Recombinant mouse TNF_alpha (E.coli_derived)
- Known as:
- Recombinant mouse TNF_alpha (E.coli_derived)
- Catalog number:
- CT305
- Product Quantity:
- 100 µg
- Category:
- -
- Supplier:
- U-CyTech
- Gene target:
- Recombinant mouse TNF_alpha (.coli_derived)
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Related articles to: Recombinant mouse TNF_alpha (E.coli_derived)
- Tumour necrosis factor (TNF) is a pleiotropic cytokine originally identified for its ability to kill cancer cells. However, a paradoxical tumour-promoting role for TNF emerged when early attempts to exploit its anti-tumour activity in cancer therapy produced conflicting outcomes, raising the question of whether TNF should be viewed as a therapeutic agent or a treatment target in cancer. Here, we demonstrate that expression of cFLIP, a catalytically inactive paralogue of caspase-8 (CASP8), determines the susceptibility of melanoma cells to TNF and thereby controls melanoma growth in a syngeneic, immune-competent mouse model of B16F10 cutaneous melanoma. B16F10 melanoma cells lacking cFLIP (cFlip cells) failed to grow in wild-type mice, whereas in TNF-deficient mice, cFlip melanoma cells formed palpable tumours and exhibited robust subcutaneous growth. These findings indicate that TNF alone is sufficient to control melanoma growth in the absence of cFLIP. Importantly, the anti-tumour activity of TNF has predominantly been investigated through targeting cellular inhibitors of apoptosis proteins (cIAPs), which promotes RIPK1 activation and TNF-induced cytotoxicity. We show that genomic ablation of cIAPs or RIPK1, in contrast to cFLIP, neither triggered TNF-induced toxicity nor affected melanoma growth in vivo. Collectively, our data underscore the central role of cFLIP in regulating melanoma responses to TNF and suggest that endogenous immune surveillance as well as immunotherapies involving TNF could strongly benefit from cFLIP targeting strategies. - Source: PubMed
Publication date: 2026/08/01
Stachelscheid JohannaKaul CäciliaGerstenberg KatrinWerthenbach J PaulSchorn FabianSteinkamp JoyZigrino PaolaPasparakis ManolisSchiffmann Lars MKashkar Hamid - Atorvastatin (ATR) is a well-established antihyperlipidemic agent that has recently gained attention in wound-healing research for its pleiotropic anti-inflammatory and antioxidant properties. Despite this therapeutic potential, its clinical repurposing for topical application remains challenging because of its poor aqueous solubility (BCS Class II) and limited penetration across the skin barrier. To address these limitations, ATR was incorporated into a self-nanoemulsifying drug delivery system (SNEDDS), which possesses inherent wound-healing properties, and subsequently incorporated into a thermoresponsive hydrogel to develop a novel ATR-SNEDDS hydrogel aimed at enhancing wound-healing efficacy. ATR-SNEDDS formulations were prepared using frankincense) FRK (oil, Tween® 20, and PEG 400 and characterized for thermodynamic stability, emulsification efficiency, droplet size, cloud point, and drug content. The optimized formulation, exhibiting nanometric droplet size, high drug content, and excellent physical stability, was then incorporated into a thermosensitive poloxamer hydrogel using the cold method, which demonstrated improved spreadability, suitable rheological properties, and complete drug release within 6 h. In a rat incisional wound model, the ATR-SNEDDS hydrogel significantly enhanced wound contraction (40% vs. diseased group; 16% vs. marketed standard), accompanied by marked reductions in oxidative stress and inflammatory markers, including malondialdehyde (68%) and TNF-α (60%), along with increased antioxidant defenses as evidenced by elevated SOD (48%) and GSH (50%). Histopathological and immunohistochemical analyses confirmed accelerated re-epithelialization, enhanced collagen deposition, and reduced inflammatory infiltration. Collectively, these findings demonstrate that the ATR-SNEDDS thermosensitive hydrogel provides a synergistic and effective platform for improving the therapeutic performance of ATR, offering promising wound-healing potential in an acute incisional wound model. - Source: PubMed
Publication date: 2026/08/01
Abdelqader Samaa OElnahas Hanan MIbrahim Tarek MMahmoud Abdulla M AZewail Moataz BEl-Dakroury Walaa A - Refined Changqin NO.1 (R-Cq1) has shown favorable therapeutic effects in traumatic brain injury (TBI), which triggers neuronal PANoptosis and involves dysregulation of gut microbiota and metabolites. - Source: PubMed
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Publication date: 2026/08/01
Yang HuiChen YeweiWang YipingZhang YinanLi YanLiu XiaoqinLiu YinTian MiQian MingZhou LinZhang JinpingLin MingbaoLiu Hang - Currently, utilized disease-modifying antirheumatic drugs (DMARDs) do not provide a complete cure for rheumatoid arthritis (RA) and are associated with side effects related to prolonged use. In contrast, natural products have demonstrated promising efficacy and low toxicity in treating various diseases. This study employed network pharmacology and virtual screening to identify natural products with potential therapeutic effects for RA, followed by molecular dynamics simulations and experimental validation. Through network pharmacology, we identified interleukin-1 beta (IL-1β), interleukin-6 (IL-6), and tumor necrosis factor-alpha (TNF-α) as RA-related targets, and subsequently prioritized neoprzewaquinone A (NEO) via virtual screening and molecular dynamics simulations for further validation. Subsequent experiments indicated that NEO could inhibit the binding of IL-1β, IL-6, and TNF-α to their respective receptors, reduce proliferation, and downregulate the migratory and invasive capacities of RA fibroblast-like synoviocytes (RA-FLS). Furthermore, NEO alleviated RA-related symptoms and diminished tissue damage in collagen-induced arthritis (CIA) mice. RNA sequencing suggested that the alleviative effect of NEO on RA may be attributed to the inhibition of the activation of the MAPK signaling pathway. Additionally, NEO appeared to reduce the phosphorylation levels of MEK and ERK. Importantly, safety evaluations did not reveal a clear increase in liver or kidney toxicity associated with NEO, within the scope of this study. Collectively, these findings suggested that NEO shows promise as a potential natural therapeutic option for RA and offers a new direction and theoretical foundation for future pharmacotherapy research in this area. - Source: PubMed
Publication date: 2026/08/01
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