TNF_alpha mAb;human (1)
- Known as:
- TNF_alpha mAb;H. sapiens (1)
- Catalog number:
- ASACSA-806E
- Product Quantity:
- 100 µg
- Category:
- -
- Supplier:
- Other suppliers
- Gene target:
- TNF_alpha mAb;human (1)
Related products to: TNF_alpha mAb;human (1)
Related articles to: TNF_alpha mAb;human (1)
- Ulcerative colitis (UC) is a chronic inflammatory bowel disease in which cytomegalovirus (CMV) reactivation has been linked to severe and steroid-refractory cases. However, the effect of CMV on cytokine regulation in UC remains unclear. This study investigated colonic and systemic cytokine profiles in CMV-positive and CMV-negative UC patients. - Source: PubMed
Publication date: 2026/05/15
Izadi NasimShirmohammadi MasoudDaryani Nasser EbrahimiBehboudi EmadBaghi Hossein BannazadehOskouee Mahin AhangarSadeghipoor ShimaYazdani ShaghayeghAzadi ArezouNaghili BehroozAghazadeh MohammadPoortahmasebi Vahdat - End-stage renal disease (ESRD) is frequently accompanied by major adverse cardiac and cerebrovascular events (MACCE) in affected patients. Therefore, there is an urgent need to develop effective biomarkers. - Source: PubMed
Publication date: 2026/05/16
Liao JieCao XuelingYu Lili - Tumor necrosis factor-alpha (TNF-α) inhibitors increase the risk of developing active tuberculosis (TB) disease through reactivation of latent TB infection (LTBI). We aimed to analyze TB infections in BCG-vaccinated children and adolescents with rheumatologic diseases treated with TNF-α inhibitors in a country of moderate risk for TB. This retrospective study included 261 children with a rheumatic disease who were treated with TNF-α inhibitors and followed up on a fixed schedule between January 2018 and December 2022. Demographic and clinical characteristics, as well as TB screening results, were recorded. The mean age of the patients was 14.0 ± 4.1 years; 56.7% were female. The mean age at initiation of TNF-α inhibitors was 11.0 ± 5.1 years, the mean duration of TNF-α inhibitor use was 4.1 ± 2.7 years, and the mean follow-up time was 4.1 ± 2.6 years. During the study period, 75 (29.0%) patients were diagnosed with LTBI: 44% at the initial evaluation and 56% during follow-up. None of them progressed to TB disease. Only two cases of active TB disease were seen without prior documented LTBI. Age and duration of TNF-α inhibitor use were significantly associated with LTBI positivity. - Source: PubMed
Publication date: 2026/05/15
Ademhan Tural DilberDoğru DenizÖzsezen BesteKaraman AzerSunman BirceNayir Büyükşahin HalimeGüzelkaş İsmailAlboğa DidemErdal Meltem AkgülEmiralioğlu Ordukaya NagehanBilginer YeldaYalçın EbruÖzçelik UğurÖzen SezaKiper Nural - Intestinal obstruction is a common surgical emergency characterised by rapid progression and high mortality. However, the underlying mechanisms remain incompletely elucidated. Here, we show, by combining single-cell RNA sequencing with in vivo pharmacological modulation in male rats, the temporal dynamics of neutrophil extracellular traps (NETs) formation and their contribution to barrier dysfunction in incarcerated small-bowel obstruction. Profiling of 23,320 intestinal cells reveals pronounced neutrophil infiltration in late-stage obstruction (24.59% of total cells) and enables identification of a discrete "NETs-associated neutrophil subset (Neu_NETs)". These Neu_NETs exhibit marked transcriptional enrichment of IL-17, NF-κB and TNF signalling pathways. Functional analyses demonstrate a time-dependent accumulation of NETs within obstructed segments that inversely correlates with the expression of intestinal tight junction proteins. In vivo administration of the PAD4 inhibitor Cl-amidine significantly attenuates NETs formation, ameliorates histopathological injury, and decreases local levels of IL-1β and TNF-α. Therefore, targeting NETs may represent a strategy for treating intestinal obstruction. - Source: PubMed
Publication date: 2026/05/15
Li ZhanchuanYe YongxinWang PengLong FeiZhang YingyiZheng XunriLin ChangweiLi XiaorongBai YangZhang Yi - Non-small cell lung cancer (NSCLC), the predominant subtype of lung cancer, remains a major global health challenge due to its complex etiology and resistance to therapy. Aberrant signaling through receptor tyrosine kinases (RTKs) and mitogen-activated protein kinases (MAPKs) drives tumor progression and immune modulation, underscoring the need for systems-level investigation. In this study, we employed mathematical modeling and experimental validation to dissect the dynamic interplay of EGFR, FGFR, and TNFR signaling in NSCLC cells and macrophages. Our flux-based sensitivity analysis revealed persistent pathway biases, highlighting DUSP1, DUSP4, and SPRY2 as critical high-flux regulators within the MAPK and PI3K/AKT cascades. Crosstalk analysis demonstrated that these proteins form an interconnected signaling axis influencing cytokine production (IL6, IL10, IL12, and TNF-α) and macrophage-mediated responses in the tumor microenvironment. Functional assays confirmed that silencing SPRY2 suppressed DUSP1 and DUSP4 expression, impaired cell migration, and induced G2/M arrest, establishing a coordinated regulatory network essential for NSCLC progression. Together, our findings integrate computational modeling with molecular validation to identify DUSP1, DUSP4, and SPRY2 as pivotal drivers of oncogenic signaling and immune regulation. These proteins represent promising therapeutic targets whose inhibition may disrupt tumor-promoting feedback loops and attenuate NSCLC growth and survival. - Source: PubMed
Publication date: 2026/05/15
Tukrul ManasiGulhane PoojaSingh Shailza