Transfected Stable Cell Lines
Reliable | High-Performance | Wide Rage
Precision reporter, kinase, immune receptor, biosimilar, Cas9, and knockout stable cell lines for diverse applications.
| Cat.No. | Product Name | Price |
|---|---|---|
| CSC-DC016359 | Panoply™ Human TNFRSF14 Knockdown Stable Cell Line | Inquiry |
| CSC-SC016359 | Panoply™ Human TNFRSF14 Over-expressing Stable Cell Line | Inquiry |
| CSC-RO0205 | Human TNFRSF14 Stable Cell Line - CHO-K1 | Inquiry |
| CSC-RO0206 | Mouse Tnfrsf14 Stable Cell Line - CHO-K1 | Inquiry |
| CLOE-1509 | Human TNFRSF14 HEK293 Cell Lysate | Inquiry |
| CLOE-1510 | Human TNFRSF14(His) HEK293 Cell Lysate | Inquiry |
| CLOE-3003 | Mouse Tnfrsf14 (Fc) HEK293 Cell Lysate | Inquiry |
| CLOE-3004 | Mouse Tnfrsf14 (Fc) CHO Cell Lysate | Inquiry |
| CSC-RH0092M | Humanized TNFRSF14 Murine Tumor Cell Line | Inquiry |
| Cat.No. | Product Name | Price |
|---|---|---|
| AD16669Z | Human TNFRSF14 adenoviral particles | Inquiry |
| LV00502Z | Human TNFRSF14 lentiviral particles | Inquiry |
| LV00503Z | Mouse Tnfrsf14 lentiviral particles | Inquiry |
| LV00504Z | Mouse Tnfrsf14 lentiviral particles | Inquiry |
| Cat.No. | Product Name | Price |
|---|---|---|
| SHH431932 | shRNA set against Human TNFRSF14 (NM_003820.2) | Inquiry |
| SHH431936 | shRNA set against Mouse TNFRSF14 (NM_178931.2) | Inquiry |
| SHL084335 | shRNA set against Mouse Tnfrsf14(NM_178931.2) | Inquiry |
| SHH431940 | shRNA set against Rat TNFRSF14 (NM_001015034.1) | Inquiry |
| SHL084334 | shRNA set against Rat Tnfrsf14(NM_001015034.1) | Inquiry |
| SHL084626 | shRNA set against Human TNFRSF14(NM_003820.2) | Inquiry |
| Cat.No. | Product Name | Price |
|---|---|---|
| CDCR370421 | Rat Tnfrsf14 ORF Clone(NM_001015034.1) | Inquiry |
| CDFH020003 | Human TNFRSF14 cDNA Clone(NM_003820.2) | Inquiry |
| CDFR003431 | Rat Tnfrsf14 cDNA Clone(NM_001015034.1) | Inquiry |
| MiUTR1H-10595 | TNFRSF14 miRNA 3'UTR clone | Inquiry |
| MiUTR1M-11989 | TNFRSF14 miRNA 3'UTR clone | Inquiry |
| MiUTR1R-08116 | TNFRSF14 miRNA 3'UTR clone | Inquiry |
| CDCB156769 | Cynomolgus TNFRSF14 ORF clone | Inquiry |
| CDCL184636 | Human HVEM ORF clone(NM_003820.2) | Inquiry |
| CDCL184637 | Mouse HVEM ORF clone(NM_178931.2) | Inquiry |
| CDCS411486 | Human TNFRSF14 ORF Clone (BC029848) | Inquiry |
| CDCS411487 | Human TNFRSF14 ORF Clone (BC002794) | Inquiry |
Recent Research Progress
HVEM, the host receptor herpesvirus entry mediator, also known as TNFRSR14, as its name suggests, facilitates herpes simplex virus (HSV) entry through interactions with a viral envelope glycoprotein. As shown in the diagram below, HVEM also bridges several signaling networks, combining ligands from the tumor necrosis factor (TNF) and immunoglobulin (Ig) superfamilies, with diverse, and often opposing, outcomes. While HVEM was first identified as a viral entry receptor for HSV, it is only recently that HVEM has emerged as an important host factor in the immunogenic pathogenesis of HSV-1 infection in the eye. Surprisingly, HVEM exacerbates the development of the disease, regardless of entry. HVEM signaling plays a multiple role in regulating immune responses to HSV and other pathogens, and there is increasing evidence that these effects are responsible for HVEM-mediated eye pathogenesis. There are dual branches of HVEM function during HSV infection: entry and immunomodulation. HVEM is broadly expressed, intersecting two important immune signaling networks and affecting autoimmunity, infection, and inflammation.
Figure 1. Schematic depicting the facilitation of bidirectional signaling of HVEM (Edwards R G, et al. 2017).
According to recent researches, HVEM, as a ligand of BTLA (B- and T-lymphocyte attenuator, also known as CD272), has emerged as a major and complex co-signaling molecule, identified as a new target to enhance anti-tumor immunity. HVEM provides a stimulation signal upon binding to TNF member LIGHT (TNFSF14) on T cells and B cells. And, HVEM can also provide suppression signals to T cells when bound to BTLA. Thus, HVEM may be viewed as a molecular switch in T cells. Despite the complexity of ligand binding, the inhibitory function of HVEM seems to be dominant. These studies further supported that the BTLA/HVEM interaction also act as an inhibitors and might be a targetable interaction. Moreover, HVEM targeting could be attractive if we imagine a joint blockade of the BTLA/HVEM inhibitory pathway and triggering of the LIGHT/HVEM co-stimulatory pathway.
Additionally, the HVEM network could be new directions in targeting novel co-stimulatory/co-inhibitory molecules for cancer therapy. The potential roles of HVEM and its ligands in tumor progression and immune response escape has been confirmed. Blockade or enhancement of these pathways may help improving cancer therapy.
Coincidentally, Tsang J Y S, et al. indicated HVEM played significant oncogenic role in breast carcinogenesis, and may also be a tumor-specific target. HVEM expression in breast cancers was associated with aggressive tumor features. It is possible that HVEM acts directly on breast cancer cells in promoting cell cycle progression, and indirectly by inhibiting the tumor immune environment. Thus, HVEM may be a synergistic target for the immunotherapy of breast cancers. What’s more, HVEM is highly expressed in ovarian serous adenocarcinoma tissues and is correlated with the patient clinicopathological features. Therefore, HVEM may provide a basis in the search for a new targeting treatment for ovarian serous adenocarcinoma.
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