fas

Mouse Apoptosis-mediating surface antigen FAS (Fas) belongs to the death receptor subfamily of the TNF receptor superfamily and is designated TNFRSF6. Mouse Fas contains 1 death domain and 3 TNFR-Cys repeats. It detected in various tissues including thymus, liver, lung, heart, and adult ovary. As a receptor for TNFSF6 FASLG, The adapter molecule FADD recruits caspase-8 to the activated receptor. The resulting death-inducing signaling complex (DISC) performs caspase-8 proteolytic activation which initiates the subsequent cascade of caspases mediating apoptosis. FAS-mediated apoptosis may have a role in the induction of peripheral tolerance, in the antigen-stimulated suicide of mature T-cells, or both.

FASN Protein, Mouse, Recombinant (His) is expressed in E. coli expression system with His tag. The predicted molecular weight is 34.23 kDa and the accession number is P19096.

FASN Protein, Human, Recombinant (His) is expressed in E. coli expression system with His tag. The predicted molecular weight is 35.26 kDa and the accession number is P49327.

Fas Ligand, also known as FASLG and CD95L, is the ligand for FAS. It is a transmembrane protein which binds to TNFRSF6 FAS. Interaction of FAS with fas Ligand is critical in triggering apoptosis of some types of cells such as lymphocytes. Fas Ligand may be involved in cytotoxic T-cell mediated apoptosis and in T-cell development. TNFRSF6 FAS-mediated apoptosis may have a role in the induction of peripheral tolerance, in the antigen-stimulated suicide of mature T-cells, or both. Fas Ligand Protein, Mouse, Recombinant (His) is expressed in yeast with His tag. The predicted molecular weight is 18.2 kDa and the accession number is AAB02915.1.

Fas CD95 Protein, Human, Recombinant (hFc) is expressed in HEK293 mammalian cells with hFc tag. The predicted molecular weight is 43.4 kDa and the accession number is P25445-1.

Fas CD95 Protein, Cynomolgus, Recombinant is expressed in HEK293 mammalian cells. The predicted molecular weight is 17.6 kDa and the accession number is F6V1W6.

Fas CD95 Protein, Mouse, Recombinant (His) is expressed in HEK293 mammalian cells with His tag. The predicted molecular weight is 18 kDa and the accession number is P25446.

Fas CD95 Protein, Human, Recombinant (His) is expressed in HEK293 mammalian cells with His tag. The predicted molecular weight is 18.2 kDa and the accession number is P25445-1.

Fas CD95 Protein, Rat, Recombinant (His) is expressed in HEK293 mammalian cells with His tag. The predicted molecular weight is 18 kDa and the accession number is A6I127.

Fas Ligand, also known as FASLG and CD95L, is the ligand for FAS. It is a transmembrane protein which binds to TNFRSF6 FAS. Interaction of FAS with fas Ligand is critical in triggering apoptosis of some types of cells such as lymphocytes. Fas Ligand may be involved in cytotoxic T-cell mediated apoptosis and in T-cell development. TNFRSF6 FAS-mediated apoptosis may have a role in the induction of peripheral tolerance, in the antigen-stimulated suicide of mature T-cells, or both. Fas Ligand Protein, Human, Recombinant (His) is expressed in yeast with His tag. The predicted molecular weight is 19.3 kDa and the accession number is P48023-1.

Fas CD95 Protein, Cynomolgus, Recombinant (hFc) is expressed in HEK293 mammalian cells with hFc tag. The predicted molecular weight is 43.8 kDa and the accession number is F6V1W6.

Fas CD95 Protein, Rat, Recombinant (hFc) is expressed in HEK293 mammalian cells with hFc tag. The predicted molecular weight is 43.7 kDa and the accession number is A6I127.

Fas Ligand, also known as FASLG and CD95L, is the ligand for FAS. It is a transmembrane protein which binds to TNFRSF6 FAS. Interaction of FAS with fas Ligand is critical in triggering apoptosis of some types of cells such as lymphocytes. Fas Ligand may be involved in cytotoxic T-cell mediated apoptosis and in T-cell development. TNFRSF6 FAS-mediated apoptosis may have a role in the induction of peripheral tolerance, in the antigen-stimulated suicide of mature T-cells, or both. Fas Ligand Protein, Rat, Recombinant (His) is expressed in yeast with His tag. The predicted molecular weight is 21.3 kDa and the accession number is A0A0U5J7X8.

