{"id":138,"date":"2023-10-16T08:48:52","date_gmt":"2023-10-16T07:48:52","guid":{"rendered":"https:\/\/ccb.flaus.net\/ccb2\/?page_id=138"},"modified":"2026-04-10T22:45:22","modified_gmt":"2026-04-10T21:45:22","slug":"lowndes","status":"publish","type":"page","link":"https:\/\/chromosome.ie\/gae\/groups\/lowndes\/","title":{"rendered":"Noel Lowndes"},"content":{"rendered":"<div class=\"wp-block-image\">\n<figure class=\"alignleft size-full is-resized\"><img loading=\"lazy\" decoding=\"async\" width=\"882\" height=\"882\" src=\"https:\/\/chromosome.ie\/wp-content\/uploads\/2024\/04\/noel-lowndes-headshot-edited.png\" alt=\"\" class=\"wp-image-1276\" style=\"width:150px\" srcset=\"https:\/\/chromosome.ie\/wp-content\/uploads\/2024\/04\/noel-lowndes-headshot-edited.png 882w, https:\/\/chromosome.ie\/wp-content\/uploads\/2024\/04\/noel-lowndes-headshot-edited-300x300.png 300w, https:\/\/chromosome.ie\/wp-content\/uploads\/2024\/04\/noel-lowndes-headshot-edited-150x150.png 150w, https:\/\/chromosome.ie\/wp-content\/uploads\/2024\/04\/noel-lowndes-headshot-edited-768x768.png 768w, https:\/\/chromosome.ie\/wp-content\/uploads\/2024\/04\/noel-lowndes-headshot-edited-600x600.png 600w\" sizes=\"auto, (max-width: 882px) 100vw, 882px\" \/><\/figure>\n<\/div>\n\n\n<p><strong>Prof Noel Lowndes<\/strong><br>Established Professor of Biochemistry<br>Director of the CCB<br>SFI Future Frontiers &amp; EMBO Member<br>noel.lowndes@universityofgalway.ie<\/p>\n\n\n\n<hr class=\"wp-block-separator has-alpha-channel-opacity is-style-wide\"\/>\n\n\n\n<p><\/p>\n\n\n\n<h4 class=\"wp-block-heading\">Research interests<\/h4>\n\n\n\n<ul class=\"wp-block-list\">\n<li>Role of phosphatidylinositol 3-kinase like kinases (PIKKs) in genome stability<\/li>\n\n\n\n<li>Kinesins &amp; 53BP1-dependent DNA double strand break repair<\/li>\n\n\n\n<li>Zinc finger protein roles in DNA double strand break signalling &amp; repair<\/li>\n\n\n\n<li>Regulation of cytokinetic abscission by ATR<\/li>\n<\/ul>\n\n\n\n<h4 class=\"wp-block-heading\">Research overview<\/h4>\n\n\n\n<p class=\"has-text-align-justify\">Pathways required to maintain genome stability are potently tumour suppressive, while genome instability is a hallmark of cancer. Our research aims to elucidate novel mechanisms controlling genome stability. While our focus is on fundamental cell biology, future translational studies may ultimately have clinical impact. We utilise genome editing, proteomics, <em>in vitro<\/em> biochemistry and microscopy to identify and dissect novel genome stability factors. Our principle models are established transformed and immortalised human cell lines (e.g. HCT293, HeLa, U2OS, hTERT-RPE1 cells). In addition, we use primary animal fibroblasts (e.g. mouse, bat).<\/p>\n\n\n\n<h4 class=\"wp-block-heading\">Keywords<\/h4>\n\n\n\n<p>ATM, ATR, abscission, checkpoints, DNA repair, kinesins, 53BP1<\/p>\n\n\n\n<h4 class=\"wp-block-heading\">Selected Figures<\/h4>\n\n\n\n<div class=\"wp-block-cb-carousel cb-single-slide\" data-slick=\"{&quot;slidesToShow&quot;:1,&quot;slidesToScroll&quot;:1,&quot;speed&quot;:300,&quot;arrows&quot;:true,&quot;dots&quot;:true,&quot;autoplay&quot;:false,&quot;autoplaySpeed&quot;:3000,&quot;infinite&quot;:true,&quot;responsive&quot;:[{&quot;breakpoint&quot;:769,&quot;settings&quot;:{&quot;slidesToShow&quot;:1,&quot;slidesToScroll&quot;:1}}]}\">\n<div