Please use this identifier to cite or link to this item:
Title: FAIM : an antagonist of Fas-killing and beyond
Authors: Huo, Jianxin
Xu, Shengli
Lam, Kong-Peng
Keywords: Science::Biological sciences
Issue Date: 2019
Source: Huo, J., Xu, S., & Lam, K.-P. (2019). FAIM : an antagonist of Fas-killing and beyond. Cells, 8(6), 541-. doi:10.3390/cells8060541
Journal: Cells 
Abstract: Fas Apoptosis Inhibitory Molecule (FAIM) is an anti-apoptotic protein that is up-regulated in B cell receptor (BCR)-activated B cells and confers upon them resistance to Fas-mediated cell death. Faim has two alternatively spliced isoforms, with the short isoform ubiquitously expressed in various tissues and the long isoform mainly found in the nervous tissues. FAIM is evolutionarily conserved but does not share any significant primary sequence homology with any known protein. The function of FAIM has been extensively studied in the past 20 years, with its primary role being ascribed to be anti-apoptotic. In addition, several other functions of FAIM were also discovered in different physiological and pathological conditions, such as cell growth, metabolism, Alzheimer’s disease and tumorigenesis. However, the detailed molecular mechanisms underlying FAIM’s role in these conditions remain unknown. In this review, we summarize comprehensively the functions of FAIM in these different contexts and discuss its potential as a diagnostic, prognostic or therapeutic target.
ISSN: 2073-4409
DOI: 10.3390/cells8060541
Rights: © 2019 The Author(s). Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (
Fulltext Permission: open
Fulltext Availability: With Fulltext
Appears in Collections:SBS Journal Articles

Files in This Item:
File Description SizeFormat 
FAIM An Antagonist of Fas-Killing and Beyond.pdf833.36 kBAdobe PDFThumbnail

Citations 20

Updated on Mar 18, 2023

Web of ScienceTM
Citations 20

Updated on Mar 17, 2023

Page view(s)

Updated on Mar 20, 2023

Download(s) 50

Updated on Mar 20, 2023

Google ScholarTM




Items in DR-NTU are protected by copyright, with all rights reserved, unless otherwise indicated.