Tumor necrosis factor decoy receptors. Medical search. Frequent questions

Decoy receptor 3 (Dcr3), also known as tumor necrosis factor receptor superfamily member 6B (TNFRSF6B), TR6 and M68, is a soluble protein of the tumor necrosis factor receptor superfamily which inhibits Fas ligand-induced apoptosis. (wikipedia.org)
TRAIL (also known as Apo2 ligand), is a trimeric protein, a TNF superfamily member, expressed as a type-II transmembrane protein and plays a physiological role in anti-tumor immune surveillance [ 1 - 6 ]. (oncotarget.com)
Product Description google Rabbit anti-Tumor necrosis factor receptor superfamily member 19 (TROY) Polyclonal Antibody (Unconjugated), suitable for IHC-Frozen. (biosensis.com)
Product Description Rabbit anti-Tumor necrosis factor receptor superfamily member 19 (TROY) Polyclonal Antibody (Unconjugated), suitable for IHC-Frozen. (biosensis.com)
Furthermore, quercetin increased the gene expressions of TNFRSF10D (Tumor necrosis factor receptor superfamily, member 10d, decoy with truncated death domain), TP53INP1 (tumor protein p53 inducible nuclear protein 1), and JUNB (jun B proto-oncogene) but decreased the gene expression of VEGFB (vascular endothelial growth factor B), CDK10 (cyclin-dependent kinase 10), and KDELC2 (KDEL [Lys-Asp-Glu-Leu] containing 2) that are associated with apoptosis pathways. (tmu.edu.tw)

Crystal structure of human RANKL complexed with its decoy receptor osteoprotegerin. (joplink.net)
and OPG (osteoprotegerin), a soluble "decoy" receptor for RANKL. (endotext.org)
Circulating osteoprotegerin (OPG), a member of the receptor activator of nuclear factor kappa-B (RANK) axis, may influence breast cancer risk via its role as the decoy receptor for both the RANK ligand (RANKL) and tumor necrosis factor-related apoptosis-inducing ligand (TRAIL). (biomedcentral.com)
TRAIL can also bind to decoy receptors (DcR1, DcR2, and osteoprotegerin receptor) that cannot induce apoptosis. (crg.eu)
5 ] Osteoblasts, bone-forming cells, also regulate osteoclast differentiation via RANKL and osteoprotegerin (OPG) expression, a decoy receptor for RANKL. (e-jbm.org)
Estrogen stimulates osteoprotegerin (OPG) which Isochlorogenic acid B in turn inhibits osteoclast differentiation by acting like a decoy receptor of RANKL therefore leading to decreased osteoclast differentiation osteoclast survival and preservation of bone.8 Inversely menopause or ovariectomy will decrease OPG and promote osteoclast differentiation survival and consequently bone resorption. (cancer8.info)
The biological activity of tissue-conditioned media was evaluated by measuring production of selected factors (IL-6, IL-8, Dickkopf-1, osteoprotegerin) by fibroblast-like synoviocytes (FLS). (bmj.com)

It acts as a decoy receptor that competes with death receptors for ligand binding. (wikipedia.org)
Tumor necrosis factor (TNF)-related apoptosis-inducing ligand (TRAIL) binds to death receptors and induces apoptosis in various cancer cell lines while sparing normal cells. (oncotarget.com)
Tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) is a potential anticancer drug that selectively induces apoptosis in a variety of cancer cells by interacting with death receptors DR4 and DR5. (crg.eu)
The apoptotic response of cells can be induced by the intrinsic and the extrinsic pathway, the former being mediated by the mitochondria and the latter activated by ligand stimulation of death receptors at the cell surface [ 1 ]. (biomedcentral.com)
T umor Necrosis Factor-α R elated A poptosis I nducing L igand (TRAIL) is a member of the Tumor Necrosis Factor (TNF) super-family of cytokines that engages the cellular apoptotic mechanism upon specific binding to death receptors (DRs) 4 and 5 on the cell surface [ 1 ]. (biomedcentral.com)
Although TRAIL and agonistic antibodies to death receptors 4 and 5 are promising candidates for cancer therapy, many tumor cells are inherently resistant or acquire resistance to TRAIL-mediated apoptosis. (biomedcentral.com)

