phosphorylase
- a role of Fas gene mutations in the pathogenesis of testicular germ cell tumors
- The apoptotic episodes surrounding the earlier stage of DC differentiation appeared to be mediated by Fas. In contrast, a Fas independent pathway is probably responsible for the apoptotic events associated with terminally differentiated DC.
- In the case of Fas-mediated apoptosis, when we transiently introduced these hybrid-ribozyme libraries into Fas-expressing HeLa cells, we were able to isolate surviving clones that were resistant to or exhibited a delay in Fas-mediated apoptosis
- DNA damage, death receptor (CD95) activation and ROS formation contribute to UVB-induced apoptosis in an essential and independent way.
- signals to mitochondria via FADD, caspase-8/10, Bid, and Bax but differentially regulate events downstream from truncated Bid compared to TRAIL receptor 2
- Caspase-10 is recruited to and activated at the native CD95 death-inducing signalling complex in a FADD-dependent manner.
- Stimulation of CD95 in the presence of caspase inhibitors induces necrosis and expression of various proinflammatory cytokines in primary T lymphocytes, such as TNF-alpha, IFN-gamma and granulocyte/macrophage colony-stimulating factor.
- molecular model of a conformational alteration of a mutated extracellular domain of Fas antigen in an adult T cell leukemia cell line
- Review. Fas introduces apoptosis-inducing signals into cells. It is implicated in peripheral lymphocyte regulation, elimination of autoreactive cells, tumors & virus-infected cells, & tissue disruption in autoimmune disease & fulminant hepatitis.
- Glutathione peroxidase-1 protects from apoptosis induced by this antigen
- IFN-gamma enhanced constitutive CD95 expression. Coincubation with anti-CD95 monoclonal antibody induced apoptosis
- Fas resistance of leukemic eosinophils to NF-kappa B activation results from Fas ligation itself and can be negated by inhibition of the nuclear translocation of p65/p50.
- Immunohistochemical expression of this protein in squamous cell carcinomas from immunosuppressed renal transplant recipients and immunocompetent individuals.
- Fas induces alpha(v)beta(8) integrin in cell migration
- Tyrosine-based sorting signal in adenovirus RID plays a role in RID's ability to down-regulate FAS and inhibit apoptosis
- Soluble HLA class I induces NK cell apoptosis upon the engagement of killer-activating HLA class I receptors through FasL-Fas interaction
- Fas-mediated apoptosis is important in regulating cell replication and death in trisomy 8 hematopoietic cells but not in cells with other cytogenetic abnormalities.
- A novel signaling mechanism shows synergy with anti-CD95 monoclonal antibodies for apoptosis and NF-kappaB nuclear translocation.
- that H(2)O(2) induces Fas upregulation by promoting cytoplasmic transport of Fas to the cell surface in human airway epithelial cells, and that the activation of the poly(ADP-ribose) polymerase-p53 pathway may be involved in this mechanism.
- fas Receptors are up-regulated in acute lung injury and the acute respiratory distress syndrome
- Delayed elevation of ceramide is proposed to promote necrosis in Fas-stimulated cells where caspase-8 activation was insufficient to trigger caspase-3-dependent apoptosis
- Ox-LDL dose-dependently up-regulated cell surface Fas expression, determining the degree of apoptosis.
- the lower expression of Fas in urinary malignant cell lines than that in normal cells might be the reason for occurrence and progression of urinary malignant tumors.
- Data suggest that frequent Fas gene mutations in nasal natural killer (NK)/T-cell lymphoma (NL) can result in resistance to apoptosis and may contribute to the pathogenesis of NL by adding to the tumor immune privilege.
- homeostatic regulation of myelopoiesis in bone marrow is mediated via an autoregulatory feedback loop via the Fas-FasL pathway
- A role for the Fas/Fas ligand apoptotic pathway in regulating myeloid progenitor cell kinetics.
- induced il-8 production is activated by activation o the p38 MAPK and ERK1/2 pathways in colonic epithelial cells
- Further evidence for role of a promoter polymorphism in the TNFRSF6 gene in genetic predisposition to Alzheimer disease.
- The Fas antigen may be involved in the apoptosis of astrocytic tumors, and the apoptotic index can be a useful parameter for assessing prognosis of astrocytic tumors.
- Bcl-2 may be involved in protecting against CD95-mediated apoptosis of cord blood CD34(+) cell.
- The Fas genotype may not appear to be a risk factor for stroke in Korean stroke patients.
- The Fas expression is positively correlated with the different degrees of differentiation
- CD95 gene mutations play little if any role in the generation of the pool of plasmablasts from systemic lupus erythematosus patients
- Fas system as an inducer of apoptosis in cutaneous leishmaniasis
- Over-expression of the splice variant Luca-15 inhibited CD95-mediated apoptosis in CEM-C7 T-cells.
- Bax, Bcl-2, fas and Fas-L antigen expression in human seminoma: correlation with the apoptotic index.
- sFas promotes a pro-apoptogen effect, which would explain the high susceptibility to apoptosis in active lupus, and that the apoptosis program itself includes release of sFas to spread the death signal.
- Dysfunction of the Fas apoptotic signaling pathway in persistent polyclonal B-cell lymphocytosis.
- Vitamin C inhibition of FAS-mediated apoptosis was associated with reduced activity of caspase-3, -8, and -10, as well as diminished levels of ROS and preservation of mitochondrial membrane integrity.
- Cross-talk between glioma cells and neutrophils through the Fas/FasL system stimulated expression of IL-6 and IL-8 in glioma cells, enhanced neutrophil viability, and stimulated cytokine production in neutrophils.