class=\"wp-block-cb-slide\">\n<figure class=\"wp-block-image size-full caption-align-center\"><img loading=\"lazy\" decoding=\"async\" width=\"913\" height=\"502\" src=\"https:\/\/chromosome.ie\/wp-content\/uploads\/2024\/03\/TIM-snip.png\" alt=\"\" class=\"wp-image-630\" srcset=\"https:\/\/chromosome.ie\/wp-content\/uploads\/2024\/03\/TIM-snip.png 913w, https:\/\/chromosome.ie\/wp-content\/uploads\/2024\/03\/TIM-snip-300x165.png 300w, https:\/\/chromosome.ie\/wp-content\/uploads\/2024\/03\/TIM-snip-768x422.png 768w, https:\/\/chromosome.ie\/wp-content\/uploads\/2024\/03\/TIM-snip-600x330.png 600w\" sizes=\"auto, (max-width: 913px) 100vw, 913px\" \/><figcaption class=\"wp-element-caption\">Characterisation of the binding surface on the Tudor domain of 53BP1 that interacts with a novel Tudor-interacting motif (TIM) in the nuclear kinesin, KIF18B. Residue W1495 (purple), which separates the known pocket for binding Histone H4K20me2 from the shallower pocket that binds KIF18B-TIM, is required to bind both . The silver stained gel on the left is an SDS-PAGE analysis of an in vitro binding assay using purified recombinant Flag-tagged 53BP1 Tudor domain (WT and mutants, as indicated) with biotinylated H4K20me2 or KIF18B-TIM peptides. Residues D1521 and Y1502 (in orange) and C1525 and S1497\/S1496 (in blue) are specific to H4K20me2 and TIM, respectively. <a href=\"https:\/\/pubmed.ncbi.nlm.nih.gov\/34192545\/\" target=\"_blank\" rel=\"noreferrer noopener\">[Source]<\/a><\/figcaption><\/figure>\n<\/div>\n\n\n\n<div class=\"wp-block-cb-slide\">\n<figure class=\"wp-block-image size-full\"><img loading=\"lazy\" decoding=\"async\" width=\"900\" height=\"344\" src=\"https:\/\/chromosome.ie\/wp-content\/uploads\/2024\/03\/ESCRT-snip.png\" alt=\"\" class=\"wp-image-615\" srcset=\"https:\/\/chromosome.ie\/wp-content\/uploads\/2024\/03\/ESCRT-snip.png 900w, https:\/\/chromosome.ie\/wp-content\/uploads\/2024\/03\/ESCRT-snip-300x115.png 300w, https:\/\/chromosome.ie\/wp-content\/uploads\/2024\/03\/ESCRT-snip-768x294.png 768w, https:\/\/chromosome.ie\/wp-content\/uploads\/2024\/03\/ESCRT-snip-600x229.png 600w\" sizes=\"auto, (max-width: 900px) 100vw, 900px\" \/><figcaption class=\"wp-element-caption\">Cytokinetic abscission occurs when the membrane remodelling ESCRT-III complex re-localises from the cytokinetic midbody to abscission sites on one side (\u201c1o cut\u201d) and then the other (\u201c2o cut\u201d) side of the midbody. The critical ESCRT-III component for abscission is CHMP4B. While ATR localises to the midbody, specifically during late cytokinesis, it does not localise to the  sites of abscission. ATR has a regulatory role, rather than in abscission <em><strong>per se<\/strong><\/em>. <a href=\"https:\/\/pubmed.ncbi.nlm.nih.gov\/35754741\/\" target=\"_blank\" rel=\"noreferrer noopener\">[Source]<\/a><\/figcaption><\/figure>\n<\/div>\n\n\n\n<div class=\"wp-block-cb-slide\">\n<figure class=\"wp-block-image size-full\"><img loading=\"lazy\" decoding=\"async\" width=\"913\" height=\"316\" src=\"https:\/\/chromosome.ie\/wp-content\/uploads\/2024\/03\/ATR-ATRIP-snip.png\" alt=\"\" class=\"wp-image-631\" srcset=\"https:\/\/chromosome.ie\/wp-content\/uploads\/2024\/03\/ATR-ATRIP-snip.png 