{"id":3969,"date":"2011-11-29T16:50:00","date_gmt":"2011-11-29T21:50:00","guid":{"rendered":"https:\/\/www.med.unc.edu\/biochem\/sancar-lab-featured-on-in-this-issue-of-pnas-published-on-november-15-2011\/"},"modified":"2024-12-04T11:43:25","modified_gmt":"2024-12-04T16:43:25","slug":"sancar-lab-featured-on-in-this-issue-of-pnas-published-on-november-15-2011","status":"publish","type":"post","link":"https:\/\/www.med.unc.edu\/biochem\/news\/sancar-lab-featured-on-in-this-issue-of-pnas-published-on-november-15-2011\/","title":{"rendered":"Sancar lab featured on &#8220;In This Issue&#8221; of PNAS, published on November 15, 2011"},"content":{"rendered":"<div>\n<p class=\"lead\">Exposure to UV radiation triggers DNA lesions that can lead to skin cancer, the most common type of cancer in the United States. Previous studies in mice have shown that levels of a protein called XPA, involved in repairing UV-induced DNA lesions, waxes and wanes with the time of day. Shobhan Gaddameedhi et al. found that the protein\u2019s level and activity in mouse skin cells are at their lowest at 4 AM and their highest at 4PM.<\/p>\n<div class=\"image-section\">\n<figure class=\"thumbnail wp-caption alignright\"><img loading=\"lazy\" decoding=\"async\" class=\"size-medium wp-image-3970\" src=\"https:\/\/www.med.unc.edu\/biochem\/wp-content\/uploads\/sites\/795\/2018\/07\/sancar-lab-featured-on-in-this-issue-of-pnas-published-on-november-15-2011-image2-294x300.jpeg\" alt=\"image2\" width=\"300\" height=\"200\" \/><figcaption class=\"caption wp-caption-text\">Circadian control of skin cancer. Image courtesy of Marian Miller (University of Cincinnati, Cincinnati, OH). Upper left quadrant: Hourtide by Edward Henry Potthast, 1920; Lower left quadrant: Sleeping Woman by Felix Valloton, 1899.<\/figcaption><\/figure>\n<\/div>\n<div>\n<hr \/>\n<p><b> Title: <\/b><a class=\"external-link\" href=\"http:\/\/www.pnas.org\/content\/108\/46\/18567.full.pdf+html\"><b>Time of UV exposure might influence skin cancer onset<\/b><\/a><\/p>\n<p style=\"margin: 0.25em 0pt 0.85em;line-height: 1.5em;color: #333333;letter-spacing: normal;text-indent: 0px;text-transform: none;background-color: #ffffff\"><b>Authors: <\/b>Shobhan Gaddameedhi, Christopher P. Selby, William K. Kaufmann, Robert C. Smart, and Aziz Sancar<\/p>\n<p style=\"margin: 0.25em 0pt 0.85em;line-height: 1.5em;color: #333333;letter-spacing: normal;text-indent: 0px;text-transform: none;background-color: #ffffff\"><b>Journal<\/b>: Proceedings of the National Academy of Sciences<\/p>\n<p><b>Issue: <\/b><span class=\"Apple-converted-space\">November 15<\/span>, 2011<b> \u2013 <\/b><span class=\"Apple-converted-space\">vol. <\/span>286, no. 46, 18567-18568<\/p>\n<p style=\"text-align: justify\"><b>About the Article:<\/b> The authors exposed two groups of mice to UV radiation\u2014one at 4 AM and the other at 4 PM\u2014and monitored the onset of skin cancer. Mice irradiated when the repair activity was at its lowest developed tumors much faster and at fivefold higher frequency compared with mice exposed to UV when the protein\u2019s repair function was at full throttle. When the authors repeated the experiment in a strain of mice lacking two key components of the circadian clock, the time of UV exposure tracked neither the protein\u2019s repair activity nor the onset of skin cancer, suggesting that circadian control of the XPA protein might influence skin cancer rates. Because mouse and human circadian clocks are similar, the time of UV exposure might likewise determine its cancer-causing potential in people, according to the authors.