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Validated All-in-One™ qPCR Primer for TNFRSF4(NM_003327.3) Search again
Product ID:
HQP018332
(click here to view gene annotation page)
Powered by BiozSpecies:
Human
Symbol:
Alias:
ACT35, CD134, IMD16, OX40, TXGP1L
Gene Description:
TNF receptor superfamily member 4
Target Gene Accession:
NM_003327.3(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 TNF-receptor superfamily. This receptor has been shown to activate NF-kappaB through its interaction with adaptor proteins TRAF2 and TRAF5. Knockout studies in mice suggested that this receptor promotes the expression of apoptosis inhibitors BCL2 and BCL2lL1/BCL2-XL, and thus suppresses apoptosis. The knockout studies also suggested the roles of this receptor in CD4+ T cell response, as well as in T cell-dependent B cell proliferation and differentiation. [provided by RefSeq].
Gene References into function
- Pimecrolimus inhibits up-regulation of OX40 and synthesis of inflammatory cytokines upon secondary T cell activation by allogeneic dendritic cells.
- Expression of CD134 and CD134 ligand in lesional and nonlesional psoriatic skin.
- CD134 positive cells are identified within inflammatory lesions of active multiple sclerosis (MS), acute MS and chronic active MS as well as in acute disseminated leukoencephalitis patients.
- T cell proliferation by direct cross-talk between OX40 ligand on human mast cells and OX40 on human T cells.
- Mutagenesis showed that Asp60 and Asp62 are required for interaction with FIV, and modeling studies localized these two residues to the outer edge of domain 1
- The expression of CD134 was markedly higher, compared to CD137, both on the day of the surgery and ten days after colorectal cancer surgery.
- Deficiencies in OX40 and CD30 signals were additive, secondary Ab responses were ablated.OX40/CD30 double-knockout OTII transgenic T cells fail to survive compared with normal T cells when cocultured with CD4(+)CD3(-) cells in vitro.
- Decrease in OX40 expression posttransplant includes the defective reconstitution of Treg cells, and the active inhibition of gene transcription by cyclosporine.
- stimulation of OX40/4-1BB rendered cells sensitive to apoptosis induced by TNF-alpha and reduced activation of NF-kappaB. OX40/4-1BB stimulation repressed the mitogen response in activated CD25+CD4+ T cells and preactivated CD8+ T cells
- CD3+ T lymphocytes co-expressing CD134 and CD137 antigens on peripheral blood revealed an increased percentages of OX-40/CD137 positive cells in patients with Graves' disease (p<0.025) compared to the controls.
- The relevance of these findings is supported by the vital functions fulfilled by OX40 in mammals as reflected by the high level of evolutionary conservation.
- The coexpression of CD25 and the costimulatory molecule CD134 on memory T-cells provides a novel marker for type 1 diabetes-associated T-cell immunity.
- OX40 ligation on CD4(+) T cells represents a potentially novel immunotherapeutic strategy that should be investigated to treat and prevent persistent virus infections, such as HIV-1 infection.
- OX40 is induced transiently on CD8(+) T cells upon activation and its signals contribute to both clonal expansion and functional reinforcement
- In the present study we found that costimulation via OX40 and TNF-R in OX40-expressing HIV-1-infected T cell lines leads to a marked reduction of HIV-1 production associated with rapid cell death.
- The expression of OX40 on CD4+ T cells in sentinel lymph nodes draining primary melanomas decreased withe more advanced tumor features, suggesting an immunosuppressive effect.
- Activity of OX40 ligand is enhanced by oligomerization and cell surface immobilization.
- the frequency of the most frequent haplotype, C-C-A-A, was significantly lower and that of the second most frequent, C-T-G-A, was significantly higher in hypertensive subjects than in controls. This difference was observed only in female patients
- Results show that the OX40-OX40L interaction suppresses IL-17 production by PHA-stimulated human PBMC and purified CD4 and CD8 cells.
- These data offer a novel approach for UCB Treg expansion using aAPCs, including those coexpressing OX40L or 4-1BBL.
- Targeting the OX40 costimulation is therapeutically important in the induction of transplant tolerance.
- CD4(+)CD25(+) effector memory T-cells expressing CD134 and GITR seem to play a role in disease mechanisms, as suggested by their close association with disease activity and their participation in the inflammatory process in Wegener's granulomatosis.
- OX40 antigen levels were significantly elevated in Systemic sclerosis patients compared with Systemic Lupus patients and controls; elevated levels were assoicated with early-onset disease
- Lack of OX40 signals in transgenic mice significantly reduces the number and proportion of killer cell lectin-like receptor G1 (KLRG1)-defective memory precursor effector T cells.