DR5, also called TRAIL R2, TRICK 2, TNFRSF10B, and MK is a type 1 TNF R superfamily, membrane protein which is a receptor for TRAIL (APO2 ligand). DR5 is a receptor for the cytotoxic ligand TNFSF10 TRAIL. The resulting death-inducing signaling complex (DISC) performs caspase-8 proteolytic activation which initiates the subsequent cascade of caspases (aspartate-specific cysteine proteases) mediating apoptosis.

ENR Protein, Mycobacterium tuberculosis, Recombinant (His) is expressed in E. coli expression system with N-6xHis tag. The predicted molecular weight is 32.6 kDa and the accession number is P9WGR0.

May play a role in the immune system processes. Protects cells from FAS-, TNF alpha- and FADD-induced apoptosis without increasing expression of the inhibitors of apoptosis BCL2 and BCLXL. Seems to activate an inhibitory pathway that prevents CASP8 activation following FAS stimulation, rather than blocking apoptotic signals downstream. May inhibit FAS-induced apoptosis by preventing CASP8 processing through CFLAR up-regulation.

Caspase-10 (CASP10) is a 521 amino acid protein member of the Cysteine-Aspartic Acid Protease (Caspase) family. CASP10 contains two DED (Death Effector) domains and is detectable in most tissues. CASP10 cleavage by Granzyme B and autocatalytic activity generate the two active subunits: Caspase-10 subunit p23 17, Caspase-10 subunit p12. Caspases are a family of cytosolic aspartate-specific cysteine proteases involved in the execution-phase of cell apoptosis, the initiation and execution. Human caspases can be subdivided into three functional groups: cytokine activation (caspase-1, -4, -5, and -13), apoptosis initiation (caspase-2, -8, -9, -and -10), and apoptosis execution (caspase-3, -6, and -7). CASP10 cleaves and activates caspases 3 and 7, but itself is processed by caspase 8. Defects in CASP10 are associated with apoptosis defects seen in type II autoimmune lymphoproliferative syndrome.

DR5, also called TRAIL R2, TRICK 2, TNFRSF10B, and MK is a type 1 TNF R superfamily, membrane protein which is a receptor for TRAIL (APO2 ligand). DR5 is a receptor for the cytotoxic ligand TNFSF10 TRAIL. The adapter molecule FADD recruits caspase-8 to the activated receptor. The resulting death-inducing signaling complex (DISC) performs caspase-8 proteolytic activation which initiates the subsequent cascade of caspases (aspartate-specific cysteine proteases) mediating apoptosis.

Albumin Protein, Macaca fascicularis, Recombinant (Yeast, His) is expressed in yeast with N-6xHis tag. The predicted molecular weight is 68.0 kDa and the accession number is A2V9Z4.

OBP28 Protein, Culex quinquefasciatus, Recombinant (His) is expressed in yeast with N-6xHis tag. The predicted molecular weight is 16.1 kDa and the accession number is B0XC79.

Macaca fascicularis Cytomegalovirus (CyCMV) (strain OT-1) glycoprotein B gB Protein (hFc) is expressed in HEK293 mammalian cells with Fc tag. The predicted molecular weight is 102.5 kDa and the accession number is E7DB34.

Neurofascin Protein, Human, Recombinant (His) is expressed in HEK293 mammalian cells with His tag. The predicted molecular weight is 104.4 kDa and the accession number is O94856-12.

OBP28 Protein, Culex quinquefasciatus, Recombinant (His & Myc) is expressed in E. coli expression system with N-10xHis and C-Myc tag. The predicted molecular weight is 22 kDa and the accession number is B0XC79.

Neurofascin Protein, Human, Recombinant (hFc) is expressed in HEK293 mammalian cells with hFc tag. The predicted molecular weight is 130 kDa and the accession number is O94856-12.

Phosphoribosylformylglycinamidine synthase involved in the purines biosynthetic pathway. Catalyzes the ATP-dependent conversion of formylglycinamide ribonucleotide (FGAR) and glutamine to yield formylglycinamidine ribonucleotide (FGAM) and glutamate. PFAS Protein, Human, Recombinant (His & Myc & SUMO) is expressed in E. coli expression system with N-10xHis-SUMO and C-Myc tag. The predicted molecular weight is 45.4 kDa and the accession number is O15067.

