クイック注文

CD95/APO-1/TNFRSF6  Protein, Antibody, ELISA Kit, cDNA Clone

発現宿主: Human Cells  
10217-H08H-50
10217-H08H-100
50 µg 
100 µg 
Add to Cart
  • Slide 1
発現宿主: Human Cells  
10217-H02H-50
10217-H02H-100
50 µg 
100 µg 
Add to Cart
  • Slide 1
発現宿主: Human Cells  
50027-M08H-50
50027-M08H-100
50 µg 
100 µg 
Add to Cart
  • Slide 1
発現宿主: Human Cells  
80043-R08H-50
80043-R08H-100
50 µg 
100 µg 
Add to Cart
  • Slide 1
発現宿主: Human Cells  
80043-R02H-50
80043-R02H-100
50 µg 
100 µg 
Add to Cart
  • Slide 1
発現宿主: Human Cells  
90273-C02H-50
90273-C02H-100
50 µg 
100 µg 
Add to Cart
  • Slide 1
発現宿主: Human Cells  
90273-CCCH-50
90273-CCCH-100
50 µg 
100 µg 
Add to Cart
  • Slide 1

CD95/APO-1/TNFRSF6 Related Area

CD95/APO-1/TNFRSF6 関連経路

CD95/APO-1/TNFRSF6 関連製品

CD95/APO-1/TNFRSF6 サマリー & タンパク質情報

CD95/APO-1/TNFRSF6 背景

遺伝子の概要: The CD95 protein encoded by this FAS gene is a member of the TNF-receptor superfamily. This CD95 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 CD95 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 CD95 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.
General information above from NCBI
サブユニット構造: Binds DAXX. Interacts with HIPK3. Part of a complex containing HIPK3 and FADD (By similarity). Binds RIPK1 and FAIM2. Interacts with BRE and FEM1B. Interacts with FADD. Interacts directly (via DED domain) with NOL3 (via CARD domain); inhibits death-inducing signaling complex (DISC) assembly by inhibiting the increase in FAS-FADD binding induced by FAS activation (By similarity). {ECO:0000250, ECO:0000250|UniProtKB:Q63199, ECO:0000269|PubMed:10535980, ECO:0000269|PubMed:10542291, ECO:0000269|PubMed:15465831, ECO:0000269|PubMed:19118384, ECO:0000269|PubMed:21109225, ECO:0000269|PubMed:7538908}.
ドメイン: Contains a death domain involved in the binding of FADD, and maybe to other cytosolic adapter proteins.
細胞内位置: Isoform 1: Cell membrane; Single-pass type I membrane protein.; Isoform 2: Secreted.; Isoform 3: Secreted.; Isoform 4: Secreted.; Isoform 5: Secreted.; Isoform 6: Secreted.
組織特異性: Isoform 1 and isoform 6 are expressed at equal levels in resting peripheral blood mononuclear cells. After activation there is an increase in isoform 1 and decrease in the levels of isoform 6. {ECO:0000269|PubMed:7575433}.
翻訳後: N- and O-glycosylated. O-glycosylated with core 1 or possibly core 8 glycans. {ECO:0000269|PubMed:19159218, ECO:0000269|PubMed:22171320}.
疾患関連性: DISEASE: Autoimmune lymphoproliferative syndrome 1A (ALPS1A) [MIM:601859]: A disorder of apoptosis that manifests in early childhood and results in the accumulation of autoreactive lymphocytes. It is characterized by non-malignant lymphadenopathy with hepatosplenomegaly, and autoimmune hemolytic anemia, thrombocytopenia and neutropenia. {ECO:0000269|PubMed:10090885, ECO:0000269|PubMed:10340403, ECO:0000269|PubMed:10515860, ECO:0000269|PubMed:11418480, ECO:0000269|PubMed:17336828, ECO:0000269|PubMed:7540117, ECO:0000269|PubMed:8929361, ECO:0000269|PubMed:9028321, ECO:0000269|PubMed:9028957, ECO:0000269|PubMed:9322534, ECO:0000269|PubMed:9821419, ECO:0000269|PubMed:9927496}. Note=The disease is caused by mutations affecting the gene represented in this entry.
シーケンスの類似性: Contains 1 death domain. {ECO:0000255|PROSITE-ProRule:PRU00064}.; Contains 3 TNFR-Cys repeats. {ECO:0000255|PROSITE-ProRule:PRU00206}.
General information above from UniProt

CD95 (APO-1/Fas) is an important inducer of the extrinsic apoptosis signaling pathway and therapy induced apoptosis of many tumor cells has been linked to the activity of CD95. is a prototype death receptor characterized by the presence of an 80 amino acid death domain in its cytoplasmic tail. This domain is essential for the recruitment of a number of signaling components upon activation by either agonistic anti-CD95 antibodies or cognate CD95 ligand that initiate apoptosis. The complex of proteins that forms upon triggering of CD95 is called the death-inducting signaling complex (DISC). The DISC consists of an adaptor protein and initiator caspases and is essential for induction of apoptosis. CD95 is also crucial for the negative selection of B cells within the germinal center (GC). Impairment of CD95-mediated apoptosis results in defective affinity maturation and the persistence of autoreactive B-cell clones. Changes in the expression of CD95 and/or its ligand CD95L are frequently found in human cancer. The downregulation or mutation of CD95 has been proposed as a mechanism by which cancer cells avoid destruction by the immune system through reduced apoptosis sensitivity. Thus, CD95 has therefore been viewed as a tumor suppressor. CD95 has been reported to be involved in the activation of NF-kappaB, MAPK3/ERK1, MAPK8/JNK, and the alternate pathways for CTL-mediated cytotoxicity. Accordingly, this protein is implicated in the pathogenesis of various malignancies and diseases of the immune system. The CD95/CD95L system was implicated in the etiology of inflammatory bowel disease (IBD) based, primarily, on the finding that CD95 is highly expressed in the intestinal epithelial cells and that epithelial apoptosis is increased in IBD.

CD95/APO-1/TNFRSF6 代替名

CD95/APO-1/TNFRSF6 関連研究

  • Mschen M, et al. (2002) The origin of CD95-gene mutations in B-cell lymphoma. Trends Immunol. 23(2): 75-80.
  • Peter ME, et al. (2003) The CD95(APO-1/Fas) DISC and beyond. Cell Death Differ. 10(1): 26-35.
  • Peter ME, et al. (2005) Does CD95 have tumor promoting activities Biochim Biophys Acta. 1755(1): 25-36.
  • Chen L, et al. (2010) Cell death in the colonic epithelium during inflammatory bowel diseases: CD95/Fas and beyond. Inflamm Bowel Dis. 16(6): 1071-6.
  • 注意:すべての製品は、"研究目的のみに使用するものであり、診断または治療目的に使用するものではありません"