913w, https:\/\/chromosome.ie\/wp-content\/uploads\/2024\/03\/ATR-ATRIP-snip-300x104.png 300w, https:\/\/chromosome.ie\/wp-content\/uploads\/2024\/03\/ATR-ATRIP-snip-768x266.png 768w, https:\/\/chromosome.ie\/wp-content\/uploads\/2024\/03\/ATR-ATRIP-snip-600x208.png 600w\" sizes=\"auto, (max-width: 913px) 100vw, 913px\" \/><figcaption class=\"wp-element-caption\">A four year old non-Seckel patient presenting at the Cleveland Clinic (Ohio, USA) with developmental delays, autism and acute leukemia was determined to be a compound ATR heterozygote inheriting a known Seckel mutation from his father (intron 2 c.151+4A&gt;G) and a novel missense mutation in the ATR allele inherited from his mother (c.140 A&gt;T; D47V). Molecular Dynamic simulations (with Leif Eriksson, University of Gothenberg, Sweden) indicate the loss of a salt bridge between ATR (in green) and ATRIP (in blue). The ATR-D47V mutation disrupts helix-coil transitions resulting in a less dynamic ATR N-terminal structure that interacts less efficiently with ATRIP resulting in reduced ATR activity <\/figcaption><\/figure>\n<\/div>\n<\/div>\n\n\n\n<div class=\"wp-block-columns is-layout-flex wp-container-core-columns-is-layout-9d6595d7 wp-block-columns-is-layout-flex\">\n<div class=\"wp-block-column is-layout-flow wp-block-column-is-layout-flow\">\n<h4 class=\"wp-block-heading\">Key Research techniques<\/h4>\n\n\n\n<ul class=\"wp-block-list\">\n<li>Genome editing<\/li>\n\n\n\n<li>Protein biochemistry &amp; proteomics<\/li>\n\n\n\n<li>DNA damage &amp; cell cycle assays<\/li>\n\n\n\n<li>Fluorescence &amp; expansion microscopy<\/li>\n<\/ul>\n<\/div>\n\n\n\n<div class=\"wp-block-column is-layout-flow wp-block-column-is-layout-flow\">\n<h4 class=\"wp-block-heading\">Lab Members<\/h4>\n\n\n\n<ul class=\"wp-block-list\">\n<li>Dr Ilze Skujina (Post-Doc)<\/li>\n\n\n\n<li>Dr Sabrinna Crowley (Post Doc)<\/li>\n\n\n\n<li>Peng Wu (PhD)<\/li>\n\n\n\n<li>Anna-Marie Meaney (PhD)<\/li>\n\n\n\n<li>Zaid Abu Diak (PhD)<\/li>\n<\/ul>\n\n\n\n<p><\/p>\n<\/div>\n<\/div>\n\n\n\n<p class=\"has-white-color has-text-color has-link-color wp-elements-acb05b5a90d57f0ce99f91c0137563fc\" style=\"font-size:4px\"><\/p>\n\n\n\n<h4 class=\"wp-block-heading\">Mentoring\/Hosting<\/h4>\n\n\n<div class=\"wp-block-image\">\n<figure class=\"alignleft size-full is-resized\"><img loading=\"lazy\" decoding=\"async\" width=\"391\" height=\"391\" src=\"https:\/\/chromosome.ie\/wp-content\/uploads\/2024\/04\/janna-luessing-edited.png\" alt=\"\" class=\"wp-image-1287\" style=\"aspect-ratio:1;object-fit:cover;width:150px\" srcset=\"https:\/\/chromosome.ie\/wp-content\/uploads\/2024\/04\/janna-luessing-edited.png 391w, https:\/\/chromosome.ie\/wp-content\/uploads\/2024\/04\/janna-luessing-edited-300x300.png 300w, https:\/\/chromosome.ie\/wp-content\/uploads\/2024\/04\/janna-luessing-edited-150x150.png 150w\" sizes=\"auto, (max-width: 391px) 100vw, 391px\" \/><\/figure>\n<\/div>\n\n\n<p><a href=\"https:\/\/chromosome.ie\/groups\/lowndes\/luessing\/\"><strong>Dr Janna Luessing<\/strong><\/a><br>Senior Researcher<br>SFI-IRC Pathway Programme<br>janna.luessing@universityofgalway.ie<\/p>\n\n\n\n<p class=\"has-white-color has-text-color has-link-color wp-elements-e693951c8d471257006de1dc6d0e0dec\">.