Cytokine directly involved in hematopoiesis. Astakine Protein, Pacifastacus leniusculus, Recombinant (His & Myc) is expressed in E. coli expression system with N-10xHis and C-Myc tag. The predicted molecular weight is 16.2 kDa and the accession number is Q56R11.

Neurofascin Protein, Human, Recombinant (hFc), Biotinylated is expressed in HEK293 mammalian cells with hFc tag. The predicted molecular weight is 130 kDa and the accession number is O94856-9.

Nucleolar protein 3 is encoded by NOL3 gene. Multiple transcript variants encoding different isoforms have been found for this gene. So far, Nucleolar protein 3 has show to have two Isoforms. Isoform 1 may be involved in RNA splicing. Isoform 2 functions as an apoptosis repressor that blocks multiple modes of cell death. It inhibits extrinsic apoptotic pathways through two different ways. Firstly, it by interacting with FAS and FADD upon FAS activation blocking death-inducing signaling complex (DISC) assembly. Secondly by interacting with CASP8 in a mitochondria localization- and phosphorylation-dependent manner, limiting the amount of soluble CASP8 available for DISC-mediated activation. It has been shown to down-regulate the enzyme activities of caspase 2, caspase 8 and tumor protein p53.

Type IV collagen is the major structural component of glomerular basement membranes (GBM), forming a 'chicken-wire' meshwork together with laminins, proteoglycans and entactin nidogen.; Canstatin, a cleavage product corresponding to the collagen alpha 2(IV) NC1 domain, possesses both anti-angiogenic and anti-tumor cell activity. It inhibits proliferation and migration of endothelial cells, reduces mitochondrial membrane potential, and induces apoptosis. Specifically induces Fas-dependent apoptosis and activates procaspase-8 and -9 activity. Ligand for alphavbeta3 and alphavbeta5 integrins.

Tumor necrosis factor receptor superfamily member 27, also known as XEDAR and EDA2R, is a type III transmembrane protein of the TNFR superfamily. EDA2R consists of extracellular domain (ECD) with 3 cysteine-rich repeats and a single transmembrane domain but lacks an N-terminal signal peptide. EDA2R is widely expressed, notably in embryonic basal epidermal cells and maturing hair follicles. Even though it does not contain a cytoplasmic death domain, EDA2R can associate with Fas and induce EDA‑A2 dependent apoptosis. Its transcription is directly induced by p53, and it mediated cell death is p53 dependent. it is down‑regulated in breast, colon, and lung cancers, particularly in cases with p53 mutations. It also plays a role in EDA‑A2 induced skeletal muscle degeneration and osteoblast differentiation. Mutations in the EDA gene are associated with the X-linked form of Hypohidrotic Ectodermal Dysplasia (HED), a disease typically characterized by abnormal hair, teeth and sweat glands.

Acts as a tumor suppressor in many tumor types; induces growth arrest or apoptosis depending on the physiological circumstances and cell type. Involved in cell cycle regulation as a trans-activator that acts to negatively regulate cell division by controlling a set of genes required for this process. One of the activated genes is an inhibitor of cyclin-dependent kinases. Apoptosis induction seems to be mediated either by stimulation of BAX and FAS antigen expression, or by repression of Bcl-2 expression. Its pro-apoptotic activity is activated via its interaction with PPP1R13B ASPP1 or TP53BP2 ASPP2. However, this activity is inhibited when the interaction with PPP1R13B ASPP1 or TP53BP2 ASPP2 is displaced by PPP1R13L iASPP. In cooperation with mitochondrial PPIF is involved in activating oxidative stress-induced necrosis; the function is largely independent of transcription. Prevents CDK7 kinase activity when associated to CAK complex in response to DNA damage, thus stopping cell cycle progression. Induces the transcription of long intergenic non-coding RNA p21 (lincRNA-p21) and lincRNA-Mkln1. LincRNA-p21 participates in TP53-dependent transcriptional repression leading to apoptosis and seems to have an effect on cell-cycle regulation. Regulates the circadian clock by repressing CLOCK-ARNTL BMAL1-mediated transcriptional activation of PER2.