- Fas-induced apoptosis of myeloid leukemia cells is restricted to G1 phase of the cell cycle and can be increased by interferon
- IL-18 and TNF-alpha function both as apoptosis-promoting factors and as apoptosis-inhibiting factors in acute liver failure
- results showed that Fas and/or Fas-Ligand, Bcl-2, and tissue transglutaminase may be involved in apoptotic pathways leading to mucosal atrophy in children with coeliac disease
- maternal serum sFas antigen decreased significantly in the first trimester of pregnancy and at term, possibly affecting immune tolerance and apoptosis for rupture of membranes; amniotic fluid sFas decreased at term compared with the second trimester
- CD95 apoptotic function is regulated by SODD/BAG4
- apoptosis mediated by Fas-FasL and engagement of CTLA-4 are involved in modulation of the immune response in patients infected with Paracoccidioides brasiliensis
- Fas is inhibited by FAP-1 in tumor cells
- Longitudinally obtained data indicate that Fas is upregulated in peripheral blood mononuclear cells of multiple sclerosis patients, especially during secondary progressive course; in relapsing remitting patients Fas levels increase even more dynamically.
- Fas-FasL interactions may contribute to mechanisms of neuronal loss and neuritic degeneration in Alzheimer disease.
- Increased expression of Fas antigen on CD4+ subset and increased serum sFas level are valuable markers of clinical activity in multiple sclerosis.
- Expression of a functional Fas death receptor by human foetal motoneurons.
- ATG-induced apoptosis in T cells involves both Fas and TNF pathways and TNF-alpha is produced much earlier than Fas and FasL expression.
- upregulation of expression by p53 upon genotoxic treatment in human breast tumor cells
- Fas-induced monocyte cytokine responses are associated with monocyte apoptosis, nuclear translocation of NF-kappa B, and cytokine gene expression and are blocked by caspase inhibition but not by inhibition of IL-1beta signaling.
- Fas/Fas-L and Bcl-2 expression participate in regulation of apoptosis in extravillous trophoblast(EVT) along invasion to decidua. Increased apoptosis in invasive phenotype of EVT may be attributable to increased Fas and Fas-L and decreased Bcl-2.
- increased expression of soluble Fas in pleural effusion associated with lung cancer
- in B cells, Gadd45 beta is induced by CD40 through a mechanism that requires NF-kappa B and this induction suppresses Fas-mediated killing
- oligomerization/depolymerization of soluble Fas antigen can regulate its activity
- Data suggest that increased intrathecal release of Fas, but not FasL or caspase 3, in the cerebrospinal fluid of infants with hydrocephalus may serve as an indicator of brain injury from progressive ventricular dilatation.
- While short-term activated T cells (two to five rounds of stimulation) are CD95 sensitive and susceptible to activation-induced cell death (AICD), T cells stimulated more than eight times acquire constitutive CD95 resistance and exhibit reduced AICD.
- CD95 was expressed at a higher level on CD45RA+ peripheral T-cells in the fetus than in the adult.
- Fas stimulation may contribute to hepatocellular carcinoma cell survival or proliferation
- induction of CD95/CD95L expression does not have a role in p53-induced apoptosis
- possible role of FAS mutations upon higher-grade transformation of FCL to DLBCL was assessed by exmining sequential biopsies; 10 polymorphisms (6 previously unreported) were observed and described.
- Radiation-induced Fas sensitization in prostate cancer cells is mediated through p53-dependent transactivation of the Fas gene, which can be blocked by androgen stimulation mainly through induction of c-jun
- Infection of primary cells with adenoviruses carrying the relevant point mutations confirmed the crucial role of putative YXX Phi and dileucine (LL) transport motifs within Ad2 10.4-14.5 for down-regulation of Fas, TRAIL-R1, TRAIL-R2, and EGFR.
- Fas polymorphism is associated with altered apoptotic capacity in lymphocyte cultures, and risk of lung cancer
- Data show that Fas ligand is expressed on cytotoxic effector and memory cells, suggesting that the Fas/FasL system is involved in the inflammatory process observed in silicosis patients.
- The Fas signal mediates transcription of IL-10 in Jurkat cells upon contact with glioma cells via a protein kinase A-independent pathway.
- Decreased expression of Fas is seen in aggressive tumors and tumors that are poorly differentiated. Deserves further investigation, which may then shed more light on immune escape mechanisms of this tumor and thus enable novel therapeutic strategies.
- Fas, DR4, and DR5 are activated in drug-sensitive cells in response to anticancer drugs depending on the cytotoxic effect of each drug
- lysosomal degradation by adenovirus E3 RIDalpha protein dependent on specific domains
- CD95/Fas binds to the expanded binding surface of the FADD death domain
- there is no significant contribution of common genetic Fas variants to the genetic risk of developing Hashimoto's thyroiditis or Graves' disease.
- Fas-mediated apoptosis is regulated by calmodulin
- Lower gene expression of CD95 correlates with detectable blood-brain barrier leakage and active inflammation in the brain as reflected by gadolinium-enhancing lesions on MRI.
- Fas activation plays a role in NFkappaB inhibition-induced apoptosis in human tumor cells
- Fas and Fas ligand expression are regulated in leukocytes during systemic inflammation
- In this study, we show that c-FLIP(L) but not c-FLIP(S) physically binds to Daxx through interaction between C-terminal domain of c-FLIP(L) and Fas-binding domain of Daxx, an alternative Fas signaling adaptor.
- changes in peripheral lymphocyte subsets, and Fas expression in these subsets, during the menstrual cycle
- death-inducing capacity of CD95 in Jurkat T cells
- Apoptosis is related to upregulation of apo-1 receptor.
