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Women, autoimmunity, and cancer: a dangerous liaison between estrogen and activation-induced deaminase?
Why women are more susceptible to autoimmune diseases is not completely clear, but new data suggest that the hormone estrogen may play an important role. A new study now shows that estrogen activates the expression of activation-induced deaminase (AID), a protein that drives antibody diversification...
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Formato: | Texto |
Lenguaje: | English |
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The Rockefeller University Press
2009
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2626682/ https://www.ncbi.nlm.nih.gov/pubmed/19139165 http://dx.doi.org/10.1084/jem.20080086 |
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author | Maul, Robert W. Gearhart, Patricia J. |
author_facet | Maul, Robert W. Gearhart, Patricia J. |
author_sort | Maul, Robert W. |
collection | PubMed |
description | Why women are more susceptible to autoimmune diseases is not completely clear, but new data suggest that the hormone estrogen may play an important role. A new study now shows that estrogen activates the expression of activation-induced deaminase (AID), a protein that drives antibody diversification by deaminating cytosine in DNA to uracil. If estrogen increases the level of AID, increased mutations could transform benign antibodies into anti-self pariahs. AID might also contribute to cancer—particularly in breast tissue, which is highly responsive to estrogen—by introducing mutations and strand breaks into the genome. |
format | Text |
id | pubmed-2626682 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2009 |
publisher | The Rockefeller University Press |
record_format | MEDLINE/PubMed |
spelling | pubmed-26266822009-07-19 Women, autoimmunity, and cancer: a dangerous liaison between estrogen and activation-induced deaminase? Maul, Robert W. Gearhart, Patricia J. J Exp Med Commentaries Why women are more susceptible to autoimmune diseases is not completely clear, but new data suggest that the hormone estrogen may play an important role. A new study now shows that estrogen activates the expression of activation-induced deaminase (AID), a protein that drives antibody diversification by deaminating cytosine in DNA to uracil. If estrogen increases the level of AID, increased mutations could transform benign antibodies into anti-self pariahs. AID might also contribute to cancer—particularly in breast tissue, which is highly responsive to estrogen—by introducing mutations and strand breaks into the genome. The Rockefeller University Press 2009-01-19 /pmc/articles/PMC2626682/ /pubmed/19139165 http://dx.doi.org/10.1084/jem.20080086 Text en This article is distributed under the terms of an Attribution–Noncommercial–Share Alike–No Mirror Sites license for the first six months after the publication date (see http://www.jem.org/misc/terms.shtml). After six months it is available under a Creative Commons License (Attribution–Noncommercial–Share Alike 3.0 Unported license, as described at http://creativecommons.org/licenses/by-nc-sa/3.0/). |
spellingShingle | Commentaries Maul, Robert W. Gearhart, Patricia J. Women, autoimmunity, and cancer: a dangerous liaison between estrogen and activation-induced deaminase? |
title | Women, autoimmunity, and cancer: a dangerous liaison between estrogen and activation-induced deaminase? |
title_full | Women, autoimmunity, and cancer: a dangerous liaison between estrogen and activation-induced deaminase? |
title_fullStr | Women, autoimmunity, and cancer: a dangerous liaison between estrogen and activation-induced deaminase? |
title_full_unstemmed | Women, autoimmunity, and cancer: a dangerous liaison between estrogen and activation-induced deaminase? |
title_short | Women, autoimmunity, and cancer: a dangerous liaison between estrogen and activation-induced deaminase? |
title_sort | women, autoimmunity, and cancer: a dangerous liaison between estrogen and activation-induced deaminase? |
topic | Commentaries |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2626682/ https://www.ncbi.nlm.nih.gov/pubmed/19139165 http://dx.doi.org/10.1084/jem.20080086 |
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