LIGHT _ CD258
- Known as:
- LIGHT _ CD258
- Catalog number:
- Y214367
- Product Quantity:
- 200ul
- Category:
- -
- Supplier:
- ABM
- Gene target:
- LIGHT _ CD258
Related genes to: LIGHT _ CD258
- Gene:
- TNFRSF14 NIH gene
- Name:
- TNF receptor superfamily member 14
- Previous symbol:
- -
- Synonyms:
- HVEM, ATAR, TR2, LIGHTR, HVEA, CD270
- Chromosome:
- 1p36.32
- Locus Type:
- gene with protein product
- Date approved:
- 1998-12-04
- Date modifiied:
- 2016-06-28
- Gene:
- TNFSF14 NIH gene
- Name:
- TNF superfamily member 14
- Previous symbol:
- -
- Synonyms:
- LIGHT, LTg, HVEM-L, CD258
- Chromosome:
- 19p13.3
- Locus Type:
- gene with protein product
- Date approved:
- 1998-12-04
- Date modifiied:
- 2017-03-02
Related products to: LIGHT _ CD258
"Light-on" LysoView 555"Light-on" LysoView 555"Light-on" LysoView 555"Light-on" LysoView 555"Light-on" LysoView 555"Light-on" LysoView 555(for isolation and cultivation of Listeria from Henry’s light.)1-Channel S.S Adaptor (40mm), Light Blue1-Channel S.S Adaptor (80mm), Light Blue1-Channel Tip Adaptor with Tip Ejector, Light Blue1-Channel Tip Adaptor, Light Blue10D6 DLC1 (Dynein Light Chain 1)17 kDa myosin light chain,Bos taurus,Bovine,LC17,MLC-3,MYL6,Myosin light chain 3,Myosin light chain A3,Myosin light chain alkali 3,Myosin light polypeptide 617 kDa myosin light chain,Homo sapiens,Human,LC17,MLC-3,MYL6,Myosin light chain 3,Myosin light chain A3,Myosin light chain alkali 3,Myosin light polypeptide 6,Smooth muscle and nonmuscle myosin light17 kDa myosin light chain,LC17,MLC-3,Mouse,Mus musculus,Myl6,Myln,Myosin light chain 3,Myosin light chain A3,Myosin light chain alkali 3,Myosin light polypeptide 6,Smooth muscle and nonmuscle myosin l Related articles to: LIGHT _ CD258
- The pathogenesis of psoriasis is associated with abnormalities in immune pathways. HVEM is known as a receptor of LIGHT (homologous to lymphotoxins, inducible, and competes with HSV glycoprotein D), which is a newly identified member of the TNF superfamily. The expression of HVEM and LTBR (another LIGHT receptor) has been found to be increased in the skin of psoriasis patients. This indicates the potential role of LIGHT and its receptors in the pathogenesis of psoriasis. Therefore, the objective of this study was to examine the effect of LIGHT on keratinocyte proliferation and its therapeutic potential in the treatment of psoriasis. - Source: PubMed
Ye Cheng-BinFei Cheng-WenCao TingZhou Xu-YangZou Ying - Alveolar macrophages (AMs) help defend the lungs against infection, but during pneumonia many alveolar macrophages die. In this issue of the JCI, Malainou et al. explored the mechanism underpinning AM death during viral pneumonia and its effect on the outcomes of bacterial superinfection, a secondary infection that occurs before the first infection is cleared. In mouse models of influenza A infection, recruited neutrophils secreted TNF superfamily member 14 (TNFSF14), and AMs increased expression of the TNFSF14 receptors TNFSFR14 and type I transmembrane lymphotoxin β receptor (LTβR). TNFSF14 signaling via the LTβR was sufficient to cause AM apoptosis. TNFSF14 deficiency or blockade preserved AMs during influenza infection and diminished bacterial burdens and mouse mortality during pneumococcal superinfection. The adoptive transfer of AMs decreased the severity of pneumococcal superinfections, if those AMs lacked the LTβR. Thus, preserving AMs by interrupting TNFRSF14-LTβR interactions can make virus-infected lungs less susceptible to severe bacterial superinfection. - Source: PubMed
Publication date: 2026/01/16
Armstrong Elise MrMizgerd Joseph P - To elucidate the mechanism through which tumor-associated neutrophil extracellular traps (NETs) contribute to the progression of colorectal cancer (CRC), characterize cellular populations within the CRC tumor microenvironment (TME), and identify potential therapeutic targets. - Source: PubMed
Publication date: 2025/11/11
Ying YaoWang HaochengWang YueHuang JunpengWu ZiyingQiu BowenChen HungchenLong MeitingMo KeCui Chunhui - T cells are important targets for therapeutic intervention in many diseases. Modifying T cell activation via immune checkpoints plays a central role in such approaches. The HVEM/LIGHT complex is one of the stimulatory immune checkpoints involved in T cell activation, and binding of these proteins results in proliferation and development of effector functions of T cells. In patients suffering from autoimmune diseases and in transplant recipients it is desirable to suppress immune responses. This could be achieved by blocking the HVEM and LIGHT interactions. Our studies concern blockage of the formation of the HVEM/LIGHT complex using peptides. To design the inhibitors of this interactions, we relied on the amino acid sequence and the structure of the LIGHT-binding fragments of HVEM. We measured the affinity of designed peptides to LIGHT using SpS technique and tested their ability to inhibit the formation of the HVEM/LIGHT complex using ELISA and cellular studies. That led to the identification of two peptides, namely CRD2e_K54E and CRD2(39-73)e that strongly bind to LIGHT and possess blocking capacities towards HVEM/LIGHT complex formation. Obtained data indicate that HVEM-derived peptides could form the basis for future therapeutics, highlighting the need for further exploration of their immunomodulatory potential. - Source: PubMed
Publication date: 2025/10/31
Ciura PiotrGumpelmair SimonSikorska EmiliaRodziewicz-Motowidło SylwiaSteinberger PeterSpodzieja MartaSieradzan Adam K - Inflammatory Bowel Disease (IBD), encompassing Crohn's disease and ulcerative colitis, is an umbrella term used to describe a group of autoimmune conditions characterized by chronic, relapsing inflammation of the gastrointestinal tract. The tumour necrosis factor superfamily member 14 (TNFSF14), also known as LIGHT, is a pleiotropic cytokine with diverse roles in immune regulation. Here, we review the multifaceted involvement of LIGHT in intestinal inflammation, particularly its dual capacity to both promote immune activation and facilitate inflammation resolution in the context of IBD. We explore the molecular mechanisms of LIGHT signalling through its receptors, Herpes Virus Entry Mediator (HVEM) and Lymphotoxin-β Receptor (LTβR), and how these distinct interactions dictate its pro-inflammatory or regulatory functions. Finally, we review the therapeutic potential of targeting this pathway, highlighting the results of recent clinical trials and exploring future strategies aimed at restoring immune homeostasis in patients with IBD. - Source: PubMed
Publication date: 2025/09/15
Mousa Rabia SInvernizzi PietroJones Joanne LMousa Hani S