- FAS expression was induced by interferon-alpha in basal carcinoma cells.
- expression of CD95 in 15/17 human melanoma cell lines analysed, but complete lack of CD95 ligand (CD95L)
- the importance of the ezrin-to-CD95 linkage in CD95-mediated apoptosis
- Fas is activated in vivo in human epidermis after UVB exposure
- No role in the CD95L/CD95 pathway for arsennic trioxide-induced apoptosis.
- Fas/CD95 pathway is activated by Ad-p53 in human gliomas
- O(6)MeG-triggered apoptosis in proliferating lymphocytes was preceded by a wave of double stranded breaks, which coincided with p53 and Fas receptor upregulation
- This review considers the role of the Fas-FasL system as a double-edged sword in the central nervous system: maintaining the immune suppressed status in normal brain and inducing neuronal cell death and inflammation in a variety of neurologic disorders.
- no evidence for an association between the Fas promoter polymorphism at position -670 and Alzheimer's disease
- TCR restimulation of activated CD4(+) T cells resulted in Fas translocation into lipid raft microdomains before binding FasL, rendering these cells sensitive to apoptosis
- Fas signaling may have a role in the regulation of endothelial function and blood pressure through modulating endothelial nitric oxide synthase expression in the Akt signal-dependent manner.
- Fas and FasL have roles in progression of breast cancer
- not a molecular prognostic factor in NSCLC
- FAS-G670A gene polymorphism is associated with the severity of villous atrophy in coeliac disease
- apoptotic effect of Herpesvirus saimiri Tip protein in T cells is mediated by Fas and requires the presence of active Lck in the cell
- Fas was expressed in sperm of infertile men.
- epidermal growth factor receptor and CD95 activation are triggered by Src family kinase Yes
- To evaluate the impact of genetic variations to apoptosis during progression of acquired immunodeficiency syndrome (AIDS), we have performed an extensive genetic analysis of Fas and Fas ligand ( FasL) genes.
- tumour-induced mesothelial apoptosis may, in part, be mediated via a Fas-dependent mechanism.
- elevated values of PBMCs apoptosis and Fas both before and 6-7 months after malignant melanonma excision
- the selective down-regulation of c-FLIP by small interfering RNA oligoribonucleotides was sufficient to sensitize Hodgkin/Reed-Sternberg cells to CD95 and tumor necrosis factor-related apoptosis-inducing ligand-induced apoptosis
- Significantly higher soluble form of fas is associated with bile duct carcinoma
- results suggest that Fas antigen stimulation not only activates caspase-8, but also a distinct signaling pathway involving protein kinase(s) to induce exposure of the N terminus of Bak protein
- REVIEW: Inherited defects in receptor-mediated lymphocyte apoptosis represent a risk factor for lymphomas and somatic mutations of these genes may also play a role in the development and/or progression of lymphomas
- thymidylate synthase and p53 have roles in regulating Fas-mediated apoptosis in response to antimetabolites
- The frequent expression and coexpression of Fas, FasL, and c-FLIP in urothelial carcinomas implicates c-FLIP as an inhibitor of the Fas-FasL-induced death pathway in these tumors.
- Assessment of Bcl-2 and Fas expression at diagnosis in acute leukemia (1) could predict responsiveness to induction chemotherapy in ALL but not in AML
- CD95 death-inducing signaling complex formation and internalization in type I and type II cells occur in lipid rafts, which are a major site of caspase-8 activation
- regulation of transcription by cyclin B1/Cdk1
- ceramide generation and clustering of CD95 in lipid rafts early in neutrophil apoptosis
- A20 also protects from Fas/CD95 and significantly blunts natural killer cell-mediated endothelial cell apoptosis by inhibiting caspase 8 activation
- Cardiomyocyte necrosis and/or apoptosis via activated tumor necrosis factor (TNF) and the Fas/Fas ligand (FasL) system may be related to the development of ongoing myocardial damage.
- Fas/CD95-induced cell death in Jurkat cells is augmented by exposure to CO via inhibition in the activation of ERK MAPK
- autoimmune biliary disease may be mediated by the Fas/FasL apoptotic system
- Study results do not support hypothesis that AA genotype in FAS gene promoter is engaged in the development of cervical neoplasia.
- the inhibitory protein c-FLIP(L) is involved in resistance to CD95-mediated apoptosis in ovarian carcinoma cells with wild-type p53
- SNARK is an NF-kappaB-regulated anti-apoptotic gene that contributes to the tumor-promoting activity of CD95 in apoptosis-resistant tumor cells
- deoxycholate induces apoptosis in colon cancer cell lines via a CD95 receptor-independent mechanism.
- tumor cell lines expressed cell surface IFN-gamma receptors, and when cultured for 2 days in the presence of IFNG, all exhibited a significant increase in expression of Fas receptors and exhibited intracellular fragmented DNA as a marker of apoptosis
- data demonstrating that in certain highly CD95 apoptosis sensitive cells NF-kappaB is robustly activated
- CD95, DR4 and DR5 localization in rafts have roles in the toxicity of resveratrol and death receptor ligands in colon carcinoma cells
- A lymphoproliferative disorder could be associated with a CD95 mutation.
- A significant increase in p21, p53, and fas mRNA expression were reported in the proximal incompetent veins. Fas overexpression did not correlate with p53 expression level and did not correlate with apoptotic cell number in the vein layers.
- high level expression in Hepacivirus infected hepatocytes and inversely correlated to number of apoptotis cells.
- Although ischemic liver injury was not serious, due to the short ischemia time, TNFR1 and TRAIL are associated with liver ischemic injury in live-donor liver transplantation but Fas is not.
