Recombinant Human TNFR1 /CD120a /TNFRSF1A Protein
- Known as:
- Recombinant Human TNFR1 /CD120a /TNFRSF1A Protein
- Catalog number:
- tn-767
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Proxinobio
- Gene target:
- Recombinant Human TNFR1 /CD120a /TNFRSF1A Protein
Related genes to: Recombinant Human TNFR1 /CD120a /TNFRSF1A Protein
- Gene:
- TNFRSF1A NIH gene
- Name:
- TNF receptor superfamily member 1A
- Previous symbol:
- TNFR1
- Synonyms:
- TNF-R, TNFAR, TNFR60, TNF-R-I, CD120a, TNF-R55
- Chromosome:
- 12p13.31
- Locus Type:
- gene with protein product
- Date approved:
- 1991-01-15
- Date modifiied:
- 2019-04-23
Related products to: Recombinant Human TNFR1 /CD120a /TNFRSF1A Protein
Related articles to: Recombinant Human TNFR1 /CD120a /TNFRSF1A Protein
- Immune checkpoint blockade (ICB) targeting PD-1/PD-L1 axis has transformed breast cancer treatment, yet how therapy reshapes the tumor microenvironment (TME) through cell-cell communication (CCC) remains unclear. Existing CCC inference methods relying on correlations have difficulty distinguishing genuine signaling from confounded associations. Here, we present a causal inference framework that uses single-cell data and leverages treatment as an instrumental variable to identify genuine CCC networks, referred to as scIVCCC, which infers causal signal transduction across cell types. Applying scIVCCC to single-cell RNA-seq data from 31 breast cancer patients before and after anti-PD-1 therapy, we constructed causal CCC networks linking exhausted T cells to tumor-associated macrophages (TAMs). Our analysis reveals a dual role of T cell-macrophage crosstalk: CD4+ and CD8+ exhausted T cells drive anti-tumor M1-like TAMs activation via TNF-TNFRSF1A, TNFSF14-LTBR, and ICAM1-ITGAL/ITGB2. Conversely, they also induce immunosuppressive M2-like polarization through pathways such as TNF-TNFRSF1B (TNFR2), TNFSF14-TNFRSF14 (HVEM), and RPS19-C5AR1, which likely contribute to therapeutic resistance. Our causal modeling suggests that receptors within these networks, such as C5AR1, TNFR2, and CSF1R, may serve as potential candidates for combination therapies to enhance anti-PD-1 efficacy. Collectively, these findings demonstrate that scIVCCC offers a robust framework for dissecting treatment-induced CCC dynamics and prioritizing actionable targets for clinical translation. - Source: PubMed
Qiu AodongZhang HanRamsey Joseph DAndrews BryanSun BoyangRen ShuangxiaLu MengyaoZhang KunCooper Gregory FLu BinfengChen LujiaLu Xinghua - Familial Mediterranean Fever (FMF) is traditionally linked to mutations. However, many patients remain genetically unexplained after routine screening. This study evaluates the utility of Next-Generation Sequencing (NGS) in patients with negative or heterozygous results from fragment analysis. - Source: PubMed
Publication date: 2026/04/19
Karaer DeryaDurak TanerAydin Leyla RezanTürel SametTokgün Pervin ElvanKilbaş GülşahAyduran SemraTokgün OnurYüksel SelçukKaraer Kadri - Allogeneic hematopoietic cell transplantation (allo-HSCT) is an essential therapeutic modality hematological malignancies, but acute graft-versus-host disease (aGvHD) persists as a leading cause of non-relapse mortality (NRM) . Cytokine biomarkers have already been used to predict aGvHD and outcomes. However, the standard guidelines for aGvHD biomarker panels remain controversial. We retrospectively analyzed the association of a biomarker panel (suppressor of tumorigenesis 2 [ST2], regenerating islet-derived 3 α [REG3α], Elafin, and tumor necrosis factor 1 [TNFR1]) in serum with the onset of 100-day aGvHD, 12-month NRM, and overall survival (OS) in 141 hematological malignancies patients at 19 ± 5 days after allo-HSCT from January 2022 to August 2023. Multivariable analysis showed that ST2 (P < .001) were strongly correlated with aGvHD, and TNFR1 was significantly associated with 12-month NRM and OS (P < .001). The panel of ST2, REG3α, Elafin, and TNFR1 demonstrated the best performance in diagnosis of 100-day aGvHD (area under the curve [AUC] = 0.79) and in the prediction of 12-month NRM (AUC = 0.74) and OS (AUC = 0.71). The 4-biomarker panel's risk classification predicted the 12-month cumulative incidence of NRM (43% vs 11%, P < .001) and 12-month OS (51% vs 82%, P < .001) for the high-risk and low-risk groups, respectively. Our results suggest that a combination of ST2, REG3α, Elafin, and TNFR1 is an excellent biomarker predictive panel for aGvHD diagnosis and outcomes after allo-HSCT. - Source: PubMed
Hao QiLiu XinyueLi TingtingWei WeiQi TianqiZhang ShuqinFei XinhongGu JiangyingWang Jingbo - Head and neck squamous cell carcinoma (HNSCC) is the most common head and neck cancer in India, where intensity-modulated radiation therapy (IMRT) is the standard treatment. Despite therapeutic advances, variability in radiation response and toxicities persists. Genetic factors, including the TNFRSF1A (-135 T>C, rs767455) polymorphism, may influence susceptibility to oral mucositis, dermatitis, and treatment response, but remain insufficiently studied in Indian populations. Functional validation through serum TNF-α profiling and predictive modeling is also lacking. - Source: PubMed
Publication date: 2026/04/08
Sarath Krishnan M PGoyal BelaGupta SweetyGupta AmitMirza Anissa Atif - Tumor necrosis factor (TNF) orchestrates immune responses but can also drive inflammation-associated tissue damage. However, the mechanisms governing tissue tolerance to TNF remain poorly understood. Here, we reveal that TNF receptor 1 (TNFR1) abundance is regulated by two upstream open reading frames (uORFs) in the 5' untranslated region of and demonstrate that this is a key determinant of TNF tolerance. uORF2 dominantly limits TNFR1 translation, and its disruption increases TNFR1 levels, leading to excessive TNF-induced gene activation and cell death in cell culture. By contrast, uORF1 dynamically regulates TNFR1 levels in response to inflammatory and stress signals. In mice, uORF2 protects against TNF-driven systemic inflammatory response syndrome and liver pathology. We additionally report that the translation of other immune receptor messenger RNAs, including , , and , is also controlled by uORFs. Thus, regulation of TNFR1 levels and possibly of other immune receptors emerges as a mechanism safeguarding against excessive immune responses and tissue damage. - Source: PubMed
Publication date: 2026/04/03
Ma BiaoLyu WenxinRizk JohnHan XiaoyueKjær MajkenPereira Almeida VinnyciusJessen MalinSauerland Max BenjaminLeung Carol Sze KiVan den Eynde Benoit JLu XinGyrd-Hansen Mads