Enoyl-ACP reductase, also known as NADH-dependent enoyl-ACP reductase and FABI, is a cell inner membrane and peripheral membrane protein which belongs to theshort-chain dehydrogenases reductases (SDR) family and FabI subfamily. Microorganisms produce many kinds of antibiotics which function in an antagonistic capacity in nature where they have much competition. Bacterial FAS provides essential fatty acids for use in the assembly of key cellular components. Among them, FABI is an enoyl-ACP reductase which catalyzes the final and rate-limiting step of bacterial FAS. The antibiotic diazaborine interferes with the activity by binding to the protein. FABI is a potential target for selective antibacterial action, because it shows low overall sequence homology with mammalian enzymes. Various compounds have been reported as inhibitors of bacterial FabI-inhibitory compounds.

Caspase 14 is a member of the caspase family. Caspases are a kind of cysteine proteinase consisting of a prodomain plus large and small catalytic subunits, that play a central role in cell apoptosis. Caspase 14 possesses an unusually short prodomain and is highly expressed in embryonic tissues but absent from most of the adult tissues except for the skin, which suggests a role in ontogenesis and skin physiology. Unlike the other short prodomain caspases(caspase-3, caspase-6, and caspase-7), Caspase 14 was not processed by multiple death stimuli including activation of members of the tumor necrosis factor receptor family and expression of proapaptotic members of the bcl-2 family. Caspase 14 has been described to be processed and activated by anti-Fas agonist antibody or TNF-related apoptosis inducing ligand in vivo. The expression and processing of this caspase may take part in keratinocyte terminal differentiation, which is essential for the skin barrier.

Death domain-containing protein CRADD, also known as Caspase and RIP adapter with death domain, RIP-associated protein with a death domain, CRADD and RAIDD, is a protein which is constitutively expressed in most tissues, with particularly high expression in adult heart, testis, liver, skeletal muscle, fetal liver and kidney. CRADD RAIDD contains oneCARD domain and onedeath domain. CRADD RAIDD contains a death domain involved in the binding of RIP protein. The CARD domain mediates the interaction with caspase-2. FADD MORT1 is a death domain (DD)-containing adaptor signaling molecule that interacts with the intracellular DD of FAS APO-I ( CD95 ) and tumor necrosis factor receptor 1 and the prodomain of caspase-8 ( Mch5 MACH FLICE). CRADD RAIDD has a dual-domain structure similar to that of FADD. CRADD RAIDD has an NH2-terminal caspase homology domain that interacts with caspase-2 and a COOH-terminal DD that interacts with RIP. CRADD RAIDD could play a role in regulating apoptosis in mammalian cells. CRADD RAIDD is a apoptotic adaptor molecule specific for caspase-2 and FASL TNF receptor-interacting protein RIP. In the presence of RIP and TRADD, CRADD RAIDD recruits caspase-2 to the TNFR-1 signalling complex.

NCKIPSD is localized exclusively in the cell nucleus. It plays a role in signal transduction and may function in the maintenance of sarcomeres and the assembly of myofibrils into sarcomeres. NCKIPSD also plays an important role in stress fiber formation. NCKIPSD gene is involved in therapy-related leukemia by a chromosomal translocation t(3;11)(p21;q23) that involves this gene and the myeloid lymphoid leukemia gene. Alternative splicing occurs in this locus and two transcript variants encoding distinct isoforms have been identified. NCKIPSD is an SH3 domain protein. Fas ligand is a cytotoxic effector molecule of T and NK cells which is characterized by an intracellular N-terminal polyproline region that serves as a docking site for SH3 and WW domain proteins. Several previously described Fas ligand-interacting SH3 domain proteins turned out to be crucial for the regulation of storage, expression, and function of the death factor. Recent observations, however, indicate that Fas ligand is also subject to posttranslational modifications including shedding and intramembrane proteolysis.

Dickkopf-like 1 (DKKL1) or soggy 1, is a glycoprotein unique to mammals that is expressed primarily in developing spermatocytes and localized in the acrosome of mature sperm. It is also expressed in the trophectoderm placental lineage. This glycoprotein is secreted by postmeiotic male germ cells. DKKL1 is a member of the Dickkopf (DKK) family, a group of proteins that are characterized as secreted antagonists of Wnt signal transduction proteins. In mammals, embryos lacking DKKL1 protein developed into viable, fertile adults. DKKL1, either directly or indirectly, facilitates the ability of sperm to penetrate the zona pellucid. DKKL1 is related to the sperm apoptotic procession. Molecular analyses identified the Fas death ligand (FasL) as a target for DkkL1 pro-apoptotic activity in adult mice. DKKL1 is considered as a negative regulator of adult testic homeostasis and identifies a novel, DKKL1 FasL- dependent, regulation that specifically controls the number of postpubertal spermatocytes.