Interstitial pH and pO2 gradients in solid tumors in vivo: high-resolution measurements reveal a lack of correlation. (ujds.in)
Single-chain antibodies (scFv) take an important role in the field, because they are less immunogenic than whole antibodies, their smaller size allows faster and deeper penetration into solid tumors, and are by definition recombinant proteins, therefore easier to produce and modify. (biomedcentral.com)

The secreted decoy receptor 3 (DcR3), a soluble protein of the tumor necrosis factor receptor (TNFR) superfamily blocks the action of TL1A. (enzolifesciences.com)
The soluble forms of membrane TNF receptors 1/2 (sTNF-R1/2) act as decoy to neutralize TNFα, and are highly abundant in cancer patients. (bmj.com)
Bone homeostasis is maintained by the interplay between the receptor activator of nuclear factor kappa-B (RANK), its soluble activation ligand (RANKL), and OPG. (biomedcentral.com)
TRAIL receptor agonists, soluble recombinant TRAIL and antibodies against DR4 and DR5 receptors, have been pursued as a promising anti-cancer strategy and showed favorable activity in pre-clinical studies [ 5 - 11 ]. (oncotarget.com)
Immunicom employs a proprietary, high-affinity, molecular capture-ligand binding matrix within the LW-02 Column to remove specific cytokine receptors, soluble TNF-Receptors 1 and 2 (sTNFR-1/2), that are shed by cancer cells into the extracellular tumor microenvironment. (immunicom.com)
2. Bulut Y, Faure E, Thomas L, Equils O, Arditi M. (2001) Cooperation of Toll-like receptor 2 and 6 for cellular activation by soluble tuberculosis factor and Borrelia burgdorferi outer surface protein A lipoprotein: role of Toll-interacting protein and IL-1 receptor signaling molecules in Toll-like receptor 2 signaling. (guidetopharmacology.org)

Binding to the decoy receptor TNFRSF6B modulates its effects. (joplink.net)

Designed tumor necrosis factor-related apoptosis-inducing ligand variants initiating apoptosis exclusively via the DR5 receptor. (crg.eu)
Tumor necrosis factor (TNF)-related apoptosis-inducing ligand (TRAIL) is a cytokine with potential therapeutic value against cancers because of its selective cytotoxicity to many transformed, but not normal, cells. (lonza.com)
Tumor necrosis element (TNF)-related apoptosis-inducing ligand (TRAIL) is a member of the TNF family that induces cancer cell death by apoptosis with some selectivity. (opioid-receptors.com)
member of the tumor necrosis factor superfamily known as TRAIL (tumor necrosis factor-related apoptosis-inducing ligand) (16). (opioid-receptors.com)
The tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) is a promising candidate for the design of bifunctional antibodies. (biomedcentral.com)

Decoy receptor 3 (DcR3) is known to block the TL1A-DR3 pathway by binding TL1A. (nih.gov)
Human decoy receptor 3 (DcR3), also called TNFRSF6B, TR6 and M68, is a member of the TNF receptor superfamily. (bio-techne.com)
Overexpression of DcR3 might be a mechanism by which certain tumors escape immune-cytotoxic attack. (bio-techne.com)

