FAIM : an antagonist of Fas-killing and beyond
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 tis...
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sg-ntu-dr.10356-1422512023-02-28T17:01:19Z FAIM : an antagonist of Fas-killing and beyond Huo, Jianxin Xu, Shengli Lam, Kong-Peng School of Biological Sciences Bioprocessing Technology Institute, A*STAR Science::Biological sciences FAIM B Cells 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. ASTAR (Agency for Sci., Tech. and Research, S’pore) Published version 2020-06-18T01:22:47Z 2020-06-18T01:22:47Z 2019 Journal Article Huo, J., Xu, S., & Lam, K.-P. (2019). FAIM : an antagonist of Fas-killing and beyond. Cells, 8(6), 541-. doi:10.3390/cells8060541 2073-4409 https://hdl.handle.net/10356/142251 10.3390/cells8060541 31167518 6 8 en Cells © 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 (http://creativecommons.org/licenses/by/4.0/). application/pdf |
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Science::Biological sciences FAIM B Cells Huo, Jianxin Xu, Shengli Lam, Kong-Peng FAIM : an antagonist of Fas-killing and beyond |
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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. |
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School of Biological Sciences |
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School of Biological Sciences Huo, Jianxin Xu, Shengli Lam, Kong-Peng |
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Article |
author |
Huo, Jianxin Xu, Shengli Lam, Kong-Peng |
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Huo, Jianxin |
title |
FAIM : an antagonist of Fas-killing and beyond |
title_short |
FAIM : an antagonist of Fas-killing and beyond |
title_full |
FAIM : an antagonist of Fas-killing and beyond |
title_fullStr |
FAIM : an antagonist of Fas-killing and beyond |
title_full_unstemmed |
FAIM : an antagonist of Fas-killing and beyond |
title_sort |
faim : an antagonist of fas-killing and beyond |
publishDate |
2020 |
url |
https://hdl.handle.net/10356/142251 |
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1759858349455704064 |