Human Cellexp Human Recombinant TNF-alpha proteins
- Known as:
- Human Cellexp Human Recombinant TNF-a proteins
- Catalog number:
- 6482-10
- Product Quantity:
- 10
- Category:
- Proteins
- Supplier:
- Biovis
- Gene target:
- Human Cellexp Recombinant TNF-alpha proteins
Related products to: Human Cellexp Human Recombinant TNF-alpha proteins
Related articles to: Human Cellexp Human Recombinant TNF-alpha proteins
- Intracerebral hemorrhage (ICH) induces dysfunction in brain microvascular endothelial cells (BMVECs), thereby contributing to secondary brain injuries. Emerging evidence implicates METTL3 and HDAC6 as critical mediators of inflammation and ferroptosis that contribute to post-ICH neurological impairment. Lovastatin exhibits anti-inflammatory, anti-oxidative, and neuroprotective properties. This study elucidated the therapeutic potential of lovastatin in attenuating BMVEC injury following ICH, while investigating the mechanistic involvement of METTL3 and HDAC6 in this protective process. - Source: PubMed
Publication date: 2025/09/09
Wang XiaolongPeng LiangshengHan LiTuo YuanzhaoChen HuahuiWang XueminXue LixiongDing Xinmin - Acute lung injury (ALI), recognized as a prevalent and severe respiratory disorder, represents a critical medical condition. During ALI, Vascular Endothelial Growth Factor A (VEGFA)-mediated M1/M2 macrophage polarization is crucial, yet its specific regulatory mechanisms remain unclear. - Source: PubMed
Publication date: 2025/09/05
Yang JinNi GuangshengXie XiaoXu Zhaojun - We herein probed the effects of ozone autohemotherapy (O3-AHT) on inflammatory response and postoperative cognitive function in patients undergoing valve replacement with cardiopulmonary bypass (CPB). - Source: PubMed
Publication date: 2025/09/17
Peng WenyongDu YulongLu WeiJiang XiaofengChai HuaTian PengshengZhu Danyan - Cardiac surgery-associated acute kidney injury (CSA-AKI) is a popular and severe complication after cardiac surgery. We aimed to set up a quick and accurate predictive model for rapid identification of CSA-AKI and to evaluate its predictive value. - Source: PubMed
Publication date: 2025/09/17
Zhang BenguiZhang DayongWang ShidongYu Hongbo - Adipocyte hypertrophy during obesity triggers chronic inflammation, leading to metabolic disorders. However, the role of adipocyte-specific inflammatory signaling in metabolic syndrome remains unclear. The linear ubiquitin chain assembly complex, LUBAC, is an E3-ligase that generates nondegradative linear ubiquitination (Lin-Ub). LUBAC regulates NF-κB/MAPK-driven inflammation and prevents cell death triggered by immune receptors like TNF receptor-1. Here, we show that mice lacking HOIP, the Lin-E3 ligase catalytic subunit of LUBAC, in adipocytes () display lipodystrophy and heightened susceptibility to obesity-induced metabolic syndrome, particularly metabolic dysfunction-associated steatotic liver disease (MASLD). Mechanistically, loss of HOIP attenuates TNF-induced NF-κB activation and promotes cell death in human adipocytes. Inhibiting caspase-8-mediated cell death is sufficient to prevent lipodystrophy and MASLD in obese mice. HOIP expression in adipose tissue positively correlates with metabolic fitness in obese individuals. Overall, our findings reveal a fundamental developmental role for Lin-Ub in adipocytes by mitigating cell death-driven adipose tissue inflammation and protecting against obesity-related metabolic syndrome. - Source: PubMed
Publication date: 2025/09/17
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