{"id":541,"date":"2020-01-23T03:01:55","date_gmt":"2020-01-23T03:01:55","guid":{"rendered":"https:\/\/medicine.nus.edu.sg\/bch\/?post_type=faculty&#038;p=541"},"modified":"2026-04-01T16:24:15","modified_gmt":"2026-04-01T08:24:15","slug":"gan-yunn-hwen","status":"publish","type":"faculty","link":"https:\/\/medicine.nus.edu.sg\/bch\/faculty\/gan-yunn-hwen\/","title":{"rendered":"Gan Yunn Hwen"},"content":{"rendered":"<h3><span style=\"font-size: 18pt; color: #000000;\">Affiliations<\/span><\/h3>\n<p align=\"justify\"><span style=\"font-size: 14pt; color: #000000;\"><strong>Associate Professor<\/strong>, Department of Biochemistry, Yong Loo Lin School of Medicine, NUS.<\/span><br \/>\n<span style=\"font-size: 14pt; color: #000000;\"><strong>Co-Director<\/strong>, Infectious Diseases Translational Research Program, Yong Loo Lin School of Medicine, NUS.<\/span><br \/>\n<span style=\"font-size: 14pt; color: #000000;\"><strong>Assistant Dean<\/strong>, Equal Opportunities and Career Development, Yong Loo Lin School of Medicine, NUS.<\/span><\/p>\n<h3><\/h3>\n<h3><span style=\"font-size: 18pt; color: #000000;\">Biodata<\/span><\/h3>\n<p align=\"justify\"><span style=\"font-size: 14pt; color: #000000;\">Yunn-Hwen Gan graduated from Purdue University with a B.Sc. (Honours) in Molecular Biology and University of Wisconsin-Madison with a Ph.D. in medical microbiology and immunology. She is a world leading researcher in melioidosis, a disease primarily in the tropics caused by the bacterium <em>Burkholderia pseudomallei<\/em>. She established the first mucosal animal model in 2002 and had helped define the field by examining pathogen\u2019s virulence as well as the host immune response to the disease. Her lab discovered a regulatory cascade that coordinately controlled two bacterial secretion systems which are absolutely critical for bacterial virulence. Other seminal findings include the discovery that glutathione deficiency is the reason for increased disease risk to melioidosis for Type 2 diabetic patients.<\/span><\/p>\n<p align=\"justify\"><span style=\"font-size: 14pt; color: #000000;\">Her current research focuses on <em>Klebsiella<\/em> induced liver abscess, a prominent disease in Asia, particularly in regions of China, Taiwan, Hong Kong, Singapore and South Korea. Her work involves identifying bacterial virulence factors of hypervirulent <em>Klebsiella pneumoniae<\/em> responsible for causing liver abscess. Her team examines host and bacterial factors that affect gut colonization and translocation. Her recent works have identified the alarming trend of the convergence of multidrug resistance and hypervirulence in <em>K. pneumoniae<\/em> in Singapore\u2019s hospital settings. Her ongoing research investigates how antibiotic resistance genes on highly evolved and adapted plasmids dominant in clinical bacterial isolates are spreading among bacterial populations, and strategies to stop the spread.<\/span><\/p>\n<p align=\"justify\"><span style=\"font-size: 14pt; color: #000000;\">She has also established multidisciplinary collaborations with chemists, clinicians and computational biologists to examine novel strategies to treat antibiotic resistant <em>Enterobacteriaceae<\/em> bacteria. One of such strategies is to establish a synthetic commensal community of bacteria to be used as probiotics for decolonization from the gut. Another strategy is to partner with AI scientists to employ synergy testing of FDA-approved compounds, including those with no known antibacterial activity on their own, on multidrug resistant bacteria.<\/span><\/p>\n<h3 style=\"margin-top: 20px;\"><\/h3>\n<h3><span style=\"font-size: 18pt; color: #000000;\">Research Interest<\/span><\/h3>\n<ul class=\"outer-ul\">\n<li><span style=\"font-size: 14pt; color: #000000;\">Novel strategies for targeting multidrug resistant enteric bacteria.<\/span><\/li>\n<li><span style=\"font-size: 14pt; color: #000000;\">Multidrug resistance plasmid transmission in clinical Gram-negative bacteria.<\/span><\/li>\n<li><span style=\"font-size: 14pt; color: #000000;\">Bacterial sensing of host environment by two component sensor\/regulator systems.