FADD pSer191 antibody Ab
- Known as:
- FADD pSer191 (anti-) Antibody
- Catalog number:
- 1488297
- Product Quantity:
- EUR
- Category:
- -
- Supplier:
- Acris antibodies
- Gene target:
- FADD pSer191 antibody
Related genes to: FADD pSer191 antibody Ab
- Gene:
- FADD NIH gene
- Name:
- Fas associated via death domain
- Previous symbol:
- -
- Synonyms:
- MORT1, GIG3
- Chromosome:
- 11q13.3
- Locus Type:
- gene with protein product
- Date approved:
- 1999-05-07
- Date modifiied:
- 2019-04-23
Related products to: FADD pSer191 antibody Ab
Related articles to: FADD pSer191 antibody Ab
- Classic Hodgkin lymphoma (CHL) is a highly curable disease. However, a subset of patients develops relapsed/refractory disease, underscoring the need for predictors of treatment response. Although immune-checkpoint inhibitors have improved outcomes, many patients still experience suboptimal responses. A deeper understanding of the CHL transcriptomic landscape may improve patient stratification and guide treatment approaches. Targeted mRNA-NGS was performed on formalin-fixed paraffine-embedded CHL-tissue using the HTG EdgeSeq Precision Immune-Oncology Panel (1,392 genes) in treatment-naive and post-chemotherapy relapsed treated with nivolumab-based protocols. Differential gene expression and pathway enrichment analyses were conducted to characterize tumor-intrinsic, and microenvironmental features associated with disease biology and treatment response. Across all CHL samples (n = 25) we observed overexpression of immune-checkpoint and immunoregulatory genes (CD274, CTLA-4, IL6, IL13), and markers of macrophage-rich/matrix-remodeling microenvironment (CD163, MMP2, TIMP1), alongside loss of B-cell identity and tumor suppression programs. Pathways analysis revealed activation of IL6/JAK/STAT3, TNF-α/NF-κB, KRAS-UP, and Inflammatory response, with reduced proliferative and metabolic activity. Immunotherapy non-responders, both in the overall (n = 5; 20%), and the treatment-naïve CHL (n = 2; 12%) displayed a proliferative, cytokine-activated, and immunologically cold phenotype. This includes shared overexpression of FADD, NFKB1, and TGFB1 and downregulation of SMAD7, together with activation of E2F, G2M, MYC, and PI3K/AKT/mTOR pathways and negative enrichment of TNF-α/NF-κB, IL6/JAK/STAT3, and Inflammatory response. Post-chemotherapy relapsed (n = 8) exhibited adaptative immunoregulatory and stress response signatures (IL15, TNFSF18, MAPK8, FUT4), along with reduced immune activation and loss of tumor-suppressor signaling. This study highlights the biological complexity and transcriptional diversity underlying CHL and its tumor microenvironment. Immunotherapy non-responders exhibited an "oncogene-driven" transcriptional profile independent of previous treatment status, whereas responders showed an "inflammatory immune-scape" phenotype, offering insight into mechanisms of resistance. Despite the limited sample size, these findings provide a foundation for larger precision-focused studies aimed at improving outcomes in CHL. - Source: PubMed
Publication date: 2026/08/05
Hamana LeticiaMarques-Piubelli Mario LWei LuKhan KhajaKakarala LakshmiShen LiWistuba Ignacio ILee Hun JuSolis Luisa MVega Francisco - 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 - Resistance to CDK4/6 inhibitors (CDK4/6i) combined with endocrine therapy presents a major barrier to improving outcomes in ER+ breast cancer. We identified FADD phosphorylation at Ser194 (phospho-FADD) as a mediator of CDK4/6i resistance in the models examined. Phospho-FADD acted as a pseudosubstrate inhibitor of the APC/C-Cdh1 complex, promoting G1/S transition and bypassing the canonical CDK4/6-Rb-E2F pathway. This CDK4/6-independent pathway was associated with PI3K hyperactivation. Clinical relevance of this