<\/p>\n\n\n\n<h4 class=\"wp-block-heading\">Selected publications<\/h4>\n\n\n\n<ul class=\"wp-block-list\">\n<li><a href=\"https:\/\/pubmed.ncbi.nlm.nih.gov\/34192545\/\" target=\"_blank\" rel=\"noreferrer noopener\">The nuclear kinesin KIF18B promotes 53BP1-mediated DNA double-strand break repair<\/a><\/li>\n\n\n\n<li><a href=\"https:\/\/pubmed.ncbi.nlm.nih.gov\/27655732\/\" target=\"_blank\" rel=\"noreferrer noopener\">A role for the p53 tumour suppressor in regulating the balance between homologous recombination and non-homologous end joining<\/a><\/li>\n\n\n\n<li><a href=\"https:\/\/pubmed.ncbi.nlm.nih.gov\/24268773\/\" target=\"_blank\" rel=\"noreferrer noopener\">ATR activates the S-M checkpoint during unperturbed growth to ensure sufficient replication prior to mitotic onset<\/a><\/li>\n\n\n\n<li><a href=\"https:\/\/pubmed.ncbi.nlm.nih.gov\/22961695\/\" target=\"_blank\" rel=\"noreferrer noopener\">Multiple facets of the DNA damage response contribute to the radioresistance of mouse mesenchymal stromal cell lines<\/a><\/li>\n\n\n\n<li><a href=\"https:\/\/pubmed.ncbi.nlm.nih.gov\/11511366\/\" target=\"_blank\" rel=\"noreferrer noopener\">Budding yeast Rad9 is an ATP-dependent Rad53 activating machine<\/a><\/li>\n<\/ul>\n\n\n\n<h4 class=\"wp-block-heading\">Most Recent Publications<\/h4>\n\n\n<ul class=\"wp-block-rss\"><li class='wp-block-rss__item'><div class='wp-block-rss__item-title'><a href='https:\/\/pubmed.ncbi.nlm.nih.gov\/41778705\/?utm_source=WordPress&#038;utm_medium=rss&#038;utm_campaign=pubmed-2&#038;utm_content=1DK1DQN9MQ-Pev5LL3ddTJG_yK_tBe12HKIeR4Hu3Mhdo8CkJJ&#038;fc=20231019070343&#038;ff=20260423104927&#038;v=2.19.0.post6+133c1fe'>The Multifaceted Role of Rad9 in the DNA Damage Response of Saccharomyces cerevisiae<\/a><\/div><\/li><li class='wp-block-rss__item'><div class='wp-block-rss__item-title'><a href='https:\/\/pubmed.ncbi.nlm.nih.gov\/39693380\/?utm_source=WordPress&#038;utm_medium=rss&#038;utm_campaign=pubmed-2&#038;utm_content=1DK1DQN9MQ-Pev5LL3ddTJG_yK_tBe12HKIeR4Hu3Mhdo8CkJJ&#038;fc=20231019070343&#038;ff=20260423104927&#038;v=2.19.0.post6+133c1fe'>Correction: Regulation of the DNA Damage Response and Gene Expression by the Dot1L Histone Methyltransferase and the 53Bp1 Tumour Suppressor<\/a><\/div><\/li><li class='wp-block-rss__item'><div class='wp-block-rss__item-title'><a href='https:\/\/pubmed.ncbi.nlm.nih.gov\/36200807\/?utm_source=WordPress&#038;utm_medium=rss&#038;utm_campaign=pubmed-2&#038;utm_content=1DK1DQN9MQ-Pev5LL3ddTJG_yK_tBe12HKIeR4Hu3Mhdo8CkJJ&#038;fc=20231019070343&#038;ff=20260423104927&#038;v=2.19.0.post6+133c1fe'>DDX17 is required for efficient DSB repair at DNA:RNA hybrid deficient loci<\/a><\/div><\/li><\/ul>\n\n\n<h4 class=\"wp-block-heading\">Quick Links<\/h4>\n\n\n\n<div class=\"wp-block-columns is-layout-flex wp-container-core-columns-is-layout-9d6595d7 wp-block-columns-is-layout-flex\">\n<div class=\"wp-block-column is-layout-flow wp-block-column-is-layout-flow\">\n<p><a href=\"https:\/\/www.universityofgalway.ie\/our-research\/people\/biological-chemical-sciences\/noellowndes\/\" target=\"_blank\" rel=\"noreferrer