<\/span><\/li>\n<li><span style=\"font-size: 14pt; color: #000000;\">Identifying risk factors for <em>Klebsiella<\/em> induced liver abscess.<\/span><\/li>\n<li><span style=\"font-size: 14pt; color: #000000;\">The influence of microbiome on\u00a0<em>Klebsiella pneumoniae\u00a0<\/em>gut colonization<\/span><\/li>\n<\/ul>\n<h3 style=\"margin-top: 20px;\"><\/h3>\n<h3><span style=\"font-size: 18pt; color: #000000;\">Projects<\/span><\/h3>\n<p><span style=\"font-size: 18pt; color: #000000;\"><strong><span style=\"text-decoration: underline;\"><em>Klebsiella<\/em> Induced Liver Abscess (KLA)<\/span><\/strong><\/span><\/p>\n<p style=\"text-align: justify;\"><span style=\"font-size: 14pt; color: #000000;\">KLA is the single most important cause of monomicrobial liver abscess and its subsequent complications in many parts of Asia, including Singapore. We examine bacterial factors and the ensuing host immune responses in the encounter between hypervirulent and its mammalian host. It is believed that many infections initiate from bacteria colonized in the intestines as they translocate across the intestinal barrier and travel via the hepatic portal vein to the liver. We are interested in examining both bacterial and host factors at play at each stage of the infection, including during the colonization stage. We routinely use a hypervirulent strain isolated from a liver abscess patient designated as a reference strain, SGH10, for our investigations. Using murine colonization and infection models, as well as primary human intestinal organoids, we hope to understand when and how the bacteria transition from a gut colonizer to a potentially deadly pathogen.<\/span><\/p>\n<p><span style=\"font-size: 14pt; color: #000000;\"><img fetchpriority=\"high\" decoding=\"async\" src=\"https:\/\/medicine.nus.edu.sg\/bch\/wp-content\/uploads\/sites\/13\/2020\/01\/B-300x215.png\" alt=\"\" class=\"alignnone wp-image-2105\" width=\"504\" height=\"361\" srcset=\"https:\/\/medicine.nus.edu.sg\/bch\/wp-content\/uploads\/sites\/13\/2020\/01\/B-300x215.png 300w, https:\/\/medicine.nus.edu.sg\/bch\/wp-content\/uploads\/sites\/13\/2020\/01\/B-1024x734.png 1024w, https:\/\/medicine.nus.edu.sg\/bch\/wp-content\/uploads\/sites\/13\/2020\/01\/B-768x550.png 768w, https:\/\/medicine.nus.edu.sg\/bch\/wp-content\/uploads\/sites\/13\/2020\/01\/B-1536x1101.png 1536w, https:\/\/medicine.nus.edu.sg\/bch\/wp-content\/uploads\/sites\/13\/2020\/01\/B-2048x1468.png 2048w\" sizes=\"(max-width: 504px) 100vw, 504px\" \/><img decoding=\"async\" src=\"https:\/\/medicine.nus.edu.sg\/bch\/wp-content\/uploads\/sites\/13\/2020\/01\/A-300x216.png\" alt=\"\" class=\"alignnone wp-image-2104\" width=\"502\" height=\"361\" srcset=\"https:\/\/medicine.nus.edu.sg\/bch\/wp-content\/uploads\/sites\/13\/2020\/01\/A-300x216.png 300w, https:\/\/medicine.nus.edu.sg\/bch\/wp-content\/uploads\/sites\/13\/2020\/01\/A-1024x736.png 1024w, https:\/\/medicine.nus.edu.sg\/bch\/wp-content\/uploads\/sites\/13\/2020\/01\/A-768x552.png 768w, https:\/\/medicine.nus.edu.sg\/bch\/wp-content\/uploads\/sites\/13\/2020\/01\/A-1536x1104.png 1536w, https:\/\/medicine.nus.edu.sg\/bch\/wp-content\/uploads\/sites\/13\/2020\/01\/A-2048x1472.png 2048w\" sizes=\"(max-width: 502px) 100vw, 502px\" \/><\/span><\/p>\n<p style=\"text-align: justify;\"><span style=\"font-size: 14pt; color: #000000;\"><strong>Figure 1.<\/strong> Scanning Electron Microscope (SEM) images of SGH10 WT strain at 40,000X magnification (left) and SGH10\u0394<em>wcaJ<\/em> capsule mutant strain at 60,000X magnification (right). (Publication link : <a href=\"https:\/\/onlinelibrary.wiley.com\/doi\/full\/10.1111\/mmi.14447\" target=\"_blank\" rel=\"noreferrer noopener\" class=\"wixui-rich-text__text\">\ud83d\udd17<\/a>)<\/span><\/p>\n<p><img decoding=\"async\" src=\"https:\/\/medicine.nus.edu.sg\/bch\/wp-content\/uploads\/sites\/13\/2020\/01\/mbio.01297-23.f007-300x193.jpg\" alt=\"\" class=\"alignnone  wp-image-6285\" width=\"873\" height=\"562\" srcset=\"https:\/\/medicine.nus.edu.sg\/bch\/wp-content\/uploads\/sites\/13\/2020\/01\/mbio.01297-23.f007-300x193.jpg 300w, https:\/\/medicine.nus.edu.sg\/bch\/wp-content\/uploads\/sites\/13\/2020\/01\/mbio.01297-23.f007-1024x660.jpg 