bypass pathway was supported by increased phospho-FADD and pAKT in 73% of paired patient biopsies at post-treatment recurrence, while the remaining cases exhibited high baseline phospho-FADD and pAKT with intrinsic non-response. Inhibition of FADD phosphorylation with the CK1α degrader DEG-77, or PI3K inhibition, restored CDK4/6i sensitivity in resistant cells. In CDK4/6i-refractory xenografts, CK1α degradation combined with CDK4/6i resulted in profound tumor regressions and increased progression-free survival compared with either single agent, including complete tumor regressions in 92% of tumors. These findings support CK1α-mediated FADD phosphorylation as a targetable resistance mechanism in a subset of CDK4/6i-resistant ER+/HER2- breast cancer. - Source: PubMed
Publication date: 2026/07/28
Awadia SahezeelZiemke Elizabeth KCurnutt Nicole MKirk EmilyThomas JulianneZimmerman AnnaMileski Maya JRam SundareshAbou Zeidane ReineGalban CraigWoo Christina MSpeers Corey WLeopold JudithRehemtulla Alnawaz - SBA, (E)-4-(2-chloro-1-(2-chloro-benzyl)-1H-indol-3-yl)but-3-en-2-one, is a derivative of natural product, named 4,4'-dimethoxychalcone. In this study, the impact of newly synthesized SBA on cell apoptosis was investigated in human oral cancer SCC-4 cells in vitro. The results showed that SBA decreased cell viability, induced S and G2/M phase arrest, and induced apoptosis in SCC-4 cells. SBA also increased ROS production, reduced mitochondrial membrane potential, and activated caspase-9 and caspase-3 in a dose-dependent manner. SBA induced the upregulation of Chk1 and Chk2 expressions, while it resulted in a reduction of cdc2 and Cyclin B1 levels. SBA also increased the levels of Fas, FasL, FADD, caspase-8, and BID. Moreover, it increased the expression of Bad, Bax, cytochrome c, AIF, EndoG, caspase-9, and caspase-3, while reducing the expression of Bcl-2, Bcl-xL, and XIAP in SCC-4 cells. Taken together, these findings suggest that SBA induces cytotoxicity in SCC-4 cells via Fas-FasL- and mitochondria-mediated pathways. - Source: PubMed
Publication date: 2026/07/28
Ma Yi-ShihLien Jin-CherngChueh Fu-ShinHuang Yi-PingYang Jiun-LongChou Yu-ChengChen Jaw-ChyunChu Yung-LinHuang An-ChengLin Tzu-ShunPeng Shu-Fen - Cervical cancer (CC) is one of the leading malignancies impacting women worldwide, with a large number of cases occurring in developing countries. However, there is a need for optimal predictive models that can precisely forecast the prognosis and guide treatment selection. Programmed cell death (PCD) and immune responses (IRs) are pivotal in understanding disease progression, diagnosis, therapeutic decision-making, and risk stratification, making them promising prognostic markers. In this study, machine learning approaches were applied to identify key prognostic genes related to PCD and IR, which led to the development of three prognostic models: a PCD index, an IR index, and a combined immune-cell death index (ICDI). The PCD and IR indices showed a positive correlation in risk scores, and all three models demonstrated comparable prognostic significance. Given the biological relevance of the immune and cell death pathways, we further investigated the ICDI derived from the key genes FADD, MUC4, CLNK, and CD8B. This analysis included validation against clinical parameters, nomograms, and exploration of immune infiltration. Profiling of drug susceptibility revealed that the high-risk cohort of patients showed resistance to rapamycin and idelalisib but were sensitive to thapsigargin and linsitinib. Overall, the ICDI shows strong potential as a prognostic marker for forecasting clinical outcomes and could facilitate personalized treatment strategies for CC patients. - Source: PubMed
Publication date: 2026/07/06
Kiruba BlessySundararajan Vino