In addition to OPG, the stimulation of osteoclastic bone resorption by RANKL is opposed by activation of the gamma interferon receptor (INFR) by gamma interferon (INF) production by activated lymphocytes and by the peptide hormone, calcitonin. (endotext.org)
OPG binds RANKL as a decoy receptor, inhibiting the activation of RANK by RANKL and preventing the differentiation of bone marrow precursor (monocyte/macrophage) cells to osteoclasts - cells that are central in the process of bone resorption [ 2 ]. (biomedcentral.com)
The discovery of the receptor activator of nuclear factor κB (RANK) ligand (RANKL) pathway, a transmembrane protein belonging to the tumour necrosis factor (TNF) superfamily, and its inhibition by osteoprotogerin (OPG) has had important implications for bone physiology as well as inflammation research. (biomedcentral.com)
Osteoclasts were formed by culturing mouse bone marrow macrophage (BMM) cells with macrophage colony-stimulating factor and receptor activator of nuclear factor-κB ligand (RANKL). (e-jbm.org)
Mechanistically, the root part of IKN suppressed RANKL-induced p38 mitogen-activated protein kinase (MAPK) activation, effectively abrogating the induction of c-Fos and nuclear factor of activated T cells 1 (NFATc1) expression. (e-jbm.org)
4 ] Macrophage colony-stimulating factor (M-CSF) and receptor activator of nuclear factor-κB (NF-κB) ligand (RANKL) are key factors in osteoclastic differentiation. (e-jbm.org)
5 , 6 ] Stimulation of osteoclast precursors with RANKL recruits cytoplasmic tumor necrosis factor receptor-associated factors (TRAFs) and activates downstream signaling pathways. (e-jbm.org)
of osteocyte mechanotransduction.6 PGE2 acts synergistically with receptor activator of nuclear element κB ligand (RANKL) to stimulate osteoclast differentiation and to initiate bone remodeling.7 Bone pressure also prospects to osteocyte apoptosis which in turn induces RANKL expression from neighboring osteoblasts. (cancer8.info)
therefore these cells are considered circulating osteoclast precursors which respond to osteoclast-specific factors and differentiate Isochlorogenic acid B into true osteoclasts.16 These osteoclast-specific factors include macrophage colony-stimulating factor and RANKL as well as OPG the endogenous decoy receptor for RANKL. (cancer8.info)

This receptor has been shown to be important for B-lineage maturation and antigen-driven B-cell differentiation, and it may regulate the migration and recruitment of dentritic and T cells during inflammatory and immunological responses. (cancerindex.org)
Activation of the receptor by CD70 ANTIGEN results in the increased proliferation of CD4-POSITIVE T-LYMPHOCYTES and CD8-POSITIVE T-LYMPHOCYTES. (bvsalud.org)

In separate work, my team identified a set of secreted proteins overexpressed in the tumor microenvironment, and developed antibodies to block their cognate receptors for therapeutic gain. (gene.com)

We propose that TR4 is a "regulatory" rather than "decoy" receptor that inhibits apoptosis signaling by TRAIL through this previously uncharacterized ligand-independent mechanism. (lonza.com)
MUC16 decreases TRAIL receptor R2 (DR5) expression and inhibits pro-caspase-8 activation at the death-inducing signaling complex (DISC). (biomedcentral.com)

The Company's LW-02 Molecular Ligand-Capturetechnology, which received FDA Breakthrough designation in 2018, is designed to remove specific factors (sTNF-R1/2) shed by cancer cells that inhibit endogenous tumor necrosis factor alpha (TNF-α), a cytokine widely recognized for its tumoricidal behavior. (immunicom.com)

Receptors for TRAIL include two death domain containing receptors, death receptor 4 (DR4) and DR5, as well as two decoy receptors, DcR1 and DcR2, lacking the intracellular signaling death domain. (thermofisher.cn)
In addition to the agonistic TRAIL receptors DR4 and DR5, TRAIL can bind to related but antagonistic receptors, including TRID or TRAIL-R3 (11, 27, 32) and TRUNDD or TRAIL-R4 (10), also coined DcR1 (decoy receptor 1) and DcR2 (decoy receptor 2), respectively. (opioid-receptors.com)
Transient overexpression of DcR1 or DcR2 in TRAIL-sensitive Sav1 tumor cells prevents cell death triggering by TRAIL (10, 11), and recent evidence indicates that tumor and normal cells can acquire resistance to TRAIL-induced killing by up-regulating TRAIL antagonistic receptors (6, 8, 9, 34). (opioid-receptors.com)
Initial binding experiments suggested that TRAIL binding affinities to TRAIL agonistic and antagonistic receptors were similar (11, Laropiprant 24), but subsequent studies demonstrated that DcR1 and Laropiprant DcR2 affinities to TRAIL were lower than that of DR4 or DR5 (8). (opioid-receptors.com)

