Disease relevance of Tnfrsf6

• Retinal glial cell responses and Fas/FasL activation in rats with chronic ocular hypertension [1].
• Conclusions: The expression of Fas and FasL increased in the course of the liver fibrosis, and would be furthered by IL-10 [2].
• Sodium butyrate potentiates Fas-dependent apoptosis in seven out of eight colon cancer cell lines [3].
• Because the clinical toxicity of butyrate is low, its ability to enhance Fas-signal delivery in cancer cells could be of therapeutic interest [3].
• Moreover, STAT-1 is critical for the induction of Fas receptor and Fas ligand expression by ischemia/reperfusion (I/R) [4].

Psychiatry related information on Tnfrsf6

• In the present study we examined the expression of Fas and Fas-L, by Western blotting and immunohistochemistry, in the human frontal cortex and hippocampus of individuals with advanced Alzheimer's disease (AD) and age-matched controls [5].
• Fas system up-regulation and the elevated activity of caspases in the testes of ETR may be a reflection of ethanol-induced testicular injury resulting in enhanced germ cells apoptosis, which may be involved in infertility associated with alcohol abuse [6].
• We suggest that Fas/FasL expression on SC may contribute to the elimination of invading autoreactive T cells in the PNS in concert with other immune defense mechanisms [7].

High impact information on Tnfrsf6

• These chemokines, and a specific set of other pro-inflammatory genes, are also upregulated in human vascular smooth muscle cells during Fas-induced apoptosis, in part through a process that requires interleukin-1alpha activation [8].
• We demonstrate that signals initiated by regulated Fas-associated death domain protein overexpression in rat vascular smooth muscle cells in the carotid artery induce expression of monocyte-chemoattractant protein-1 and interleukin-8, and cause massive immigration of macrophages in vivo [8].
• Partial deletion of the Fas intracellular domain prevented apoptosis [9].
• Unlike normal lymphocytes, leukemic T cells incorporated ET-18-OCH(3) into rafts coaggregating with Fas and underwent apoptosis [9].
• Fas-associated death domain protein, procaspase-8, procaspase-10, c-Jun amino-terminal kinase, and Bid were recruited into rafts, linking Fas and mitochondrial signaling routes [9].

Chemical compound and disease context of Tnfrsf6

• Induction of apoptosis and Fas receptor/Fas ligand expression by ischemia/reperfusion in cardiac myocytes requires serine 727 of the STAT-1 transcription factor but not tyrosine 701 [4].
• Tumor necrosis factor alpha and interleukin 1beta up-regulate gastric mucosal Fas antigen expression in Helicobacter pylori infection [10].
• After 42 days, creatinine clearance; blood CsA level; apoptosis; inflammation and tubulointerstitial fibrosis in renal tissue; and the expression of Bax, Bcl2, Fas, FasL, and transforming growth factor (TGF)-beta protein were determined [11].
• In a previous study, we demonstrated that apoptosis in rats with adriamycin (ADR)-induced cardiomyopathy occurred through a Fas-dependent pathway [12].
• Both Kupffer cells and LPS/Kupffer cell-conditioned supernatants induced expression of Fas and Fas ligand on malignant glioma cells [13].

Biological context of Tnfrsf6

• METHODS: The effects of cAMP on taurolithocholate-3-sulfate-(TLCS)- or glycochenodesoxycholate (GCDC)-induced CD95 (Fas/APO-1) activation and apoptosis were studied in 24-hour cultured rat hepatocytes and in perfused rat liver [14].
• BACKGROUND AND AIMS: Hydrophobic bile acids induce CD95 (Fas, APO-1)-dependent hepatocyte apoptosis, which involves epidermal growth factor receptor (EGFR)-catalyzed CD95 tyrosine phosphorylation [15].
• The activation of glial cells and upregulation of Fas and FasL suggest that glial cells may contribute to Fas-mediated cell death in the neurodegeneration process of chronic ocular hypertensive retinal insult [1].
• Tumor necrosis factor (enzyme-linked immunoassay), Fas/FasL, and caspase-3 (Western), tumor necrosis factor and Fas/FasL mRNA (reverse-transcription polymerase chain reaction), and NF-kappaB DNA binding (electrophoretic mobility shift assay) were determined [16].
• Nuclear factor-kappaB mediates Kupffer cell apoptosis through transcriptional activation of Fas/FasL [16].