1024w, https:\/\/medicine.nus.edu.sg\/bch\/wp-content\/uploads\/sites\/13\/2020\/01\/mbio.01297-23.f007-768x495.jpg 768w, https:\/\/medicine.nus.edu.sg\/bch\/wp-content\/uploads\/sites\/13\/2020\/01\/mbio.01297-23.f007-1536x990.jpg 1536w, https:\/\/medicine.nus.edu.sg\/bch\/wp-content\/uploads\/sites\/13\/2020\/01\/mbio.01297-23.f007-2048x1320.jpg 2048w\" sizes=\"(max-width: 873px) 100vw, 873px\" \/><\/p>\n<p style=\"text-align: justify;\"><strong><span style=\"font-size: 14pt; color: #000000;\">Figure 2. <\/span><\/strong><span style=\"font-size: 14pt; color: #000000;\">Transcriptional phenotypic switch between T3F and capsule hypermucoviscosity in response to changing iron levels. (A) Low iron condition results in hypermucoid capsule production and repressed T3F, leading to low biofilm formation and cell adhesion. (B) Iron-rich condition results in expression of T3F and downregulation of capule mucoviscosity, leading to high biofilm formation and cell adhesion. (Publication link : <a href=\"https:\/\/journals.asm.org\/doi\/full\/10.1128\/mbio.01297-23\" target=\"_blank\" rel=\"noreferrer noopener\" class=\"wixui-rich-text__text\">\ud83d\udd17<\/a>)<\/span><\/p>\n<p><img loading=\"lazy\" decoding=\"async\" src=\"https:\/\/medicine.nus.edu.sg\/bch\/wp-content\/uploads\/sites\/13\/2020\/01\/image002-300x195.png\" alt=\"\" class=\"alignnone  wp-image-6287\" width=\"890\" height=\"578\" srcset=\"https:\/\/medicine.nus.edu.sg\/bch\/wp-content\/uploads\/sites\/13\/2020\/01\/image002-300x195.png 300w, https:\/\/medicine.nus.edu.sg\/bch\/wp-content\/uploads\/sites\/13\/2020\/01\/image002-1024x666.png 1024w, https:\/\/medicine.nus.edu.sg\/bch\/wp-content\/uploads\/sites\/13\/2020\/01\/image002-768x500.png 768w, https:\/\/medicine.nus.edu.sg\/bch\/wp-content\/uploads\/sites\/13\/2020\/01\/image002.png 1203w\" sizes=\"(max-width: 890px) 100vw, 890px\" \/><\/p>\n<p style=\"text-align: justify;\"><strong><span style=\"font-size: 14pt; color: #000000;\">Figure 3. <\/span><\/strong><span style=\"font-size: 14pt; color: #000000;\">Genomic Islands GIE492 and ICEKp10 enable hypervirulent\u00a0<em>K. pneumoniae<\/em> to kill several commensal bacterial taxa during interspecies interactions in the gut. Thus, acquisition of GIE492 and ICEKp10 could enable better carriage in host populations and explain the dominance of the CG23-I HvKp lineage. (Publication link : <a href=\"https:\/\/academic.oup.com\/ismej\/article\/18\/1\/wrae054\/7636998\" target=\"_blank\" rel=\"noreferrer noopener\" class=\"wixui-rich-text__text\">\ud83d\udd17<\/a>)<\/span><\/p>\n<p><span style=\"font-size: 18pt; color: #000000;\"><strong><span style=\"text-decoration: underline;\">Multidrug resistance plasmid transmission in\u00a0<em>Klebsiella pneumoniae<\/em><\/span><\/strong><\/span><\/p>\n<p style=\"text-align: justify;\"><span style=\"font-size: 14pt; color: #000000;\">We are interested in understanding the factors driving the transmission of carbapenem-resistance and multi-drug resistance plasmids in hospitals. We track plasmid and resistance genes dominance over time in a multi-centre collaboration, then apply molecular genetics to determine plasmid and bacterial host factors favouring spread and stability of carriage. In particular, we focus on the emergence of hypervirulent and carbapenem-resistant <em>K. pneumoniae<\/em> strains and aim to define factors and conditions leading to this convergence.<\/span><\/p>\n<p><span style=\"font-size: 14pt; color: #000000;\"><img loading=\"lazy\" decoding=\"async\" src=\"https:\/\/medicine.nus.edu.sg\/bch\/wp-content\/uploads\/sites\/13\/2020\/01\/EID_fig-1.png\" alt=\"\" class=\"alignnone wp-image-5265 size-full\" width=\"2281\" height=\"886\" srcset=\"https:\/\/medicine.nus.edu.sg\/bch\/wp-content\/uploads\/sites\/13\/2020\/01\/EID_fig-1.png 2281w, https:\/\/medicine.nus.edu.sg\/bch\/wp-content\/uploads\/sites\/13\/2020\/01\/EID_fig-1-300x117.png 300w, https:\/\/medicine.nus.edu.sg\/bch\/wp-content\/uploads\/sites\/13\/2020\/01\/EID_fig-1-1024x398.png 1024w, https:\/\/medicine.nus.edu.sg\/bch\/wp-content\/uploads\/sites\/13\/2020\/01\/EID_fig-1-768x298.png 768w, https:\/\/medicine.nus.edu.sg\/bch\/wp-content\/uploads\/sites\/13\/2020\/01\/EID_fig-1-1536x597.png 1536w, https:\/\/medicine.nus.edu.sg\/bch\/wp-content\/uploads\/sites\/13\/2020\/01\/EID_fig-1-2048x795.png 2048w\" sizes=\"(max-width: 2281px) 100vw, 2281px\" \/><\/span><\/p>\n<p style=\"text-align: justify;\"><span style=\"font-size: 14pt; color: #000000;\"><strong>Figure 4.