<\/p>\n<p style=\"text-align: justify\"><b>Group Page:<\/b> <a href=\"https:\/\/sancarlab.unc.edu\/\">Sancar Lab<\/a><\/p>\n<p style=\"text-align: justify\"><a class=\"external-link\" href=\"http:\/\/www.pnas.org\/content\/108\/46\/18567.full.pdf+html\"><img decoding=\"async\" class=\"image-inline\" src=\"resolveuid\/5250be9ed0d41887494379d2d9858996\/@@images\/image\/preview\" \/><\/a><\/p>\n<\/div>\n<\/div>\n<div id=\"simple-translate\" class=\"simple-translate-system-theme\">\n<div>\n<div class=\"simple-translate-button isShow\" style=\"height: 22px;width: 22px;top: 722px;left: 110px\"><\/div>\n<div class=\"simple-translate-panel \" style=\"width: 300px;height: 200px;top: 0px;left: 0px;font-size: 13px\">\n<div class=\"simple-translate-result-wrapper\" style=\"overflow: hidden\">\n<div class=\"simple-translate-move\"><\/div>\n<div class=\"simple-translate-result-contents\">\n<p class=\"simple-translate-result\" dir=\"auto\">\n<p class=\"simple-translate-candidate\" dir=\"auto\">\n<\/div>\n<\/div>\n<\/div>\n<\/div>\n<\/div>\n","protected":false},"excerpt":{"rendered":"<p><!-- description --> <\/p>\n<p class='lead'>Exposure to UV radiation triggers DNA lesions that can lead to skin cancer, the most common type of cancer in the United States. Previous studies in mice have shown that levels of a protein called XPA, involved in repairing UV-induced DNA lesions, waxes and wanes with the time of day. Shobhan Gaddameedhi et al. found that the protein&#8217;s level and activity in mouse skin cells are at their lowest at 4 AM and their highest at 4PM.<\/p>\n","protected":false},"author":4454,"featured_media":3970,"comment_status":"closed","ping_status":"closed","sticky":false,"template":"","format":"standard","meta":{"_acf_changed":false,"layout":"","cellInformation":"","apiCallInformation":"","footnotes":"","_links_to":"","_links_to_target":""},"categories":[2],"tags":[10,16,4,17],"class_list":["post-3969","post","type-post","status-publish","format-standard","has-post-thumbnail","hentry","category-news","tag-news_faculty","tag-news_2011","tag-recent-news","tag-sancar_news","odd"],"acf":[],"yoast_head":"<!-- This site is optimized with the Yoast SEO plugin v26.8 - https:\/\/yoast.com\/product\/yoast-seo-wordpress\/ -->\n<title>Sancar lab featured on &quot;In This Issue&quot; of PNAS, published on November 15, 2011 | Biochemistry and Biophysics<\/title>\n<meta name=\"robots\" content=\"index, follow, max-snippet:-1, max-image-preview:large, max-video-preview:-1\" \/>\n<link rel=\"canonical\" href=\"https:\/\/www.med.unc.edu\/biochem\/news\/sancar-lab-featured-on-in-this-issue-of-pnas-published-on-november-15-2011\/\" \/>\n<meta property=\"og:locale\" content=\"en_US\" \/>\n<meta property=\"og:type\" content=\"article\" \/>\n<meta property=\"og:title\" content=\"Sancar lab featured on &quot;In This Issue&quot; of PNAS, published on November 15, 2011 | Biochemistry and Biophysics\" \/>\n<meta property=\"og:description\" content=\"Exposure to UV radiation triggers DNA lesions that can lead to skin cancer, the most common type of cancer in the United States. Previous studies in mice have shown that levels of a protein called XPA, involved in repairing UV-induced DNA lesions, waxes and wanes with the time of day. 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