Anatomical context of Tnfrsf6

• Pneumocystis cell wall beta-glucans induce dendritic cell costimulatory molecule expression and inflammatory activation through a Fas-Fas ligand mechanism [17].
• Here we asked whether Fas/Fas ligand system interacts with NO using rat granulosa cell culture [18].
• We further showed that NO inhibited Fas/FasL system-induced apoptosis by suppressing activation of the caspases, pointing to a cross-talk between Fas/FasL system-induced apoptosis pathway and NO-mediated antiapoptotic pathway in ovarian follicle atresia [18].
• Suppressing Akt phosphorylation and activating Fas by safrole oxide inhibited angiogenesis and induced vascular endothelial cell apoptosis in the presence of fibroblast growth factor-2 and serum [19].
• Simultaneously, Fas protein clumped on cell membrane, instead of homogenously distributed [19].

Associations of Tnfrsf6 with chemical compounds

• We additionally determined that IL-1beta and TNF-alpha secretion by beta-glucan-stimulated DCs was partially regulated by Fas-FasL [17].
• Calcineurin/NFAT-induced up-regulation of the Fas ligand/Fas death pathway is involved in methamphetamine-induced neuronal apoptosis [20].
• Regulation of CD95 (APO-1/Fas) receptor and ligand expression by lipopolysaccharide and dexamethasone in parenchymal and nonparenchymal rat liver cells [21].
• Sodium butyrate does not increase Fas receptor cell surface expression and does not modify cell levels of Bcl-2, Bcl-xL, Bcl-xS and Bax [3].
• Apoptosis could be induced by serum deprivation to model decreased availability of survival factors, by etoposide as an example of DNA-damaging agents, by ligation of mesangial cell Fas, and by protein synthesis inhibition by cycloheximide [22].

Physical interactions of Tnfrsf6

• Fas ligand (FasL) induces apoptotic cell death when bound to Fas antigen [23].

Regulatory relationships of Tnfrsf6

• These data suggest that C5b-9 through PI3K signaling can rescue OLG from Fas-mediated apoptosis by regulating caspase-8 processing [24].
• In conclusion, we demonstrated the involvement of Fas/FasL system in inducing apoptosis through activation of a caspase-mediated cascade in rat granulosa cells, which is coupled with a decrease in inducible NO synthase expression [18].
• Over the past few years, a number of experimental evidences suggested the involvement of Fas Ligand (FasL) expressing Sertoli cells to induce apoptosis of Fas bearing germ cells [25].
• As a result, activated JNK can not only phosphorylate the transcription factor c-Jun and up-regulate Fas L expression but can also phosphorylate 14-3-3 and promote Bax translocation to mitochondria, increase the release of cytochrome c and increase caspase-3 activation [26].
• The chemokine fractalkine inhibits Fas-mediated cell death of brain microglia [27].

Other interactions of Tnfrsf6

• In the present study, we examined the possible involvement of the caspase-8 and Fas pathway in OLG apoptosis and the role of C5b-9 in this process [24].
• Expressions of Fas, Fas ligand, and TNF-alpha type 1 receptor were enhanced in fasting and I/R rats [28].
• We detected strong immunoreactivity for TNFR1 and Fas in the somatolactotrope cell line GH3 [29].
• We also show that Fas activation, a molecular event known to play a critical role in anoikis, is not suppressed by TGF-alpha [30].
• CR suppressed this age-enhanced p53 and Fas receptor mRNA expression, but expression of the other genes was not altered significantly by aging or CR [31].

Analytical, diagnostic and therapeutic context of Tnfrsf6

• Caspase activity assays and Western blot analysis showed that H9c2 cells treated with Dox for 16 h had marked increase in the levels of caspases-2, -3, -8, -9, -12, Fas, and cleaved poly(ADP ribose) polymerase (PARP) [32].
• Apoptotic lymphomonocytes (identified by TUNEL) infiltrating the brain and the spinal cord were decreased in rats treated i.c.v. with FasL-p. The data suggest that the Fas/Fas-ligand pathway may be modulated by treatments with peptides of Fas-Ligand and that it may be at work within the central nervous system in EAE [33].
• Semi-quantitative RT-PCR and Western-blot were used to analyze mRNA and protein expressions of Fas and FasL from freshly isolated HSC [2].
• The mRNA of Fas and FasL in group C were significantly increased time-dependently compared to those of control group [2].
• Tolerance induction ameliorates allograft vasculopathy in rat aortic transplants. Influence of Fas-mediated apoptosis [34].

References