- CD95 requires different signalling thresholds for induction of apoptosis and activation of NF-kappaB
- activation of p38 MAPK and c-Jun N-terminal kinase pathways by hepatitis B virus X protein mediates apoptosis via induction of Fas/FasL and TNFR1/TNFa expression
- Repression of FAS mRNA expression is the consequence of feedback inhibition of FAS expression by long chain fatty acyl-CoAs, which are formed by FACL3 during its upregulation by vitamin D3 in prostate cancer cells.
- association among Gal-1, Fas/Fas ligand-mediated cell death, and the mitochondrial pathway
- Cells expressing Fas mutations from patients with the autoimmune lymphoproliferative syndrome reveals that formation of signaling protein oligomeric transduction structures can be disrupted by distinct mechanisms
- analysis of Fas-mediated apoptosis in human thyroid epithelial cells
- Ability of Hsp72 to inhibit Fas-mediated apoptosis is limited to type II cells where involvement of the intrinsic pathway is required for efficient effector caspase activation.
- Fas-670 polymorphism is not associated with inflammatory bowel disease in Chinese patients.
- H2O2 induces apoptosis of L02 cells by increasing cytosolic (Ca2+)i, and inducing Fas mRNA and protein expression.
- Fas is expressed in ovarian neoplasms, and FasL is upregulated in malignant ovarian neoplasms
- TNF receptor-associated factor 2 (TRAF2) overexpression does not only block apoptosis induction by CD95 antigen but also converts this death receptor into a mediator of invasiveness in pancreatic adenocarcinoma
- decreased cell-surface expression of Fas and resistance to Fas-mediated apoptosis may occur independently of loss of wt p53 expression in esophageal adenocarcinoma
- loss of Fas plays an important role in the tumor formation and in the evasion of tumor cells from immune surveillance
- Carriage of the TNFRSF6-670 polymorphism in the neonate was not associated with pre-eclampsia or intrauterine growth restriction.
- The fas Receptor Expression was evaluated by flow cytometry.
- Cytochrome c acts as a catalyst of phosphatidylserine oxidation during Fas-triggered A549 cell apoptosis
- The A(-670)G polymorphisms in the promoter region of Fas and high levels of sFas are associated with the presence of anti-ganglioside antibodies in Guillain-Barre syndrome.
- increased CD95 expression on CD3+ cells and the increased levels of sCD95 in plasma may modify the immunological situation of the recipients after liver transplantation
- The extracellular domains of Fas are sufficient to drive membrane FasL-induced formation of supramolecular Fas-FasL complexes, whereas soluble FasL-induced Fas aggregation is dependent on lipid rafts and the intracellular domain of Fas.
- Not an effective markers of silent myocardial ischemia in type 2 diabetes.
- Fas is effective in preventing human CD8(+) cytotoxic T lymphocyte-mediated cell killing, which may prevent xenograft rejection.
- Fas, Fas ligand (FasL) on activated T lymphocytes induces activation-induced cell death
- The data suggest that lower expression of surface Fas, but higher levels of apoptosis-inhibiting sFas, contribute to the resistance of fibroblasts in lung fibrosis against apoptosis.
- CD95 capping and the subsequent cellular polarization is a ROCK signaling-regulated process that does not correlate with the induction of apoptosis
- results show that IFN-induced up-regulation of Fas sensitizes MM cells to Fas-mediated apoptosis and suggest that attenuation of Stat3 activation may be a potentially important event in this process.
- expression in oral and oropharyngeal squamous cell carcinomas is associated with tumor stage and grade
- cMet/Fas interaction may inhibit self-association of Fas receptor such that reduced DISC formation occurs in these cells after Fas receptor ligation. cMet/Fas interaction may help explain why endothelial cells are resistant to Fas-mediated apoptosis.
- CD47 associates with Fas upon its activation and augments Fas-mediated apoptosis.
- Polymorphisms of the gene encoding Fas have been linked to a variety of autoimmune diseases. Fas gene polymorphisms might be genetic markers for AIH and PBC.
- FAS polymorphisms contribute to susceptibility of lung cancer.
- Expression of P-glycoprotein does not induce resistance to caspase-8 and -3 activation or anti-Fas-induced cell apoptosis.
- Human cells transformed with Ad12 demonstrated reduced expression of cell surface Fas antigen.
- tumor necrosis factor (alpha)- and Fas-induced apoptosis is blocked by inositol hexakisphosphate in human cells
- The positive rates of Fas were not significantly different among gallbladder carcinoma, adenoma, dysplasia and chronic cholecystitis.
- NF-kappaB may regulate Fas-mediated apoptosis in HIVAN by controlling the expression of Fas ligand in renal epithelium
- Data strongly indicate that an increment of soluble FAS/soluble FASL ratio after treatment could be an excellent marker of chemosensitivity in colorectal cancer.
- We also showed that, in contrast to the stimulation of Fas by an agonistic antibody, Fas aggregation did not occur after irradiation.
- serum sAPO-1 appears to have an important relationship to serum lipid levels and body adiposity in healthy adults
- Plasma levels may be a marker for chronic hepatitis C infections.
- Decreased expression of Fas is associated with disease progression in urothelial cancers
- Defective Fas expression exacerbates neurotoxicity in a model of Parkinson's disease.
- Altogether, these findings reveal that NO inhibits YY1 DNA-binding activity through S-nitrosation and consequently results in upregulation of Fas expression and tumor cell sensitization to Fas-induced apoptosis.
- Our data indicate an association between preterm premature rupture of membranes and increased prevalence of neonatal AG genotype at -670 Fas promoter gene.
