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Validated All-in-One™ qPCR Primer for TNFSF14(NM_003807.4) Search again
Product ID:
HQP021496
(click here to view gene annotation page)
Powered by BiozSpecies:
Human
Symbol:
Alias:
CD258, HVEML, LIGHT, LTg
Gene Description:
TNF superfamily member 14
Target Gene Accession:
NM_003807.4(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 tumor necrosis factor (TNF) ligand family. This protein is a ligand for TNFRSF14, which is a member of the tumor necrosis factor receptor superfamily, and which is also known as a herpesvirus entry mediator (HVEM). This protein may function as a costimulatory factor for the activation of lymphoid cells and as a deterrent to infection by herpesvirus. This protein has been shown to stimulate the proliferation of T cells, and trigger apoptosis of various tumor cells. This protein is also reported to prevent tumor necrosis factor alpha mediated apoptosis in primary hepatocyte. Two alternatively spliced transcript variant encoding distinct isoforms have been reported. [provided by RefSeq].
Gene References into function
- Effects in transgenic mice indicate that human LIGHT may function as a major regulator of T cell activation, and implicate LIGHT signaling pathways in inflammation focused on mucosal tissues.
- LIGHT (TNFSF14),5 its membrane-anchored ligand, was also present in atheromatous lesions and highest in regions rich in macrophage-derived foam cells.
- Role of calcium-signaling pathway in the transcriptional control
- LIGHT may act as an anti-apoptotic agent against TNFalpha-mediated liver injury by blocking the activation of both caspase-3 and caspase-8.
- LIGHT, a new member of the TNF superfamily [review]
- Data show that mRNA encoding LIGHT and its receptors [HVEM, LTbetaR, and TR6 (DcR3)] are present in placentas and cytotrophoblast cells at term.
- Soluble LIGHT blocks TR6-Fc costimulated proliferation, lymphokine production, and cytotoxicity of T cells in the presence of T cell receptor ligation.
- LIGHT-sensitized IFN-gamma-mediated apoptosis of MDA-MB-231 cells is probably through down-regulation of anti-apoptosis Bcl-2 family members; it could be caspase (especially caspase-3)-independent, even though extensive caspase activation was observed.
- LIGHT signaling is mediated through both death receptor and mitochondria pathways
- LIGHT-herpesvirus entry mediator mediated signaling as an important immune regulatory mechanism in mucosal inflammatory responses.
- Mechanisms protecting trophoblast cells from LIGHT-mediated apoptosis were studied.
- LIGHT expression by human intestinal T cells suggests the possibility that LIGHT may play a key role in regulation of the mucosal immune system.
- LIGHT protein can be activated on mucosal T cells through a gut-specific CD2-dependent signaling mechanism.
- Data suggest that LIGHT constitutively expressed in human melanoma cells and microvesicles may contribute to regulate T-cell responses to tumor cells.
- NF-kappaB signal plays a key role in LIGHT-mediated upregulation of CD86 expression.
- both LTbetaR and HVEM can discriminatively mediate the expression of different genes in cultured human umbilical vein endothelial cells, including LIGHT, a proinflammatory cytokine
- A transgenic mouse model resembling Crohn's disease (CD) suggests that up-regulation of LIGHT may be an important mediator of CD pathogenesis.
- LIGHT could serve as a molecular link between lipid metabolism, inflammation, and thrombus formation, which are all features of atherosclerotic plaques.
- platelet-derived LIGHT is biologically active and can induce an inflammatory response in monocytes and particularly within endothelial cells measured as up-regulation of adhesion molecules and release of chemokines
- Blockade of TNFSF14 signaling caused a substantial reduction in the expression of lymphotoxin beta receptor (LTbetaR)-controlled migration factors within the islets and disrupts organization of tertiary structures, leading to prevention of diabetes.
- LIGHT system may regulate early to middle stages of placental development via cell-specific, temporally programmed expression of the ligand and its receptors, and may also assist in preserving placental immune privilege.
- in addition to activating NF-kappaB/p52, LIGHT also activates Stat3 through the NIK pathway
- attenuated Salmonella typhimurium expressing LIGHT inhibited growth of primary tumors, as well as the dissemination of pulmonary metastases, in various mouse tumor models employing murine carcinoma cell lines in immunocompetent mice
- The plasma levels of LIGHT seem to be similar in hemodialysis (HD) patients and healthy subjects and were not affected by gender, age, the mean period of HD history, disease etiology, type of medication and type of using dialysis membrane.
- platelet-associated LIGHT is involved in adhesion of platelets to endothelium while soluble LIGHT induces a pro-inflammatory state in vascular endothelial cells
- Lymphotoxin-beta receptor ligand LIGHT activates both the the noncanonical and classical NF-kappa B pathways leading to proinflammatory gene expression in vascular endothelial cells.
- the allele T of C-770T and the haplotype TTGA of the promoter SNPs in LIGHT gene might decrease the expression of LIGHT and subsequently increase the susceptibility to vascular dementia in females
- derangement of LIGHT may be important for atherogenetic process of ischemic stroke.
- LIGHT was upregulated in both synovial fluid and synovium of rheumatoid arthritis patients compared with osteoarthritis patients.
- LIGHT acts synergistically with PAR-2 activation to promote enhanced release of the proatherogenic interleukin-8 & monocyte chemoattractant protein-1. The interaction between LIGHT & PAR-2 is biologically active, promoting potent inflammatory effects.