On activated T cells, TL1A functions specifically via its surface-bound receptor DR3, (a member of the death-domain containing TNF receptor family) to promote cell survival and secretion of proinflammatory cytokines. (enzolifesciences.com)
Since Cdon is upregulated in ECs treated by inflammatory cytokines, including TNF (tumor necrosis factor)-α and Il (interleukin)-1β, we then tested whether Cdon inhibition would promote endothelium integrity in acute inflammatory conditions and found that both fibrinogen and IgG extravasation were decreased in association with an increased Cdh5 (cadherin-5) expression in the brain cortex of EC-specific Cdon knockout mice administered locally with Il-1β. (oskar-bordeaux.fr)
Tissue explants were treated with proinflammatory cytokines relevant to RA pathogenesis (interleukin 1β (IL-1β), tumour necrosis factor (TNF), interferon γ, IL-15, IL-17, IL-23). (bmj.com)
Recently, adipose tissue has been shown to synthesise and release highly bioactive substances: classical adipokines (eg, leptin, adiponectin) and various proinflammatory factors such as cytokines, chemokines, growth factors and complement components. (bmj.com)

The intracellular domain of the p75 neurotrophin receptor (p75ICD) lacks catalytic activity but contains a motif similar to death domains found in the cytoplasmic regions of members of the tumor necrosis factor receptor family and their downstream targets. (embl-heidelberg.de)

An antagonist decoy receptor (designated as TRID for TRAIL receptor without an intracellular domain) that may explain the resistant phenotype of normal tissues was identified. (embl-heidelberg.de)

In contrast, cancer cells shift their metabolism toward lactate production even in the presence of oxygen [ 4 ], partly through genetic modifications that stabilize the transcription factor Hypoxia Inducible Factor (HIF) involved in the adaptation of the cells to hypoxia, under nonhypoxic conditions as well as generating an adaptive response to the hypoxic microenvironment (Figure 1 ). (hindawi.com)
Recent studies indicate that some hematopoietic growth factors, namely granulocyte macrophage colony stimulating factor (GMCSF) and granulocyte colony stimulating factor (GCSF), are abundantly released in the tumor microenvironment and play a key role in regulating tumor-nerve interactions and tumor-associated pain by activating receptors on dorsal root ganglion (DRG) neurons. (biomedcentral.com)

This study provides the first prospective data on OPG and breast cancer risk by hormone receptor subtype. (biomedcentral.com)
A tumor necrosis factor receptor subtype that has specificity for TUMOR NECROSIS FACTOR ALPHA and LYMPHOTOXIN ALPHA. (childrensmercy.org)
A tumor necrosis factor receptor subtype found in a variety of tissues and on activated LYMPHOCYTES . (nih.gov)

An antagonist decoy receptor and a death domain-containing receptor for TRAIL. (embl-heidelberg.de)
Upon activation, the IL-1 receptor antagonist (IL-1Ra)/IL-1β ratio was higher in AAT than in SM cultures. (bmj.com)

TRAIL induces apoptosis after binding to death receptor 4 (DR4 or TRAIL-R1) and/or death receptor 5 (DR5 or TRAIL-R2) [ 1 , 2 , 4 - 7 ]. (oncotarget.com)
The "decoy receptors" TRAIL-R3 (TR3) and TRAIL-R4 (TR4) were believed to negatively regulate TRAIL-induced cytotoxicity by competing for ligand binding with TRAIL-R1 (TR1) and TRAIL-R2 (TR2). (lonza.com)
Binding of the trimeric TRAIL to its receptors TRAIL-R1 and TRAIL-R2 induces caspase activation and apoptosis [ 4 ], either through the extrinsic pathway alone or recruiting the intrinsic apoptotic pathway [ 5 ]. (biomedcentral.com)