- The combination of some polymorphisms of Fas or FasL significantly influenced CD4+ T cell production and viral load decrease, showing that these genes can play a role in the immunoreconstitution triggered by antiretroviral therapy.
- Functional promoter haplotypes of FAS are associated with the phenotype of SLE characterized by thrombocytopenia.
- p75(NTR) and Fas receptors could share common signalling pathways.
- The lipolytic pathway responsible for the generation of free fatty acids (FFA) during Fas/CD95-induced apoptosis in Jurkat cells, was characterized.
- An association between -670A > G polymorphism in promoter of FAS protein and the grade of necrosis in periportal areas in patients with chronic hepatitis C
- Colon cancer cells can escape the immune surveillance and killing via decreasing Fas expression, and can counterattack the immune system via increasing FasL expression
- overexpression of c-FLIP protects ALK+ ALCL cells from FAS-induced apoptosis and may contribute to ALCL pathogenesis.
- Based on the FAP-1- and dynamin-dependent regulation of Fas translocation, we have created human melanoma lines with different levels of surface expression of Fas.
- Increased concentrations of soluble Fas in sera is associated with B-cell chronic lymphocytic leukemia
- thymosin beta-4 increases colon carcinoma apoptosis resistance triggered by FasL and apoptosis inhibitors by downregulating Fas and upregulating Survivin expression
- CD95-death-induces a signaling complex formation resulting in a robust sensitization for CD95-mediated apoptosis in autoimmune lipodystrophy.
- Coligation of Fas with CD55 or CD59 inhibits the apoptotic signal, whereas CD28 recruitment amplifies the Fas signaling pathway.
- c-FLIP confers Tax-mediated resistance toward CD95-mediated apoptosis.
- Tax inhibits Fas-mediated apoptosis by up-regulating c-FLIP expression in HTLV-I-infected cells, and NF-kappaB activity plays an essential role in the up-regulation of c-FLIP
- UV light induces a redistribution of Fas-receptor in lipid rafts
- This work suggests for the first time a possible harmful effect of Fas -670 AA genotype on liver graft survival, whereas the Fas and FasL polymorphisms are not associated with acute or chronic rejection in liver graft recipients.
- Novel autocrine regulatory loop whereby activated chondrocytes may amplify CD95 signals by inducing synthesis of CD95 ligand.
- Inhibition of Flip by antisense oligonucleotide reverted the resistance of CD LPLs to FAS-induced apoptosis.
- Fas downregulation and a consequential increased resistance to FasL-triggered apoptosis resulting from upregulated MMP-7 in colorectal cancer cells could be a key mechanism for their escape from the immune surveillance
- A single A>G nucleotide substitution at position -670 in the maternal but not neonatal TNFRSF6 gene coding for Fas is associated with a higher risk for hemolysis, elevated liver enzymes, low platelets (HELLP) syndrome.
- Germ-line polymorphism of Fas gene promoter -670 may be associated with the risk of cervical cancer in a Japanese population.
- The alteration of the up-regulated Fas expression might be characterized during the tumor progression stage.
- Study concludes that polymorphisms of FASL and FAS associate with type II diabetes and estimates of insulin resistance in Danish white subjects.
- IFN-gamma primes VSMCs to Fas-induced apoptosis, in part by relocation of Fas to the cell surface, a process that involves PI3K, Akt, and Jak-2/Stat1
- Cyclosporin A (CyA) and bongkrekic acid (BK) prevented Fas-induced apoptosis in two type I cell lines (H9 and SKW6.4) and two type II cell lines (Jurkat and CEM).
- Fas ligation suppresses CD3/CD28-initiated NF-kappaB activity by decreasing the levels of the NF-kappaB p65 subunit through a caspase-dependent mechanism.
- Increased Fas expression results in a higher susceptibility to Fas-mediated apoptosis, which contributes to increased levels of intracellular activated caspase-3 and accelerates apoptosis of T lymphocytes in patients with systemic lupus erythematosus.
- Results suggest that P. aeruginosa type III secretion system not only accounts for higher expression of Fas and release of FasL but also leads to overproduction of NO and to a NO/iNOS-dependent up-regulation of Fas-FasL proteins.
- caspase-2 is activated at the DISC but does not play an initiating role in the CD95-induced apoptosis.
- Genetic evidence is provided for the two-pathway model of CD95-mediated apoptosis, pathways which differ in efficiency of death-inducing signaling complex formation and requirement of mitochondria for caspase activation.
- The lower Fas expression in activated CD4+ CCR5+ T cells might contribute to disease pathogenesis by prolonging cell survival and favoring their migration into the CNS
- Postmenopausal women with elevated levels in Fas antigen showdifferent leukocyte and hemoglobin levels.
- We conclude that hypoxia triggers a p53-dependent gene expression pattern distinct from that induced by other stress agents and that Fas/CD95 is a critical regulator of p53-dependent apoptosis upon hypoxia.
- no age-dependent changes in the Fas/Fas ligand system could be detected in human islets
- The ability of MHC class II to modulate activation of the pro-apoptotic receptor Fas by blocking the accessory molecule FADD and to delay apoptosis induction could allow for cytokine secretion by H pylori-infected gastric epithelial cells.
- sFas, sFas-L, and MMP-3, which were significantly elevated in sera of active untreated adult-onset Still's disease patients and paralleled disease activity, may be involved in the pathogenesis of this disease
- Fas and FasL serum concentrations in patients coinfected with HIV and HCV indicate programmed cell death.
- Alkyl resorcinol exerts its cytotoxic effect in both hepatocellular cell lines through apoptotic cell death. For Hep3B, cells with mutated p53 and Fas, apoptosis would proceed by p53- or Fas-independent pathways.