<\/strong> Conjugation frequency of pKPC2 and pNDM1 among various\u00a0<span class=\"wixui-rich-text__text\"><em>Enterobacterales<\/em>\u00a0<\/span>donor-recipient pairs. (A) Conjugation frequency of pKPC2 and pNDM1 from\u00a0<em><span class=\"wixui-rich-text__text\">K. pneumoniae<\/span><\/em>\u00a0SGH10 plasmid donor strain to a panel of\u00a0<em><span class=\"wixui-rich-text__text\">Enterobacterales<\/span><\/em>\u00a0recipient strains; and B) from the panel of\u00a0<span class=\"wixui-rich-text__text\"><em>Enterobacterales<\/em><\/span>\u00a0plasmid donor strains to\u00a0<em><span class=\"wixui-rich-text__text\">K. pneumoniae<\/span><\/em>\u00a0SGH10 recipient strain. Each symbol represents 1 experimental replicate with a total of 12 replicates. Data points that are not seen on the graphs indicate no detectable transconjugant.\u00a0(Publication link : <a href=\"https:\/\/wwwnc.cdc.gov\/eid\/article\/28\/8\/21-2542_article\" target=\"_blank\" rel=\"noreferrer noopener\" class=\"wixui-rich-text__text\">\ud83d\udd17<\/a>)<\/span><\/p>\n<p><span style=\"font-size: 18pt; color: #000000;\"><strong><span style=\"text-decoration: underline;\">Novel strategies to target transmission of carbapenem-resistance in <em>Enterobacterales<\/em><\/span><\/strong><\/span><\/p>\n<div data-packed=\"true\" data-vertical-text=\"false\" class=\"txtNew\" id=\"comp-k9gsq0am\">\n<p class=\"font_8\" style=\"text-align: justify;\"><span style=\"font-size: 14pt; color: #000000;\">We engage in extensive collaborations with clinical colleagues, computational biologists, and chemists to develop strategies for combating carbapenem resistant <em>Enterobacterales <\/em>(CRE). Our efforts involve evaluating the efficacy and clinical potential of innovative synthetic antibacterial compounds and materials. Furthermore, we explore combinatorial therapy guided by AI platform to identify novel drug combinations capable of effectively eradicating CRE.<\/span><\/p>\n<\/div>\n<p><span style=\"font-size: 14pt; color: #000000;\"><img loading=\"lazy\" decoding=\"async\" src=\"https:\/\/medicine.nus.edu.sg\/bch\/wp-content\/uploads\/sites\/13\/2020\/01\/Untitled-1-1.png\" alt=\"\" class=\"alignnone wp-image-5266\" width=\"900\" height=\"586\" srcset=\"https:\/\/medicine.nus.edu.sg\/bch\/wp-content\/uploads\/sites\/13\/2020\/01\/Untitled-1-1.png 22498w, https:\/\/medicine.nus.edu.sg\/bch\/wp-content\/uploads\/sites\/13\/2020\/01\/Untitled-1-1-300x195.png 300w, https:\/\/medicine.nus.edu.sg\/bch\/wp-content\/uploads\/sites\/13\/2020\/01\/Untitled-1-1-1024x667.png 1024w, https:\/\/medicine.nus.edu.sg\/bch\/wp-content\/uploads\/sites\/13\/2020\/01\/Untitled-1-1-768x500.png 768w, https:\/\/medicine.nus.edu.sg\/bch\/wp-content\/uploads\/sites\/13\/2020\/01\/Untitled-1-1-1536x1001.png 1536w, https:\/\/medicine.nus.edu.sg\/bch\/wp-content\/uploads\/sites\/13\/2020\/01\/Untitled-1-1-2048x1335.png 2048w\" sizes=\"(max-width: 900px) 100vw, 900px\" \/><\/span><\/p>\n<p style=\"text-align: justify;\"><span style=\"font-size: 14pt; color: #000000;\"><strong>Figure 5.<\/strong> OIM1-6&#8217;s DNA binding properties and resulting DNA damage. (A) Flow cytometry analysis demonstrates picogreen displacement by OIM1-6 inside bacterial cytoplasm, indicating the DNA-binding properties of OIM1-6. Picogreen is a DNA binding dye with fluorescence level measured under Alexa Fluor 488 channel. (B) Confocal images showing the treatment of OIM1-6 leads to more foci formation in <em>E. coli<\/em> Gam-GFP strain as compared to the untreated cells. The hydrogen peroxide cells served as positive control with elevated level of foci formation. The presence of foci is indicative of double-stranded DNA breaks caused by the drug treatment. (Publication link : <a href=\"https:\/\/journals.asm.org\/doi\/epub\/10.1128\/aac.00355-23\" target=\"_blank\" rel=\"noreferrer noopener\" class=\"wixui-rich-text__text\">\ud83d\udd17<\/a>)<\/span><\/p>\n<p><img loading=\"lazy\" decoding=\"async\" src=\"https:\/\/medicine.nus.edu.sg\/bch\/wp-content\/uploads\/sites\/13\/2020\/01\/adtp202300332-fig-0001-m-1024x443.jpg\" alt=\"\" class=\"alignnone size-large wp-image-5929\" width=\"1200\" height=\"686\" \/><\/p>\n<p style=\"text-align: justify;\"><span style=\"font-size: 14pt; color: #000000;\"><strong>Figure 6.