FADD

Last update 08 May 2025

Basic Info

Synonyms

FADD, Fas associated via death domain, FAS-associated death domain protein

+ [5]

Introduction

Apoptotic adapter molecule that recruits caspases CASP8 or CASP10 to the activated FAS/CD95 or TNFRSF1A/TNFR-1 receptors (PubMed:16762833, PubMed:19118384, PubMed:20935634, PubMed:23955153, PubMed:24025841, PubMed:7538907, PubMed:9184224). The resulting aggregate called the death-inducing signaling complex (DISC) performs CASP8 proteolytic activation (PubMed:16762833, PubMed:19118384, PubMed:20935634, PubMed:7538907, PubMed:9184224). Active CASP8 initiates the subsequent cascade of caspases mediating apoptosis (PubMed:16762833). Involved in interferon-mediated antiviral immune response, playing a role in the positive regulation of interferon signaling (PubMed:21109225, PubMed:24204270).

100 Clinical Results associated with FADD

100 Translational Medicine associated with FADD

0 Patents (Medical) associated with FADD

2,494

Literatures (Medical) associated with FADD

01 Sep 2025·Comparative Biochemistry and Physiology Part D: Genomics and Proteomics

Biochemical indices, histological observations and transcriptome sequencing reveal the response mechanism of largemouth bass (Micropterus salmoides) to transport stress

Article

Author: Qiang, Jun ; Wang, Qing Chun ; Hua, Jixiang ; Duan, Xue Jun ; Tao, Yi Fan

In this study, transport conditions were simulated to investigate changes in intestinal tissue structure, oxidative stress, apoptosis and transcriptome levels during transport stress of largemouth bass (Micropterus salmoides). The results showed that the serum cortisol and lactic acid levels in largemouth bass significantly increased with increasing transport time, and the glucose content peaked after 8 h of transport. After 8 h and 12 h, the Reactive oxygen species, superoxide dismutase, malondialdehyde, and lipid peroxide contents in the intestine were significantly higher than those in the control group and the stressed group at 4 h. Additionally, more of the mucous membrane of intestinal tissue was exfoliated, resulting in edema, and the intestinal villi height and density significantly decreased. The differentially expressed genes were further analyzed after 0 h, 8 h, and 12 h of transport stress. There were significant differences in genes associated with the p53 signaling pathway (igfbp1a, ccnb1, cdk1, and igfbp6b) and apoptosis (bcl2l11, parp3, pik3r1, fadd, aifm1, and lmnb1). Combined with the increasing amount of apoptotic cells after stress, these results indicated that transport stress had a substantial effect on intestinal cell apoptosis. The intestinal antioxidant activity and tissue structure of the stressed groups recovered to the pre-stress level after 7 d of recovery from 8 h of transport; however, these parameters did not return to pre-stress levels after 7 d of recovery from 12 h of transport. This finding further demonstrated that long-term transport stress induced apoptosis and tissue damage in the largemouth bass intestine through p53 signaling.

01 Jun 2025·Toxicology Reports

MnTBAP, a peroxynitrite scavenger, attenuates cisplatin-induced apoptosis and cytotoxicity in organ of Corti cells

Article

Author: Bhatia, Pankaj ; Doyon-Reale, Nicole ; Shahab, Monazza ; Jamesdaniel, Samson ; Rosati, Rita

Cisplatin, a widely used anti-cancer drug, induces apoptosis in cochlear hair cells. In previous studies, cisplatin-induced nitration and degradation of proteins such as LMO4 disrupted their anti-apoptotic signaling. Cotreatment with SRI110, a peroxynitrite decomposition catalyst, attenuated cisplatin-induced ototoxicity in rodents. However, it is not known if other compounds that target nitrative stress would also confer similar otoprotection. Manganese (III) tetrakis (4-benzoic acid) porphyrin (MnTBAP), a cell-permeable superoxide dismutase mimetic, is a peroxynitrite decomposition catalyst that selectively scavenges peroxynitrite. This study demonstrates that cotreatment of UB/OC1 cells MnTBAP prevented cisplatin-induced cytotoxicity and nitrative stress. Furthermore, the mRNA levels of pro-apoptotic genes such as Caspase-3, Caspase-9, Fas, Fadd, and Bcl2 that were upregulated by cisplatin treatment were attenuated by MnTBAP cotreatment. The cisplatin-induced downregulation of Prdx2, an antioxidant gene, was significantly attenuated by MnTBAP cotreatment. Immunoblot analysis demonstrated that cisplatin-induced reduction in the expression of LMO4 protein was attenuated when the cells were cotreated with MnTBAP. Together, these results indicate that MnTBAP cotreatment attenuates cisplatin-induced apoptosis and mitigates associated cytotoxicity in UB/OC1 cell lines suggesting that peroxynitrite decomposition catalysts could emerge as promising interventional compounds for preventing cisplatin-induced ototoxicity.

01 Jun 2025·Phytomedicine

Eupalinolide B targets DEK and PANoptosis through E3 ubiquitin ligases RNF149 and RNF170 to negatively regulate asthma

Article

Author: Ding, Ningpo ; Liu, Ruobai ; Bai, Qiaoyun ; Yan, Guanghai ; Song, Yilan ; Li, Liangchang ; Wang, Chongyang ; Wang, Zhiguang ; Piao, Hongmei

PURPOSEWe investigated the mechanism by which eupalinolide B (EB) regulates DEK protein ubiquitination and degradation, and its impact on DEK-mediated receptor-interacting protein kinase 1 (RIPK)-PANoptosis pathway in allergic asthma.STUDY DESIGN AND METHODSIn vitro studies were conducted on human bronchial epithelial cells (BEAS-2B) treated with EB and human-recombinant DEK. Mass spectrometry analysis, RNA sequencing, molecular docking, and functional assays were used to assess the interactions and effects of EB, DEK, and ring finger protein 149 and 170 (RNF149 and RNF170). In vivo experiments involved a house dust mite-induced asthma model in mice and evaluation of airway inflammation, DEK expression, and PANoptosis markers.RESULTSIn vitro, EB could bind to DEK. RNF149 and RNF170 were identified as regulatory factors of DEK, polyubiquitinating the K349 site in the DEK coding DNA sequence region 270-350 through K48 linkages and leading to its degradation. RNA sequencing showed that DEK overexpression upregulated the expression of genes such as RIPK1, FADD, and Caspase 8. Treatment with DEK siRNA or EB reduced the activation of the RIPK1-PANoptosis pathway in BEAS-2B-DEK cells. In vivo, EB significantly reduced the levels of DEK in house dust mite-induced mice and alleviated pulmonary inflammatory cell infiltration, goblet cell hyperplasia, collagen fiber deposition, and eosinophil proportion in BALF. Knocking out the DEK gene reduced RIPK1-induced PANoptosis, and inhibited airway inflammation and cell apoptosis.CONCLUSIONEB promotes the degradation of DEK by RNF149 and RNF170, inhibits the RIPK1-PANoptosis pathway, and may effectively suppress asthma. EB may become a potential drug for treating airway inflammation in asthma.

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FADD

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