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Focal Point of Fanconi Anemia Signaling
Among human genetic diseases, Fanconi Anemia (FA) tops all with its largest number of health complications in nearly all human organ systems, suggesting the significant roles played by FA genes in the maintenance of human health. With the accumulated research on FA, the encoded protein products by F...
Autores principales: | , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
MDPI
2021
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8657418/ https://www.ncbi.nlm.nih.gov/pubmed/34884777 http://dx.doi.org/10.3390/ijms222312976 |
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author | Zhan, Sudong Siu, Jolene Wang, Zhanwei Yu, Herbert Bezabeh, Tedros Deng, Youping Du, Wei Fei, Peiwen |
author_facet | Zhan, Sudong Siu, Jolene Wang, Zhanwei Yu, Herbert Bezabeh, Tedros Deng, Youping Du, Wei Fei, Peiwen |
author_sort | Zhan, Sudong |
collection | PubMed |
description | Among human genetic diseases, Fanconi Anemia (FA) tops all with its largest number of health complications in nearly all human organ systems, suggesting the significant roles played by FA genes in the maintenance of human health. With the accumulated research on FA, the encoded protein products by FA genes have been building up to the biggest cell defense signaling network, composed of not only 22+ FA proteins but also ATM, ATR, and many other non-FA proteins. The FA D2 group protein (FANCD2) and its paralog form the focal point of FA signaling to converge the effects of its upstream players in response to a variety of cellular insults and simultaneously with downstream players to protect humans from contracting diseases, including aging and cancer. In this review, we update and discuss how the FA signaling crucially eases cellular stresses through understanding its focal point. |
format | Online Article Text |
id | pubmed-8657418 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2021 |
publisher | MDPI |
record_format | MEDLINE/PubMed |
spelling | pubmed-86574182021-12-10 Focal Point of Fanconi Anemia Signaling Zhan, Sudong Siu, Jolene Wang, Zhanwei Yu, Herbert Bezabeh, Tedros Deng, Youping Du, Wei Fei, Peiwen Int J Mol Sci Review Among human genetic diseases, Fanconi Anemia (FA) tops all with its largest number of health complications in nearly all human organ systems, suggesting the significant roles played by FA genes in the maintenance of human health. With the accumulated research on FA, the encoded protein products by FA genes have been building up to the biggest cell defense signaling network, composed of not only 22+ FA proteins but also ATM, ATR, and many other non-FA proteins. The FA D2 group protein (FANCD2) and its paralog form the focal point of FA signaling to converge the effects of its upstream players in response to a variety of cellular insults and simultaneously with downstream players to protect humans from contracting diseases, including aging and cancer. In this review, we update and discuss how the FA signaling crucially eases cellular stresses through understanding its focal point. MDPI 2021-11-30 /pmc/articles/PMC8657418/ /pubmed/34884777 http://dx.doi.org/10.3390/ijms222312976 Text en © 2021 by the authors. https://creativecommons.org/licenses/by/4.0/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 (https://creativecommons.org/licenses/by/4.0/). |
spellingShingle | Review Zhan, Sudong Siu, Jolene Wang, Zhanwei Yu, Herbert Bezabeh, Tedros Deng, Youping Du, Wei Fei, Peiwen Focal Point of Fanconi Anemia Signaling |
title | Focal Point of Fanconi Anemia Signaling |
title_full | Focal Point of Fanconi Anemia Signaling |
title_fullStr | Focal Point of Fanconi Anemia Signaling |
title_full_unstemmed | Focal Point of Fanconi Anemia Signaling |
title_short | Focal Point of Fanconi Anemia Signaling |
title_sort | focal point of fanconi anemia signaling |
topic | Review |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8657418/ https://www.ncbi.nlm.nih.gov/pubmed/34884777 http://dx.doi.org/10.3390/ijms222312976 |
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