<\/strong> Workflow of the IDentif.AI-guided drug combinatorial study against CRE. Two clinical isolates from the most representative CRE species (hv<em>Kp<\/em>\u00a0ENT646 and\u00a0<em>E. coli<\/em>\u00a0C31) are investigated by IDentif.AI. The workflow begins by selecting 12 FDA-approved drugs, and they are individually assessed via dose-response experiment in vitro. Relevant concentration levels are selected. Subsequently, 155 OACD-designed combinations are experimentally validated, and the respective data are analyzed by IDentif.AI. Top combinations selected by the platform are comprehensively analyzed.\u00a0(Publication link : <a href=\"https:\/\/onlinelibrary.wiley.com\/doi\/10.1002\/adtp.202300332\" target=\"_blank\" rel=\"noreferrer noopener\" class=\"wixui-rich-text__text\">\ud83d\udd17<\/a>)<\/span><\/p>\n<div data-packed=\"true\" data-vertical-text=\"false\" class=\"txtNew\" id=\"comp-k9gsqc2v\">\n<p class=\"font_8\"><span style=\"font-size: 18pt; color: #000000;\"><strong><span style=\"text-decoration: underline;\">Interaction of\u00a0<em>Burkholderia pseudomallei<\/em>\u00a0with host cells<\/span><\/strong><\/span><\/p>\n<\/div>\n<div data-packed=\"true\" data-vertical-text=\"false\" class=\"txtNew\" id=\"comp-k9gsqf3s\">\n<p class=\"font_8\" style=\"text-align: justify;\"><span style=\"font-size: 14pt; color: #000000;\"><em>B. pseudomallei<\/em>\u00a0is unique among bacterial pathogens in its ability to fuse host cells into multinucleated giant cells (MNGCs). Fusion is dependent on bacterial intracellular motility through the polymerization of actin into \u201cactin comet tails\u201d and the Type 6 Secretion System (T6SS5). We discovered that the process of cell fusion results in genomic instability and formation of micronuclei. Host cells sense danger brought on by unnatural cell fusion and this then triggers the cGAS-STING innate immune signalling pathway that ultimately leads to autophagic cell death. This could be the body\u2019s defense against cellular transformation.<\/span><\/p>\n<p class=\"font_8\" style=\"text-align: justify;\"><span style=\"font-size: 14pt; color: #000000;\">One of the routes of infection is through breaks in skin, such as those experienced by farmers with exposure to soil.\u00a0 We also examine the interaction of the bacteria with primary keratinocytes and the response of the host at this encounter.<\/span><\/p>\n<\/div>\n<p><span style=\"font-size: 14pt; color: #000000;\"><img loading=\"lazy\" decoding=\"async\" src=\"https:\/\/medicine.nus.edu.sg\/bch\/wp-content\/uploads\/sites\/13\/2020\/01\/MNGC-1024x1005.png\" alt=\"\" class=\"alignnone wp-image-2106 size-large\" width=\"640\" height=\"628\" srcset=\"https:\/\/medicine.nus.edu.sg\/bch\/wp-content\/uploads\/sites\/13\/2020\/01\/MNGC-1024x1005.png 1024w, https:\/\/medicine.nus.edu.sg\/bch\/wp-content\/uploads\/sites\/13\/2020\/01\/MNGC-300x294.png 300w, https:\/\/medicine.nus.edu.sg\/bch\/wp-content\/uploads\/sites\/13\/2020\/01\/MNGC-768x754.png 768w, https:\/\/medicine.nus.edu.sg\/bch\/wp-content\/uploads\/sites\/13\/2020\/01\/MNGC-1536x1507.png 1536w, https:\/\/medicine.nus.edu.sg\/bch\/wp-content\/uploads\/sites\/13\/2020\/01\/MNGC-2048x2010.png 2048w\" sizes=\"(max-width: 640px) 100vw, 640px\" \/><\/span><\/p>\n<p style=\"text-align: justify;\"><span style=\"font-size: 14pt; color: #000000;\"><strong>Figure 7.<\/strong> MNGC formation in HepG2 liver epithelial cell. Bacteria (<em>Burkholderia spp.