- in human lens epithelial cells, Fas is induced by 4-hydroxynonenal in a concentration- and time-dependent manner; results show an important role of 4-HNE in regulation of the expression and functions of Fas
- These results suggest that the FAS-1377G>A and -670A>G and FASL-844C>T polymorphisms do not significantly affect the susceptibility to lung cancer in Koreans.
- sFas concentrations are increased and sFasL are decreased in subjects at high cardiovascular risk, suggesting that these proteins may be novel markers of vascular injury.
- The mean sFas values were found higher in rheumatoid arthritis (RA), polymyositis/dermatomyositis (PM/DM) and osteoarthritis (OA) than in control although no differences were found in systemic sclerosis (SSc) and Sjogren's syndrome (SS) patients.
- The main pathway by which Fas signaling regulates the levels of Bim expression in human T-cell blasts is the death-domain- and caspase-independent generation of discrete levels of H2O2, which results in the net increase of Foxo3a levels.
- We show that Fas-mediated apoptosis requires endoplasmic reticulum-mediated calcium release in a mechanism dependent on phospholipase C-gamma1 (PLC-gamma1) activation and Ca2+ release from inositol 1,4,5-trisphosphate receptor (IP3R) channels.
- FAST K synergizes with TIA-1/TIAR proteins to regulate Fas alternative splicing
- CD95 palmitoylation facilitates formation of SDS-stable receptor aggregates that initiate apoptosis signaling
- Fas cell death signaling requires palmitoylation
- CD95 alters NOSI expression to contribute to diabetic gastroparesis.
- Our results suggest that growth factor may contribute to the resistance of cancer cells to Fas-mediated apoptosis in an autocrine or paracrine fashion.
- These findings indicate that functional polymorphisms in FAS and FASL contribute to increased apoptosis of tumor infiltration lymphocytes and risk of breast cancer.
- lymphocyte expression of CD95 is influenced by acute exercise in healthy children and adolescents
- Results suggest that EGFR-catalyzed CD95-tyrosine phosphorylation is involved in the CD95/CD95-oligomerization process, which is induced by proapoptotic stimuli and is required for apoptosis induction.
- Soluble Fas concentrations in the umbilical cord were significantly lower than in maternal serum.
- These results demonstrate that NBS1 suppresses the CD95 death receptor-dependent apoptotic pathway after gamma-irradiation and evidence is given that this is achieved by regulation of the PI3-K/AKT survival pathway.
- induction of the short c-FLIP isoforms inhibits the onset of CD95-induced apoptosis in primary CD40-stimulated ALL cells despite high CD95 expression.
- We have tested two SNPs in the FAS gene in 223 Italian patients with non-familial AD from Southern Italy. No significant differences in allelic and genotypic distributions were found between cases and controls.
- Mechanisms other than the Fas-Fas ligand pathway may induce T cell apoptosis in MDS
- analysis of 5' region mutations of the FAS/CD95 gene in nodal diffuse large B-cell lymphoma
- polymorphism of the Fas gene at position -670 does not influence susceptibility to type 1 autoimmune hepatitis, but may affect the early development of cirrhosis
- results demonstrated that FAS promoter polymorphism was significantly associated with the level of soluble FAS production in normal subjects
- Patients with active and inactive juvenile-onset systemic lupus erythematosis have a different profile of Fas and Bcl-2 expression.
- The results suggest that both N-glycosylation sites of the extracellular domain of Fas are occupied with large N-glycans that play a role in the expression of the glycoprotein.
- Germ-line functional polymorphisms affecting either the levels of expression or the biological activity of both Fas and FasL genes could be contributing to the genetic risk to develop T-cell lymphoblastic lymphomas
- The frequent expression and coexpression of Fas, FasL and c-FLIP in colorectal carcinoma implicates c-FLIP as an inhibitor of the Fas-FasL-induced death pathway in these tumours.
- FAS A-670G was not associated with the risk of developing esophageal cancer
- The serum levels of soluble FAS were studied in patients with multiple organ failure with complicating peritonitis.
- The SPF45 regulates alternative splicing of the apoptosis regulatory gene CD95; 2.1-A crystal structure of SPF45-UHM in complex with a ULM peptide from SF3b155 is reported.
- Fas was significantly more frequently overexpressed in thyroid cancer, indicating its role in thyroid tumorigenesis.
- Fas/FasL gene polymorphysms are possible that different mechanisms function in apoptosis balance in papillary thyroid cancer development
- Fas receptor and Apaf-1 were down-regulated in stage III colorectal cancer cell line.
- Bcl-X(L) conferred complete resistance to apoptosis induced by fas ligation in atherosclerotic carotid artery.
- The purpose of this study was to examine the association between 4 Fas single nucleotide polymorphisms and risk of differentiated thyroid carcinoma and salivary gland carcinoma.
- FAS polymorphism is associated with prostate cancer development
- Fas-bearing cancer cells undergo apoptosis by FasL produced by disc cells, which may be considered as a potential biochemical explanation for the disc's resistance to metastatic cancer.
- and CAPE sensitize astrocytoma cells to Fas-induced apoptosis in a redox-dependent manner
- Serum level of FAS was determined during chemotherapy of lung neoplasms.
- Fas antagonism by Met is abrogated in human fatty liver disease.
- There was no relationship between Fas-1377 G-->A polymorphism and lung cancer
- the cytotoxic granules-dependent cell death in ALPS may compensate for Fas deficiency in T lymphocytes. Furthermore, a novel AICD pathway is identified as a unique alternative to Fas apoptosis in human peripheral T lymphocytes.
- The FAS-1377, FAS-670, and FASL-844 polymorphisms were not found to be markers of melanoma risk.
