Cellular Dynamics of Fas-Associated Death Domain in the Regulation of Cancer and Inflammation

被引:8
|
作者
Ranjan, Kishu [1 ]
Pathak, Chandramani [2 ]
机构
[1] Yale Univ, Sch Med, Dept Pathol, New Haven, CT 06511 USA
[2] MGM Inst Hlth Sci, MGM Sch Biomed Sci, Navi Mumbai 410209, Maharashtra, India
关键词
cancer; FADD; apoptosis; RIP kinases; autophagy; NF-kappa B; inflammation; therapy; NF-KAPPA-B; TUMOR-NECROSIS-FACTOR; FADD GENE-TRANSFER; GLIOMAS IN-VITRO; KINASE RIP; C-FLIP; NUCLEAR-LOCALIZATION; CASPASE-8; ACTIVATION; PROGRAMMED NECROSIS; SIGNALING PATHWAY;
D O I
10.3390/ijms25063228
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Fas-associated death domain (FADD) is an adaptor protein that predominantly transduces the apoptosis signal from the death receptor (DR) to activate caspases, leading to the initiation of apoptotic signaling and the coordinated removal of damaged, infected, or unwanted cells. In addition to its apoptotic functions, FADD is involved in signaling pathways related to autophagy, cell proliferation, necroptosis, and cellular senescence, indicating its versatile role in cell survival and proliferation. The subcellular localization and intracellular expression of FADD play a crucial role in determining its functional outcomes, thereby highlighting the importance of spatiotemporal mechanisms and regulation. Furthermore, FADD has emerged as a key regulator of inflammatory signaling, contributing to immune responses and cellular homeostasis. This review provides a comprehensive summary and analysis of the cellular dynamics of FADD in regulating programmed cell death and inflammation through distinct molecular mechanisms associated with various signaling pathways.
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页数:23
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