<\/em>)\u00a0is shown in\u00a0red, the cell periphery in<span class=\"color_33\">\u00a0green<\/span>\u00a0and the cell nuclei in\u00a0<span class=\"color_18\">blue<\/span>. (Publication link : <a href=\"https:\/\/www.pnas.org\/doi\/10.1073\/pnas.2006908117\" target=\"_blank\" rel=\"noreferrer noopener\" class=\"wixui-rich-text__text\">\ud83d\udd17<\/a>)<\/span><\/p>\n<div style=\"width: 640px;\" class=\"wp-video\"><video class=\"wp-video-shortcode\" id=\"video-541-1\" width=\"640\" height=\"360\" preload=\"metadata\" controls=\"controls\"><source type=\"video\/webm\" src=\"https:\/\/static-movie-usa.glencoesoftware.com\/webm\/10.1073\/628\/1d42b8919b5f6970a828721f24503e6331a0376c\/pnas.2006908117.sm01.webm?_=1\" \/><a href=\"https:\/\/static-movie-usa.glencoesoftware.com\/webm\/10.1073\/628\/1d42b8919b5f6970a828721f24503e6331a0376c\/pnas.2006908117.sm01.webm\">https:\/\/static-movie-usa.glencoesoftware.com\/webm\/10.1073\/628\/1d42b8919b5f6970a828721f24503e6331a0376c\/pnas.2006908117.sm01.webm<\/a><\/video><\/div>\n<p style=\"text-align: justify;\"><span style=\"font-size: 14pt; color: #000000;\"><strong>Movie 1.<\/strong> <em>B. thailandensis<\/em>\u00a0infected multinucleated giant cell containing highly condensed mitotic-like chromosomes. Cell rounds up, initiates cytokinesis but eventually abort the process. HepG2 cells were infected with mApple fluorescent\u00a0<em>B. thailandensis<\/em>\u00a0(in Red) and stained with CellMask plasma membrane dye (in Magenta) and Hoechst 33342 DNA dye (in Blue).<\/span><\/p>\n<h3 style=\"margin-top: 20px;\"><\/h3>\n<h3><span style=\"font-size: 18pt; color: #000000;\">Publications<\/span><\/h3>\n<ol class=\"font_8 wixui-rich-text__text\">\n<li class=\"font_8\" style=\"text-align: justify;\">\n<p class=\"font_8 wixui-rich-text__text\">Yong M, Low WW, Mishra S, Williams G, Mileto S, Lim C, Chwa C, Oo G, Cheam G, Chen Y, Chung The H, Pham TD, Lyras D, Gan YH. Differential gut transmission of IncP plasmid clades involving hypervirulent\u00a0<\/span><span class=\"wixui-rich-text__text\">Klebsiella pneumoniae<\/span><span>\u00a0reveals plasmid-specific ecological adaptation.\u00a0<span>\u00a0<\/span><strong><span class=\"wixui-rich-text__text\">Nat Commun.<\/span><\/strong><span>\u00a0<\/span> 2025. doi: 10.1038\/s41467-025-66413-4. <a href=\"https:\/\/www.nature.com\/articles\/s41467-025-66413-4\">\ud83d\udd17<\/a><\/span><\/li>\n<li class=\"font_8\" style=\"text-align: justify;\">\n<p class=\"font_8 wixui-rich-text__text\">Oo G, Low WW, Yong M, Stanton TD, Ayuni NN, Bifani P, Wyres KL, Gan YH. Anti-plasmid defense in hypervirulent Klebsiella pneumoniae involves Type I-like and Type IV restriction modification systems.<span>\u00a0<\/span><strong><span class=\"wixui-rich-text__text\">Emerg Microbes Infect.<\/span><\/strong><span>\u00a0<\/span>2025 Dec;14(1):2558877. doi: 10.1080\/22221751.2025.2558877. Epub 2025 Sep 22. PMID: 40916842; PMCID: PMC12456054. <span><a href=\"https:\/\/www.tandfonline.com\/doi\/full\/10.1080\/22221751.2025.2558877\">\ud83d\udd17<\/a><\/span><\/p>\n<\/li>\n<li class=\"font_8\" style=\"text-align: justify;\">\n<p class=\"font_8 wixui-rich-text__text\">Koh CH, Lambu MR, Tan C, Wei G, Kok ZY, Zhang K, Vu QHN, Panneerselvam M, Ooi YJ, Tan SH, Wang Z, Tatina MB, Ng JTY, Guo A, Tonanon P, Dang TT, Gan YH, Mu Y, Hammond PT, Chi YR, Webster RD, Pullarkat SA, Li Q, Greenberg EP, Gr\u00fcndling A, Pethe K, Chan-Park MB. Carbene formation as a mechanism for efficient intracellular uptake of cationic antimicrobial carbon acid polymers.\u00a0<strong><span class=\"wixui-rich-text__text\">Nat Commun.<\/span><\/strong><span> 2025 Jul 12;16(1):6460. doi: 10.1038\/s41467-025-61724-y. 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PMID: 20335533. \u00a0<a href=\"https:\/\/www.ncbi.nlm.nih.gov\/pubmed\/20335533\" target=\"_blank\" rel=\"noreferrer noopener\" class=\"wixui-rich-text__text\">\ud83d\udd17<\/a><\/span><\/p>\n<\/li>\n<li class=\"font_8\" style=\"text-align: justify;\">\n<p class=\"font_8 wixui-rich-text__text\"><span class=\"wixui-rich-text__text\">Lee YH, Chen Y, Ouyang X, Gan YH. Identification of tomato plant as a novel host model for<span>\u00a0<\/span><em>Burkholderia pseudomallei.<\/em><span>\u00a0<\/span><strong>BMC Microbiol.