noopener\">University Profile<\/a><\/p>\n<\/div>\n\n\n\n<div class=\"wp-block-column is-layout-flow wp-block-column-is-layout-flow\">\n<p class=\"has-text-align-center\"><a href=\"https:\/\/pubmed.ncbi.nlm.nih.gov\/?term=Lowndes+NF&amp;cauthor_id=27655732\" target=\"_blank\" rel=\"noreferrer noopener\">PubMed<\/a><\/p>\n<\/div>\n\n\n\n<div class=\"wp-block-column is-layout-flow wp-block-column-is-layout-flow\">\n<p class=\"has-text-align-right\"><a href=\"https:\/\/scholar.google.com\/citations?user=5FRU7T4AAAAJ&amp;hl=en\" target=\"_blank\" rel=\"noreferrer noopener\">Google Scholar<\/a><\/p>\n<\/div>\n<\/div>\n\n\n\n<h4 class=\"wp-block-heading\">Get in Touch!<\/h4>\n\n\n\n<div class=\"wp-block-group\"><div class=\"wp-block-group__inner-container is-layout-constrained wp-block-group-is-layout-constrained\">\n<p>noel.lowndes@universityofgalway.ie<\/p>\n<\/div><\/div>\n","protected":false},"excerpt":{"rendered":"<p>Prof Noel LowndesEstablished Professor of BiochemistryDirector of the CCBSFI Future Frontiers &amp; EMBO Membernoel.lowndes@universityofgalway.ie Research interests Research overview Pathways required to maintain genome stability are potently tumour suppressive, while genome instability is a hallmark of cancer. Our research aims to&#8230; <a class=\"more-link\" href=\"https:\/\/chromosome.ie\/gae\/groups\/lowndes\/\">Continue Reading &rarr;<\/a><\/p>","protected":false},"author":1,"featured_media":0,"parent":7,"menu_order":0,"comment_status":"closed","ping_status":"closed","template":"","meta":{"_editorskit_title_hidden":false,"_editorskit_reading_time":0,"_editorskit_is_block_options_detached":false,"_editorskit_block_options_position":"{}","_eb_attr":"","_monsterinsights_skip_tracking":false,"_monsterinsights_sitenote_active":false,"_monsterinsights_sitenote_note":"","_monsterinsights_sitenote_category":0,"footnotes":""},"categories":[3],"tags":[],"class_list":["post-138","page","type-page","status-publish","hentry","category-groups"],"_links":{"self":[{"href":"https:\/\/chromosome.ie\/gae\/wp-json\/wp\/v2\/pages\/138","targetHints":{"allow":["GET"]}}],"collection":[{"href":"https:\/\/chromosome.ie\/gae\/wp-json\/wp\/v2\/pages"}],"about":[{"href":"https:\/\/chromosome.ie\/gae\/wp-json\/wp\/v2\/types\/page"}],"author":[{"embeddable":true,"href":"https:\/\/chromosome.ie\/gae\/wp-json\/wp\/v2\/users\/1"}],"replies":[{"embeddable":true,"href":"https:\/\/chromosome.ie\/gae\/wp-json\/wp\/v2\/comments?post=138"}],"version-history":[{"count":63,"href":"https:\/\/chromosome.ie\/gae\/wp-json\/wp\/v2\/pages\/138\/revisions"}],"predecessor-version":[{"id":2189,"href":"https:\/\/chromosome.ie\/gae\/wp-json\/wp\/v2\/pages\/138\/revisions\/2189"}],"up":[{"embeddable":true,"href":"https:\/\/chromosome.ie\/gae\/wp-json\/wp\/v2\/pages\/7"}],"wp:attachment":[{"href":"https:\/\/chromosome.ie\/gae\/wp-json\/wp\/v2\/media?parent=138"}],"wp:term":[{"taxonomy":"category","embeddable":true,"href":"https:\/\/chromosome.ie\/gae\/wp-json\/wp\/v2\/categories?post=138"},{"taxonomy":"post_tag","embeddable":true,"href":"https:\/\/chromosome.ie\/gae\/wp-json\/wp\/v2\/tags?post=138"}],"curies":[{"name":"wp","href":"https:\/\/api.w.org\/{rel}","templated":true}]}}