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Validated All-in-One™ qPCR Primer for TNFSF9(NM_003811.3) Search again
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:
Summary
The protein encoded by this gene is a cytokine that belongs to the tumor necrosis factor (TNF) ligand family. This transmembrane cytokine is a bidirectional signal transducer that acts as a ligand for TNFRSF9/4-1BB, which is a costimulatory receptor molecule in T lymphocytes. This cytokine and its receptor are involved in the antigen presentation process and in the generation of cytotoxic T cells. The receptor TNFRSF9/4-1BB is absent from resting T lymphocytes but rapidly expressed upon antigenic stimulation. The ligand encoded by this gene, TNFSF9/4-1BBL, has been shown to reactivate anergic T lymphocytes in addition to promoting T lymphocyte proliferation. This cytokine has also been shown to be required for the optimal CD8 responses in CD8 T cells. This cytokine is expressed in carcinoma cell lines, and is thought to be involved in T cell-tumor cell interaction.
Gene References into function
- 4-1BBL provides a costimulatory signal for T cell activation, thereby allowing T cell expansion as well as cytokine production and the development of cytolytic effector function.
- Stimulation of 4-1BBL on DCs with 4-1BB-Fc or with 4-1BB-transfected Jurkat cells resulted in acquisition of capacity for the immature DCs to produce IL-12, suggesting that 4-1BBL may be an important mediator for maturation of CD11c(+) myeloid DCs
- 4-1 BB ligand can costimulate human CD28- T cells, resulting in cell division, inflammatory cytokine production, increased perforin levels, enhancement of cytolytic effector function, as well as the up-regulation of the anti-apoptotic protein Bcl-X(L).
- First evidence of expression and synthesis of CD137 and its ligand by human brain cells.
- Data show that reverse signaling via 4-1BB-ligand enhanced interleukin-12beta mRNA and the secretion of IL-12 p70 in various antigen-presenting cells, including monocytes.
- 4-1BB/4-1BBL and Fas/FasL pathways play important roles in vascular injury in Takayasu's arteritis.
- Data suggest that levels of soluble 4-1BB and 4-1BB ligand in sera at the time of diagnosis may be indicative of the severity and outcome of rheumatoid arthritis.
- trimeric CD137L (4-1BBL) requires cross-linking for its T cell co-stimulation activity
- Signaling through 4-1BB-L allows B cells to proliferate and the expression of its ligand, by the intra-tumoral mesh of follicular dendritic cells (FDC), could thus serve as a paracrine loop facilitating growth and survival of MCL cells
- Significantly lower CD137 ligand is associated with colorectal cancer patients
- Elevated plasma levels of 4-1BBL in multiple sclerosis patients may function as a self-regulatory mechanism of the 4-1BB/4-1BBL pathway involved in the disease process.
- Here we document a function for the TNF family member 4-1BB ligand (4-1BBL) in sustaining TLR-induced TNF production
- Reverse signalling by CD137 ligand is mediated by protein tyrosine kinases, p38 mitogen activated protein kinase (MAPK), extracellular signal-regulated kinase (ERK)1,2, MAP/ERK kinase (MEK), Phosphoinositide-3-kinase (PI3-K) and protein kinase A (PKA).
- selective immunosuppression through MSCs may perhaps occur partly through an increase in CD137L+ on T-lymphocytes
- T cells that had become non-responsive to anti-CD3 could be reactivated to proliferate when costimulated with 4-1BBL, either alone or combined with CD80/CD86.
- CD80 and 4-1BBL induce auto- and transcostimulation in tumor cells
- deliver new insights into the multiple effects of reverse signaling of CD137L in human DC during the initiation of an adaptive immune response