<\/strong><span>\u00a0<\/span>2010 Jan 29;10:28. doi: 10.1186\/1471-2180-10-28. PMID: 20109238; PMCID: PMC2823722. \u00a0<a href=\"https:\/\/www.ncbi.nlm.nih.gov\/pmc\/articles\/PMC2823722\/\" target=\"_blank\" rel=\"noreferrer noopener\" class=\"wixui-rich-text__text\">\ud83d\udd17<\/a><\/span><\/p>\n<\/li>\n<li class=\"font_8\" style=\"text-align: justify;\">\n<p class=\"font_8 wixui-rich-text__text\"><span class=\"wixui-rich-text__text\">Breitbach K, Sun GW, K\u00f6hler J, Eske K, Wongprompitak P, Tan G, Liu Y, Gan YH, Steinmetz I. Caspase-1 mediates resistance in murine melioidosis.<span>\u00a0<\/span><strong>Infect Immun.<\/strong><span>\u00a0<\/span>2009 Apr;77(4):1589-95. doi: 10.1128\/IAI.01257-08. Epub 2009 Jan 29. PMID: 19179418; PMCID: PMC2663179. \u00a0<a href=\"https:\/\/iai.asm.org\/content\/77\/4\/1589\" target=\"_blank\" rel=\"noreferrer noopener\" class=\"wixui-rich-text__text\">\ud83d\udd17<\/a><\/span><\/p>\n<\/li>\n<li class=\"font_8\" style=\"text-align: justify;\">\n<p class=\"font_8 wixui-rich-text__text\"><span class=\"wixui-rich-text__text\">Ye Z, Lee CM, Sun GW, Gan YH.<span>\u00a0<\/span><em>Burkholderia pseudomallei<\/em><span>\u00a0<\/span>infection of T cells leads to T-cell costimulation partially provided by flagellin.<span>\u00a0<\/span><strong>Infect Immun.<\/strong><span>\u00a0<\/span>2008 Jun;76(6):2541-50. doi: 10.1128\/IAI.01310-07. Epub 2008 Mar 17. PMID: 18347031; PMCID: PMC2423057. \u00a0<a href=\"https:\/\/iai.asm.org\/content\/76\/6\/2541\" target=\"_blank\" rel=\"noreferrer noopener\" class=\"wixui-rich-text__text\">\ud83d\udd17<\/a><\/span><\/p>\n<\/li>\n<li class=\"font_8\" style=\"text-align: justify;\">\n<p class=\"font_8 wixui-rich-text__text\"><span class=\"wixui-rich-text__text\">Hii CS, Sun GW, Goh JW, Lu J, Stevens MP, Gan YH. Interleukin-8 induction by<span>\u00a0<\/span><em>Burkholderia pseudomallei<\/em><span>\u00a0<\/span>can occur without Toll-like receptor signaling but requires a functional type III secretion system.<span>\u00a0<\/span><strong>J Infect Dis.<\/strong><span>\u00a0<\/span>2008 Jun 1;197(11):1537-47. doi: 10.1086\/587905. PMID: 18419546. \u00a0<a href=\"https:\/\/www.ncbi.nlm.nih.gov\/pubmed\/18419546\" target=\"_blank\" rel=\"noreferrer noopener\" class=\"wixui-rich-text__text\">\ud83d\udd17<\/a><\/span><\/p>\n<\/li>\n<li class=\"font_8\" style=\"text-align: justify;\">\n<p class=\"font_8 wixui-rich-text__text\"><span class=\"wixui-rich-text__text\">Ye Z, Gan YH. Flagellin contamination of recombinant heat shock protein 70 is responsible for its activity on T cells.<span>\u00a0<\/span><strong>J Biol Chem.<\/strong><span>\u00a0<\/span>2007 Feb 16;282(7):4479-4484. doi: 10.1074\/jbc.M606802200. Epub 2006 Dec 18. PMID: 17178717. \u00a0<a href=\"https:\/\/www.ncbi.nlm.nih.gov\/pubmed\/17178717\" target=\"_blank\" rel=\"noreferrer noopener\" class=\"wixui-rich-text__text\">\ud83d\udd17<\/a><\/span><\/p>\n<\/li>\n<li class=\"font_8\" style=\"text-align: justify;\">\n<p class=\"font_8 wixui-rich-text__text\"><span class=\"wixui-rich-text__text\">Koo GC, Gan YH. The innate interferon gamma response of BALB\/c and C57BL\/6 mice to<span>\u00a0<\/span><em>in vitro Burkholderia pseudomallei\u00a0<\/em>infection.<span>\u00a0<\/span><strong>BMC Immunol.<\/strong><span>\u00a0<\/span>2006 Aug 18;7:19. doi: 10.1186\/1471-2172-7-19. PMID: 16919160; PMCID: PMC1559720. \u00a0<a href=\"https:\/\/www.ncbi.nlm.nih.gov\/pubmed\/16919160\" target=\"_blank\" rel=\"noreferrer noopener\" class=\"wixui-rich-text__text\">\ud83d\udd17<\/a><\/span><\/p>\n<\/li>\n<li class=\"font_8\" style=\"text-align: justify;\">\n<p class=\"font_8 wixui-rich-text__text\"><span class=\"wixui-rich-text__text\">Gan YH. Interaction between<span>\u00a0<\/span><em>Burkholderia pseudomallei<\/em><span>\u00a0<\/span>and the host immune response: sleeping with the enemy?<span>\u00a0<\/span><strong>J Infect Dis.<\/strong><span>\u00a0<\/span>2005 Nov 15;192(10):1845-50. doi: 10.1086\/497382. Epub 2005 Oct 7. PMID: 16235187.\u00a0<a href=\"https:\/\/www.ncbi.nlm.nih.gov\/pubmed\/16235187\" target=\"_blank\" rel=\"noreferrer noopener\" class=\"wixui-rich-text__text\">\ud83d\udd17<\/a><\/span><\/p>\n<\/li>\n<li class=\"font_8\" style=\"text-align: justify;\">\n<p class=\"font_8 wixui-rich-text__text\"><span class=\"wixui-rich-text__text\">Sun GW, Lu J, Pervaiz S, Cao WP, Gan YH. Caspase-1 dependent macrophage death induced by<span>\u00a0<\/span><em>Burkholderia pseudomallei<\/em>.