- A higher expression of apoptotic molecules (Fas and FasL) on lymphocytes occurs before the onset of acute ischaemia and contributes to the plaque rupture and acute coronary syndrome.
- stimulation of the beta integrin signal of T cells by contact with tumor cells may trigger a novel protective signaling through the Phosphatidylinositol 3-kinase/Akt pathway of T cells against Fas-mediated apoptosis
- Disruption of actin by cytochalasin D (cytD) or lantrunculin A remarkably reduced CD95/Fas-induced apoptosis of HIV-specific CD8+ T cells while their spontaneous apoptosis was unaffected.
- Recombinant fourth FAS1 domain of BigH3 has been crystallized and characterized.
- This study aimed to explore, whether polymorphisms in BCL2, Cyclin D1, FAS, EGF and EGFR genes affect survival in a cohort of patients with squamous cell esophageal cancer treated with CT+RT with a view to identify the potential therapeutic targets.
- Allografted cells undergo Fas-mediated apoptosis induced by CD8+ T cells. Our objective was to prevent human keratinocytes from immunologically induced apoptosis by blocking the Fas ligand/Fas interaction.
- reconstitution of ATM kinase activity decreases FLIP protein levels and restores Fas sensitivity in Hodgkin lymphoma-derived cells
- no significant associations found between Fas or FasL promoter polymorphism with hepatitis B virus clearance & HBeAg clearance; -1377G>A in Fas promoter region showed protective effect to hepatocellular carcinoma occurrence
- Paeoniflorin inhibits A549 cell proliferation via Fas/FasL apoptosic pathway.
- risk of breast cancer may be elevated among women with polymorphisms in the FAS gene and detectable PAH-DNA adducts.
- The a functional Fas promoter polymorphism is significantly associated to susceptibility, clinical manifestation, and survival in ATL.
- The increase in Fas and CTLA4 molecules in multiple sclerosis patients may lead to lymphocyte apoptosis, which suggests possible mechanisms underlying the therapeutic response to IFN-beta.
- Resistance to Ara-c up-regulates FAS activity.
- CK2 regulates endometrial carcinoma cell sensitivity to TRAIL and Fas by regulating FLIP levels.
- display reduced capacity for Fas-mediated death-inducing signaling complex formation
- TNF-alpha sensitizes primarily resistant endometrial stromal cells to Fas-mediated apoptosis.
- CD95L-induced endosomal acidification, ceramide formation, and downstream events, such as p47(phox) phosphorylation, ROS formation, CD95 activation, and apoptosis.
- Semaphorin3A (Sema3A) triggers a proapoptotic program that sensitizes leukemic T cells to Fas (CD95)-mediated apoptosis.
- lower level of soluble Fas may provide proper microenvironment for increased apoptosis of trabecular meshwork cells in primary open angle glaucoma
- FAS -1377 G-->A polymorphism may be associated with an increased risk of lymph node metastasis in Korean cervical cancer patients.
- Soluble Fas and soluble Fas ligand are increased in the joints of patients with rheumatoid arthritis and osteoarthritis.
- Therefore, CHX treatment is granting the CD95-mediated pathway the ability to bypass the mitochondria requirement to apoptosis, much alike to what is observed in Type I cells.
- Association between the Fas exon 3 A>G polymorphism and osteosarcoma risk.
- In thyroid glands of patients with Graves disease the regulation of Fas/Fas ligand/Bcl-2 favors apoptosis of infiltrating lymphocytes.
- fluctuations in CSF sHLA-G and sFas levels observed when MRI disease activity resolved suggest that sHLA-G could play an immunomodulatory role in multiple sclerosis through Fas/FasL-mediated mechanisms
- in HCV and HIV infections, the concentration of sFas, but not sFasL, in serum correlates with the concentration of ssDNA in liver tissue
- The role of alpha(v)beta(3) and Fas as the mediators of streptococcal pyrogenic exotoxin (SPE) B-induced apoptosis is described.
- This study identifies mitogen-activated protein kinase/ERK/Mcl-1 as an important survival signaling pathway in the resistance of melanoma cells to Fas-mediated apoptosis.
- Study indicated that c-FLIP(L) might be a suppressor of Fas-mediated apoptosis in Fas antigen expressing colon carcinoma cells.
- Fas is upregulated in cells deficient for SBDS protein. Inhibition of SBDS results in accelerated apoptosis through the Fas pathway.
- In transgenic mice with mutations in the Fas/FasL pathways, impaired function of memory CD8+ T cells increases their susceptibility to recurrent/latent infections.
- data suggest that there is a different regulation and function of the Fas/FasL system in early human pregnancies. Aberration of the Fas-mediated apoptosis may represent one of the execution-step necessary for pregnancy loss in missed miscarriage cases.
- Our findings suggest that the changes in the expression of apoptotic proteins (Fas/FasL and caspase 8) in the thyroid gland of patients with autoimmune Graves Disease and Hashimoto's thyroiditis reflect their involvemetn in the pathogenesis.
- Binding of CD95 Ligand to CD95 on glioblastoma cells recruit Yes and the p85 subunit of phosphatidylinositol 3-kinase to CD95, which signal invasion via the glycogen synthase kinase 3-beta pathway and subsequent expression of matrix metalloproteinases.
- Fas activation induces apoptosis of endometrial epithelial cells (EEC) via p38 MAPK and JNK, thereby promoting trophoblast outgrowth on EEC.
- FAS and FASL genotypes of the hosts are important determinants in the pathogenesis of gastric atrophy and intestinal metaplasia in H. pylori-infected individuals.
