{"id":3,"date":"2014-05-23T19:56:56","date_gmt":"2014-05-23T19:56:56","guid":{"rendered":"https:\/\/lipsick.su.domains\/?page_id=2"},"modified":"2024-07-18T20:28:23","modified_gmt":"2024-07-18T20:28:23","slug":"sample-page","status":"publish","type":"page","link":"https:\/\/lipsick.su.domains\/","title":{"rendered":"Overview"},"content":{"rendered":"<p style=\"text-align: left;\">Cancer is caused by mutations in oncogenes and tumor suppressor genes.\u00a0 Mutations are changes in the DNA sequence that may alter gene function.\u00a0 Gain-of-function mutations can activate oncogenes, whereas loss-of-function mutations can inactivate tumor suppressor genes.\u00a0 Our laboratory studies the Myb oncogene family that is mutated in human cancers of blood cells (leukemia), brain, breast, and salivary gland.\u00a0 The proteins encoded by Myb genes bind to DNA and regulate the expression of other genes that control cell division, differentiation, and cell death.\u00a0 The Myb proteins interact with a highly conserved multi-protein complex called the MuvB core.\u00a0 The same complex also interacts with proteins of the Rb tumor suppressor family and the E2F transcription factor family.\u00a0 Work from our laboratory has shown that Myb acts in opposition to Rb-E2F to epigenetically regulate gene expression.<\/p>\n<p><img loading=\"lazy\" decoding=\"async\" class=\"wp-image-441 alignnone\" src=\"http:\/\/lipsick.su.domains\/wp-content\/uploads\/2014\/05\/mitosis1.jpg\" alt=\"mitosis1\" width=\"224\" height=\"307\" \/><a href=\"http:\/\/lipsick.su.domains\/wp-content\/uploads\/2014\/05\/fly-myb-worm-lin9-lin52-model.jpg\"><img loading=\"lazy\" decoding=\"async\" class=\" size-medium wp-image-889 alignnone\" src=\"http:\/\/lipsick.su.domains\/wp-content\/uploads\/2014\/05\/fly-myb-worm-lin9-lin52-model-273x300.jpg\" alt=\"fly myb worm lin9 lin52 model\" width=\"273\" height=\"300\" srcset=\"https:\/\/lipsick.su.domains\/wp-content\/uploads\/2014\/05\/fly-myb-worm-lin9-lin52-model-273x300.jpg 273w, https:\/\/lipsick.su.domains\/wp-content\/uploads\/2014\/05\/fly-myb-worm-lin9-lin52-model.jpg 401w\" sizes=\"auto, (max-width: 273px) 100vw, 273px\" \/><\/a><\/p>\n<p><em>Left: Abnormal mitosis in a Drosophila Myb null mutant.<\/em><br \/>\n<em> DNA (blue), condensed chromatin (magenta), and microtubules (green). [<a href=\"https:\/\/www.pnas.org\/content\/99\/11\/7438.long\">Manak, et al, PNAS, 2002<\/a>; <a href=\"https:\/\/pubmed.ncbi.nlm.nih.gov\/17450131\/\">Manak, et al, Nature Cell Biology, 2007<\/a>]<br \/>\n<\/em><\/p>\n<p><em>Right: Model of the MuvB-interacting domain of Drosophila melanogaster Myb protein binding to the Myb-interacting domains of C elegans Lin9 and Lin52.\u00a0 Amino acids that are required for binding in vitro and biological activity in vivo are underlined.\u00a0 The nematode C elegans lost its own animal-type Myb gene and protein over 500 million years ago.\u00a0 This model is based on a crystallographic structure of the homologous domains of human proteins: B-Myb, Lin9, and Lin52. The model is consistent with in vitro biochemistry and in vivo genetic studies [<a href=\"https:\/\/www.pnas.org\/content\/115\/40\/10016.long\">Guiley, et al, PNAS, 2018<\/a>; <a href=\"https:\/\/bio.biologists.org\/content\/9\/5\/bio051508\">Vorster, et al, Biology Open, 2020<\/a>]<\/em><\/p>\n<p>The work described in these webpages was funded by research grants from the <a href=\"https:\/\/www.nih.gov\/\">National Institutes of Health<\/a>.<\/p>\n","protected":false},"excerpt":{"rendered":"<p>Cancer is caused by mutations in oncogenes and tumor suppressor genes.\u00a0 Mutations are changes in the DNA sequence that may alter gene function.\u00a0 Gain-of-function mutations can activate oncogenes, whereas loss-of-function mutations can inactivate tumor suppressor genes.\u00a0 Our laboratory studies the Myb oncogene family that is mutated in human cancers of blood cells (leukemia), brain, breast, &hellip; <a href=\"https:\/\/lipsick.su.domains\/\" class=\"more-link\">Continue reading <span class=\"screen-reader-text\">Overview<\/span> <span class=\"meta-nav\">&rarr;<\/span><\/a><\/p>\n","protected":false},"author":1,"featured_media":0,"parent":0,"menu_order":0,"comment_status":"closed","ping_status":"closed","template":"","meta":{"footnotes":""},"class_list":["post-3","page","type-page","status-publish","hentry"],"_links":{"self":[{"href":"https:\/\/lipsick.su.domains\/index.php?rest_route=\/wp\/v2\/pages\/3","targetHints":{"allow":["GET"]}}],"collection":[{"href":"https:\/\/lipsick.su.domains\/index.php?rest_route=\/wp\/v2\/pages"}],"about":[{"href":"https:\/\/lipsick.su.domains\/index.php?rest_route=\/wp\/v2\/types\/page"}],"author":[{"embeddable":true,"href":"https:\/\/lipsick.su.domains\/index.php?rest_route=\/wp\/v2\/users\/1"}],"replies":[{"embeddable":true,"href":"https:\/\/lipsick.su.domains\/index.php?rest_route=%2Fwp%2Fv2%2Fcomments&post=3"}],"version-history":[{"count":41,"href":"https:\/\/lipsick.su.domains\/index.php?rest_route=\/wp\/v2\/pages\/3\/revisions"}],"predecessor-version":[{"id":995,"href":"https:\/\/lipsick.su.domains\/index.php?rest_route=\/wp\/v2\/pages\/3\/revisions\/995"}],"wp:attachment":[{"href":"https:\/\/lipsick.su.domains\/index.php?rest_route=%2Fwp%2Fv2%2Fmedia&parent=3"}],"curies":[{"name":"wp","href":"https:\/\/api.w.org\/{rel}","templated":true}]}}