Th17 cell proliferation is promoted by tumor necrosis factor (TNF)-like ligand 1A (TL1A), which binds to death receptor 3 (DR3) expressed on Th17 cells. (nih.gov)
Our research further revealed that inhibiting IRE1 activity in cancer-surveilling dendritic cells augments anti-tumor immunity. (gene.com)
We are currently developing strategies that aim to kill cancer cells by directly disrupting their inherent stress-adaptation mechanisms or by augmenting the anti-tumor immune response. (gene.com)
Accumulating evidence shows that cancer stem cells are key drivers of tumor formation, progression, and recurrence. (hindawi.com)
However, cancer cells overcome these controls, in particular by acquiring genetic mutations leading to the activation of oncogenes (pten, myc) or loss of tumor suppressors (p53) [ 1 ]. (hindawi.com)
Typically, rapidly proliferating tumor cells have glycolytic rates up to 200 times higher than those of their normal tissue of origin, even in the presence of oxygen [ 3 ]. (hindawi.com)
In normal cells, the fate of pyruvate depends on many factors, one of which is oxygen availability. (hindawi.com)
During tumor development, stromal cells are co-opted to the tumor milieu and provide favorable conditions for the tumor. (cancerindex.org)
Hypoxia stimulates cancer cells to acquire a more malignant phenotype via activation of hypoxia-inducible factor 1 (HIF-1). (cancerindex.org)
TL1A (TNFSF15), a ligand belonging to the tumor necrosis factor (TNF) family, is expressed predominantly by endothelial cells and monocytes. (enzolifesciences.com)
Background TNFα is a cytokine produced by immune cells and by tumor cells. (bmj.com)
More recent data show that OPG is also produced in breast tumor cells, and that it can promote tumor growth and metastasis [ 5 , 6 ]. (biomedcentral.com)
ADI downregulates survivin, upregulates DR5 receptor and sensitizes cancer cells to TRAIL induced apoptosis. (oncotarget.com)
The occurrence of DR5-responsive tumor cells indicates that a DR5 receptor-specific TRAIL variant will permit tumor-selective therapies. (crg.eu)
Tumour cells in the bone marrow cavity secrete a variety of paracrine factors that stimulate bone formation. (biomedcentral.com)
7 - 9 ] Activation of these signaling pathways induces the expression of transcription factors such as c-Fos and nuclear factor of activated T cells (NFATc1), a master transcription factor for osteoclastogenesis. (e-jbm.org)
quality-of-life/clinical function, circulating CT-DNA and tumor cells, and markers of an immunologic response (including in tissue) will also be evaluated. (immunicom.com)
sTNF-Rs serve as decoys, binding to tumor necrosis factor alpha (TNF-α) before it can bind to its membrane-embedded sTNF-R receptors to trigger several cell death pathways, as well as modulate antitumor cytotoxic T-cells and macrophage activity. (immunicom.com)
More specifically, we recently identified Dhh (desert hedgehog) as a downstream effector of Klf2 (Kruppel-like factor 2) in endothelial cells (ECs). (oskar-bordeaux.fr)
Apoptosis plays a critical role in cellular homeostasis and prevents the development of tumor cells. (biomedcentral.com)
TRAIL preferentially induces apoptosis in transformed and tumor cells, but does not appear to kill normal cells although it is expressed at a significant level in most normal tissues. (thermofisher.cn)
It is constitutively expressed in most tissues and is a key mediator of tumor necrosis factor signaling in the vast majority of cells. (childrensmercy.org)
Defects can occur at any point along these pathways, leading to malignant transformation of the affected cells, tumour metastasis and resistance to anticancer drugs. (biomedcentral.com)
TRAIL has gained considerable interest in oncology since it displays specific antitumoral activity against a wide range of tumor cells (14, 41, 47) without significant side effects, at least in mice and monkeys (3, 21, 22). (opioid-receptors.com)
Toll-like receptors (TLRs) enable innate immune cells, such as macrophages, to recognize a wide variety of microbial ligands, thereby promoting inflammation. (frontiersin.org)
In addition, the presence of EVs reduced inflammatory responses in Pam 3 CSK 4 -treated endothelial cells and HEK Dual reporter cells, demonstrating that TLR2-EVs can act as decoy receptors. (frontiersin.org)
Cytokine that binds to TNFRSF6/Fas, a receptor that transduces the apoptotic signal into cells. (lu.se)
T umor Necrosis Factor-α R elated A poptosis I nducing L igand (TRAIL) and agonistic antibodies to death receptor 4 and 5 are promising candidates for cancer therapy due to their ability to induce apoptosis selectively in a variety of human cancer cells, while demonstrating little cytotoxicity in normal cells. (biomedcentral.com)
Several types of non-hematopoietic tumors secrete hematopoietic colony stimulating factors, which act on myeloid cells and tumor cells[ 7 ]. (biomedcentral.com)
2017) IL-1R8 is a checkpoint in NK cells regulating anti-tumour and anti-viral activity. (guidetopharmacology.org)
After sensitization with cytotoxic drugs, scFv62-TRAIL induced apoptosis only in K V 10.1-positive cancer cells, but not in non-tumor cells, nor in tumor cells lacking K V 10.1 expression. (biomedcentral.com)
We could design a strategy that selectively kills tumor cells based on a K V 10.1-specific antibody. (biomedcentral.com)
Dysregulation of apoptosis of tumor cells plays an important role in the pathogenesis of pancreatic cancer and their resistance to therapies [ 5 ]. (oncotarget.com)