Interleukin 1 family member 7, or interleukin 37 (IL1F7 IL37 IL-1H4) is a secretory protein belonging to the Interleukin 1 family. IL-1F7 was localized in human peripheral monocytic cells. It has been localized the expression of IL-1F7b protein in discrete cell populations including plasma cells and tumor cells. These data suggest that IL-1F7 may be involved in immune response, inflammatory diseases, and or cancer. Through constructing an adenoviral vector that allows high-level expression in murine and human cells, it has been demonstrated that the ability of adenovirus-mediated gene transfer of IL1F7 to induce an IL-12- and Fas ligand-dependent anti-tumor response. Complete inhibition of tumor growth was observed following multiple injections of IL1F7 in most animals. These results suggest that IL1F7 could play a role in both innate and adaptive immune responses, similar to IL-18. Moreover, IL1F7 could be useful for cancer gene therapy.

SerpinB9, also known as Cytoplasmic antiproteinase 3, CAP-3, Peptidase inhibitor 9, SERPINB9 and PI-9, is a cytoplasm protein that belongs to the serpin family and Ov-serpin subfamily. Serpin-B9 ( CAP-3 PI-9 ) is the only known human intracellular inhibitor of granzyme B (GrB), the effector molecule in immunity against cytomegalovirus (CMV) and in renal allograft rejection. Serpin-B9 and SPI-6 expression in immune-privileged cells, APCs, and CTLs protect these cells against the actions of granzyme B, and when expressed in tumor cells or virally infected hepatocytes, confers resistance to killing by CTL and NK cells. Expression of increasing levels of Serpin-B9 ( CAP-3 PI-9 ) in target cells may progressively inhibit immune surveillance by blocking NK and CTL-induced cytotoxicity through the perforin granzyme pathway and then through the Fas FasL pathway. Serpin-B9 ( CAP-3 PI-9 ) is selectively up-regulated in hepatocytes in response to infiltration of the liver by NK cells that express perforin and enzymatically active granzyme B. Upregulated expression of Serpin-B9 ( CAP-3 PI-9 ) in NSCLC cells may serve to protect them from apoptosis induced by GrB.

Interleukin (IL)‑12B, which encodes the p40 subunit common to IL‑12 and IL‑23, as one of the genes for which expression in fibroblast‑like synoviocytes from patients with rheumatoid arthritis (RA‑FLS) is induced by DcR3.Decoy receptor 3 (DcR3) competitively binds to three ligands, Fas ligand, lymphotoxin‑related inducible ligand that competes for glycoprotein D binding to herpesvirus entry mediator on T cells and tumor necrosis factor‑like ligand 1A (TL1A), to prevent their effects. Recent studies have suggested that DcR3 directly affects cells as a ligand.

Acts as a tumor suppressor in many tumor types; induces growth arrest or apoptosis depending on the physiological circumstances and cell type. Involved in cell cycle regulation as a trans-activator that acts to negatively regulate cell division by controlling a set of genes required for this process. One of the activated genes is an inhibitor of cyclin-dependent kinases. Apoptosis induction seems to be mediated either by stimulation of BAX and FAS antigen expression, or by repression of Bcl-2 expression. Its pro-apoptotic activity is activated via its interaction with PPP1R13B ASPP1 or TP53BP2 ASPP2. However, this activity is inhibited when the interaction with PPP1R13B ASPP1 or TP53BP2 ASPP2 is displaced by PPP1R13L iASPP. In cooperation with mitochondrial PPIF is involved in activating oxidative stress-induced necrosis; the function is largely independent of transcription. Prevents CDK7 kinase activity when associated to CAK complex in response to DNA damage, thus stopping cell cycle progression. Induces the transcription of long intergenic non-coding RNA p21 (lincRNA-p21) and lincRNA-Mkln1. LincRNA-p21 participates in TP53-dependent transcriptional repression leading to apoptosis, but seems to have to effect on cell-cycle regulation. Regulates the circadian clock by repressing CLOCK-ARNTL BMAL1-mediated transcriptional activation of PER2.