- These results indicate that T. gondii inhibits Fas/CD95-mediated apoptosis in type II cells primarily by decreasing the apoptogenic function of mitochondria.
- placental FasL expression was significantly lower in abnormal pregnancies than in normal ones. However, no such difference was observed for Fas expression.
- These results show that the Fas/FasL-system mediated by caspase-3 activation plays a role in Clonorchis sinensis-infected hepatocyte apoptosis.
- Soluble Fas could play a role in germ cell apoptosis in varicocele-associated infertility.
- high IL-7 levels associated with lymphopenic conditions may simultaneously induce sensitivity to Fas-mediated apoptosis in nonactivated T cells and increase Fas-induced costimulatory signals in T cells recognizing low-affinity antigens.
- a functional link between HuR as repressor of alternative Fas splicing and the molecular mechanisms modulating programmed cell death.
- Gastrin and somatostatin play important roles in the regulation and control of cell apoptosis in large intestinal carcinoma, and the mechanism may be directly related to the aberrant expression of Fas and Fas ligand.
- Our results suggest a systemic nature of uveitis with persistent activation of the immune system. Apoptosis may play regulatory role in ocular inflammation of patients with uveitis.
- In Graves' disease patients, the intensity of Fas expression on CD4 and CD8 lymphocytes was reduced and sFas levels in serum were simultaneously increased when compared with Hashimoto's thyroiditis patients and controls.
- there is a functional link among apoptosis induction, U2AF65 cleavage, and the regulation of Fas alternative splicing
- a specific domain in Fas, topologically and functionally distinct from the death domain, which regulates neuritogenesis via recruitment of ezrin and activation of Rac1
- a homogeneous subset of CD27-,IgD-,CD95+ memory B cells with an activated phenotype was identified in lupus patients.
- genetic variants in the FAS gene may affect the risk of vitiligo in Chinese populations
- very high expression of CD40 on BCP-ALL blasts is an independent prognostic marker indicative of superior relapse-free survival that may in part be due to CD40-dependent death receptor up-regulation
- Up-regulation of Fas expression in CD8+ T cells is related to increased apoptosis of circulating CD8+ T cells in patients with gastric cancer.
- suggest that antineuronal antibodies may contribute to neuronal dysfunction observed in patients with neurogenic chronic intestinal pseudo-obstruction via autoantibody-mediated activation of autophagy involving the Fas receptor complex.
- Promoter genetic variants may be related to sarcoidosis disease risk in African-Americans.
- In chronic kidney disease patients, the decrease in renal function is followed by a decrease in sFas (serum FAS Protein) clearance and an increase in serum sFas; sFAS is increased in patients
- lack of Fas in primary breast cancer is associated with perilymphatic fat infiltration
- CD95 stimulation results in the formation of a novel death effector domain protein-containing complex
- To test whether polymorphisms in IL-1, NF-KB, FAS, and FASL genes are associated with risk of silicosis
- This review summarizes the functional relevance of FasL-Fas signaling-a quintessential death ligand/receptor system-in different neurological disease models ranging from traumatic, inflammatory and ischemic to neurodegenerative processes [review].
- there is an association of a Fas Antigen (Fas)-670 (A/G) gene polymorphism with the risk of cervical cancer in a North Indian population.
- These results reveal a cytochrome c-independent branch of FAS-induced apoptosis involving cleavage and cytoplasmic release of mitochondrial Cyt b
- Bbrief cross-linking (15 min) of Fas/APO-1 on Jurkat T cells or primary human T cells renders these cells appetizing to human monocyte-derived macrophages.
- Immunohistochemistry using antibodies to determine the protein expression of Fas, Fas-L, Bax, Bcl-2, p53 and c-Myc in skin of venous ulcer patients.
- HGF and EGF can interfere with CD95-mediated apoptosis and the action of cytotoxic T-cells through multiple mechanisms in human hepatocytes
- In contrast with classical mechanisms of splicing regulation, RBM5 does not affect early events of splice site recognition that lead to Fas exon 6 definition.
- leptin at a physiological serum concentration, may regulate the remodeling of the human endometrial epithelium by stimulating cell proliferation and enhancing the Fas-specific intracellular apoptotic signaling pathway.
- analysis of the expression of fatty acid synthase, Ki-67 and p53 in squamous cell carcinomas of the larynx
- Cytomegalovirus (CMV) infection development and mRNA fas transcription levels (CD95) in resting (GO) and proliferating (S-phase) human lung embryo fibroblasts (HLEF-110044 line) were studied
- SBDS loss results in abnormal accumulation of Fas at the plasma membrane, where it sensitizes the cells to stimulation by Fas ligand
- In chronic HCV infection, steatosis up-regulates hepatocyte CD95/Fas and thus increases apoptosis, which facilitates inflammation and fibrosis.
- Data show that Fas activation opens clathrin-independent portals in mature T cells, which drive rapid internalization of surface proteins such as CD59 and depend upon actin-regulating Rho GTPases.
- results indicate that the apoptosis markers Fas receptor and caspase-3 might play a significant role in glaucoma neuropathy at the stage of absolute glaucoma
- Fas resistance can be caused by reduced Fas expression, which is a result of an unidentified mode of regulation
- PTEN influences Fas signaling, at least in part, by regulating PEA-15 phosphorylation and activity that, in turn, regulate the ability of Bcl-2 to suppress Fas-induced apoptosis.
- human Fas-FADD death domain complex 2.7 A crystal structure
- FAS and FASLG SNP may be associated with idiopathic azoospermia or severe oligozoospermia.
- Loss of Fas expression might play a role in tumorigenesis in some prostate cancers possibly by inhibiting apoptosis mediated by Fas.