Osteoclast differentiation and activation factor. (joplink.net)
This interacts with its cognate receptor RANK, which is expressed on osteoclast precursors and promotes osteoclast differentiation. (biomedcentral.com)
This study aimed to assess the association between plasma Growth Differentiation Factor-8 (GDF-8)/Myostatin levels and outcome of IS patients. (bvsalud.org)

Mechanistically, the CCL20/CCR6 signaling pathway upregulates HIF-1α by stimulating nuclear factor kappa B-driven transactivation of the HIF1A gene. (cancerindex.org)

The shelf life is related to many factors, storage state, buffer ingredients, storage temperature and the stability of the protein itself. (joplink.net)
This gene encodes a member of the beta chemokine receptor family, which is predicted to be a seven transmembrane protein similar to G protein-coupled receptors. (cancerindex.org)
The ligand of this receptor is macrophage inflammatory protein 3 alpha (MIP-3 alpha). (cancerindex.org)
In an HCT116 xenograft model ADI-TRAIL localized to the tumor and induced dose-dependent tumor regression, the fusion protein was superior to rhTRAIL administered at the same molar amounts. (oncotarget.com)
The activity of this protein may be modulated by binding to the decoy receptors TNFRSF10C/TRAILR3, TNFRSF10D/TRAILR4, and TNFRSF11B/OPG that cannot induce apoptosis. (thermofisher.cn)
The binding of TRAIL protein to its receptors has been shown to trigger the activation of MAPK8/JNK, caspase 8, and caspase 3. (thermofisher.cn)
TRAIL, also called Apo2L, is a cytotoxic protein that induces apoptosis of many transformed cell lines but not of normal tissues, even though its death domain-containing receptor, DR4, is expressed on both cell types. (embl-heidelberg.de)
In response to TRAIL, these receptors recruit the adaptor protein FADD (Fas-associated death domain), through death domain homophilic interactions (5), and the initiators procaspase-8 and -10, through death effector domain interactions with FADD, hence forming the macromolecular complex called DISC (death-inducing signaling complex). (opioid-receptors.com)
Especially, the potassium channel K V 10.1 (Ether-á-go-go) is attractive as target since this surface protein is virtually not detected in normal tissue outside the central nervous system, but is expressed in approximately 70% of tumors from different origins. (biomedcentral.com)

2004) Intestinal inflammation in mice deficient in Tir8, an inhibitory member of the IL-1 receptor family. (guidetopharmacology.org)
A member of the tumor necrosis factor receptor superfamily found on most T-LYMPHOCYTES. (bvsalud.org)