<span>\u00a0<\/span><strong>Cell Microbiol.<\/strong><span>\u00a0<\/span>2005 Oct;7(10):1447-58. doi: 10.1111\/j.1462-5822.2005.00569.x. PMID: 16153244. \u00a0<a href=\"https:\/\/www.ncbi.nlm.nih.gov\/pubmed\/16153244\" target=\"_blank\" rel=\"noreferrer noopener\" class=\"wixui-rich-text__text\">\ud83d\udd17<\/a><\/span><\/p>\n<\/li>\n<li class=\"font_8\" style=\"text-align: justify;\">\n<p class=\"font_8 wixui-rich-text__text\"><span class=\"wixui-rich-text__text\">Chen K, Sun GW, Chua KL, Gan YH. Modified virulence of antibiotic-induced<span>\u00a0<\/span><em>Burkholderia pseudomallei<\/em><span>\u00a0<\/span>filaments.<span>\u00a0<\/span><strong>Antimicrob Agents Chemother.<\/strong><span>\u00a0<\/span>2005 Mar;49(3):1002-9. doi: 10.1128\/AAC.49.3.1002-1009.2005. PMID: 15728895; PMCID: PMC549247. \u00a0<a href=\"https:\/\/aac.asm.org\/content\/49\/3\/1002\" target=\"_blank\" rel=\"noreferrer noopener\" class=\"wixui-rich-text__text\">\ud83d\udd17<\/a><\/span><\/p>\n<\/li>\n<li class=\"font_8\" style=\"text-align: justify;\">\n<p class=\"font_8 wixui-rich-text__text\"><span class=\"wixui-rich-text__text\">Chua KL, Chan YY, Gan YH. Flagella are virulence determinants of<span>\u00a0<\/span><em>Burkholderia pseudomallei<\/em>.<strong>\u00a0Infect Immun.<\/strong><span>\u00a0<\/span>2003 Apr;71(4):1622-9. doi: 10.1128\/IAI.71.4.1622-1629.2003. PMID: 12654773; PMCID: PMC152022. \u00a0<a href=\"https:\/\/www.ncbi.nlm.nih.gov\/pubmed\/12654773\" target=\"_blank\" rel=\"noreferrer noopener\" class=\"wixui-rich-text__text\">\ud83d\udd17<\/a><\/span><\/p>\n<\/li>\n<li class=\"font_8\" style=\"text-align: justify;\">\n<p class=\"font_8 wixui-rich-text__text\"><span class=\"wixui-rich-text__text\">Gan YH, Chua KL, Chua HH, Liu B, Hii CS, Chong HL, Tan P. Characterization of<span>\u00a0<\/span><em>Burkholderia pseudomallei\u00a0<\/em>infection and identification of novel virulence factors using a<span>\u00a0<\/span><em>Caenorhabditis elegans<\/em><span>\u00a0<\/span>host system.<span>\u00a0<\/span><strong>Mol Microbiol.<\/strong><span>\u00a0<\/span>2002 Jun;44(5):1185-97. doi: 10.1046\/j.1365-2958.2002.02957.x. PMID: 12068805.\u00a0<a href=\"https:\/\/www.ncbi.nlm.nih.gov\/pubmed\/12068805\" target=\"_blank\" rel=\"noreferrer noopener\" class=\"wixui-rich-text__text\">\ud83d\udd17<\/a><\/span><\/p>\n<\/li>\n<li class=\"font_8\" style=\"text-align: justify;\">\n<p class=\"font_8 wixui-rich-text__text\"><span class=\"wixui-rich-text__text\">Liu B, Koo GC, Yap EH, Chua KL, Gan YH. Model of differential susceptibility to mucosal<span>\u00a0<\/span><em>Burkholderia pseudomallei<\/em><span>\u00a0<\/span>infection.<span>\u00a0<\/span><strong>Infect Immun.<\/strong><span>\u00a0<\/span>2002 Feb;70(2):504-11. doi: 10.1128\/IAI.70.2.504-511.2002. PMID: 11796576; PMCID: PMC127661. \u00a0<a href=\"https:\/\/www.ncbi.nlm.nih.gov\/pubmed\/11796576\" target=\"_blank\" rel=\"noreferrer noopener\" class=\"wixui-rich-text__text\">\ud83d\udd17<\/a><\/span><\/p>\n<\/li>\n<\/ol>\n<ol><\/ol>\n","protected":false},"featured_media":427,"parent":0,"menu_order":8,"template":"","faculty_category":[12,58],"class_list":["post-541","faculty","type-faculty","status-publish","has-post-thumbnail","hentry","faculty_category-academic-faculty","faculty_category-academic-faculty-academic-faculty"],"acf":[],"yoast_head":"<!-- This site is optimized with the Yoast SEO plugin v26.4 - https:\/\/yoast.com\/wordpress\/plugins\/seo\/ -->\n<title>Gan Yunn Hwen - Department of Biochemistry \u2013 School of Medicine, National University of Singapore<\/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:\/\/medicine.nus.edu.sg\/bch\/faculty\/gan-yunn-hwen\/\" \/>\n<meta property=\"og:locale\" content=\"en_US\" \/>\n<meta property=\"og:type\" content=\"article\" \/>\n<meta property=\"og:title\" content=\"Gan Yunn Hwen - Department of Biochemistry \u2013 School of Medicine, National University of Singapore\" \/>\n<meta property=\"og:description\" content=\"Affiliations Associate Professor, Department of Biochemistry, Yong Loo Lin School of Medicine, NUS. 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