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Title: Regulatory mechanisms of hypoxia-inducible factor 1 activity: Two decades of knowledge
Authors: Koyasu, Sho  kyouindb  KAKEN_id
Kobayashi, Minoru  kyouindb  KAKEN_id  orcid https://orcid.org/0000-0003-3843-3584 (unconfirmed)
Goto, Yoko
Hiraoka, Masahiro
Harada, Hiroshi  kyouindb  KAKEN_id  orcid https://orcid.org/0000-0001-7507-3173 (unconfirmed)
Author's alias: 子安, 翔
小林, 稔
後藤, 容子
平岡, 眞寛
原田, 浩
Keywords: gene expression
hypoxia-inducible factor 1 (HIF-1)
molecular mechanism
tumor hypoxia
Issue Date: 3-Mar-2018
Publisher: Blackwell Publishing Ltd
Journal title: Cancer Science
Volume: 109
Issue: 3
Start page: 560
End page: 571
Abstract: Hypoxia‐inducible factor 1 (HIF‐1) is a transcriptional activator of various genes related to cellular adaptive responses to hypoxia. Dysfunctions in the regulatory systems of HIF‐1 activity have been implicated in the pathogenesis of various diseases including malignant tumors and, thus, elucidating the molecular mechanisms underlying the activation of HIF‐1 is eagerly desired for the development of novel anti‐cancer strategies. The importance of oxygen‐dependent and ubiquitin‐mediated proteolysis of the regulatory subunit of HIF‐1 (HIF‐1α) was first reported in 1997. Since then, accumulating evidence has shown that HIF‐1α may become stable and active even under normoxic conditions; for example, when disease‐associated genetic and functional alterations in some genes trigger the aberrant activation of HIF‐1 regardless of oxygen conditions. We herein review the last two decades of knowledge, since 1997, on the regulatory mechanisms of HIF‐1 activity from conventional oxygen‐ and proteolysis‐dependent mechanisms to up‐to‐the‐minute information on cancer‐associated genetic and functional alteration‐mediated mechanisms.
Rights: © 2017 The Authors. Cancer Science published by John Wiley & Sons Australia, Ltd on behalf of Japanese Cancer Association. This is an open access article under the terms of the Creative Commons Attribution‐NonCommercial License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited and is not used for commercial purposes.
URI: http://hdl.handle.net/2433/230435
DOI(Published Version): 10.1111/cas.13483
PubMed ID: 29285833
Appears in Collections:Journal Articles

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