They represent the first line of defense against pathogens in the lower airspace and recognize microbial ligands via pattern recognition receptors ( 4 , 5 ). (frontiersin.org)

By contrast, ligand binding by TR4 is dispensable for its apoptosis inhibitory function, thereby excluding the possibility that TR4 was a "decoy" to inhibit apoptosis by binding up TRAIL. (lonza.com)

Unfortunately, even among those patients who undergo resection for pancreatic cancer and have tumor-free margins, the 5-year survival rate after resection is 10% to 25% [ 3 ]. (oncotarget.com)

PI3K is activated by growth factors resulting in, among others, the activation of Akt and mTOR. (hindawi.com)
several of these TNF receptors use caspase activation as a signalling mechanism. (embl-heidelberg.de)
Although some aspects of the signaling pathways downstream of p75 have been elucidated recently, mechanisms of receptor activation and proximal signaling events are unknown. (embl-heidelberg.de)

However, clinical success has been limited due to poor PK and development of resistance to death receptor-induced apoptosis. (oncotarget.com)
There is an intense effort invested into the search for innovative therapies that can complement classical chemotherapy, radiation and surgery to overcome the limitations derived from chemo-resistance, toxicity of non-specific drugs and incomplete elimination of tumor tissue. (biomedcentral.com)

Our contributions to elucidating the mechanisms of apoptosis led to clinical investigation of a novel class of molecules called Pro-Apoptotic Receptor Agonists, and aided in the advancement of apoptosis-promoting cancer medicines such as venclexta. (gene.com)

In the 1990's, the Human Genome Project inspired my team to discover several novel members of the TNF cytokine superfamily, most notably, Apo2L/TRAIL and its "death" and "decoy" receptors. (gene.com)

It was found to be expressed in a variety of different tissues and at high levels in many malignant tumors. (bio-techne.com)

Oral carcinogenesis is known as multifactorial process which engaged plentiful genetic events that transform normal activity of tumor suppressor genes and oncogenes. (ujds.in)

Several growth factors in addition to TGF beta reside in bone matrix and can be released upon resorption to exert their biological effects, often osteoclast stimulation. (endotext.org)

The selective removal of decoy sTNF-Rs by the LW-02 Column allows the patient's immune system to identify and aggressively attack the cancer. (immunicom.com)
Toll-like receptors (TLRs) are the major pattern recognition receptors of the innate immune system that sense a wide range of "danger" signals or pathogen-associated molecular patterns (PAMPs) ( 6 - 8 ). (frontiersin.org)
Patients with severe immune-mediated inflammatory diseases, e.g. rheumatoid arthritis, Crohn's disease or psoriasis, often respond well and relatively quickly to treatment with biologic medicines such as tumour necrosis factor (TNF) inhibitors. (bpac.org.nz)

G-/GMCSF activates the JAK family of receptor tyrosine kinases, which unfolds its activity by not only regulating enzymes and target proteins within its local milieu, but importantly also by activating the STAT family of transcription factors, which subsequently dimerize and translocate to the cell nucleus to regulate gene expression[ 13 ]. (biomedcentral.com)

Because of this event, growth factor production increases as well as increase in total of receptors on cell surface and increased intracellular signal messengers. (ujds.in)

Anatomy3

Organisms1

Diseases1

Chemicals and Drugs22

Phenomena and Processes3

Superfamily member5

Osteoprotegerin7

Death receptors6

Solid tumors2

Soluble6

Binding to the decoy receptor TNFRSF6B1

Apoptosis-induci5

DcR33

RANKL9

Antigen2

Overexpressed in the tumor microenvironment1

Inhibits2

20181

DCR24

Cytokines4

Cytoplasmic1

Intracellular domain1

Microenvironment2

Subtype3

Antagonist2

TRAIL-R13

Cells33

Differentiation3

Signaling pathway1

Protein9

Member2

Ligands1

Inhibit1

Pancreatic Cancer1

Activation3

Resistance2

Agonists1

Apo2L1

Tissues1

Suppressor1

Osteoclast1

Immune3

Proteins1

Cell surface1