{"id":477,"date":"2016-03-30T16:49:36","date_gmt":"2016-03-30T16:49:36","guid":{"rendered":"https:\/\/sites.rutgers.edu\/wei-xing-zong\/?p=477"},"modified":"2025-09-25T14:52:06","modified_gmt":"2025-09-25T14:52:06","slug":"rutgers-scientists-identify-a-defective-protein-causing-damage-and-serious-illness","status":"publish","type":"post","link":"https:\/\/sites.rutgers.edu\/wei-xing-zong\/rutgers-scientists-identify-a-defective-protein-causing-damage-and-serious-illness\/","title":{"rendered":"Rutgers Scientists Identify a Defective Protein Causing Damage and Serious Illness"},"content":{"rendered":"

Heart and Liver Disease Linked to Antioxidant Shutdown<\/strong>
\nBy Robin Lally<\/p>\n

A protein that should help fight infection and keep us healthy may be targeted for treating devastating illnesses like heart and liver disease, according to a new Rutgers study.<\/p>\n

Rutgers scientists have discovered that a protein which is supposed to prevent cell damage is not working efficiently in laboratory mice with heart and liver disease.<\/figcaption><\/figure>\n

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In research published in\u00a0Molecular Cell<\/em>,<\/a>\u00a0Rutgers scientists discovered that a protein (p62), which is supposed to act as an antioxidant to prevent cell damage, was not working efficiently in laboratory mice with liver and heart disease that mimicked these conditions in humans.<\/p>\n

This caused oxidative stress \u2013 too much oxygen that damages healthy cells \u2013 and allowed the release of harmful molecules, called free radicals, which resulted in serious illness. One of the body\u2019s first lines of defense, the cells’ antioxidant response system is supposed to prevent these harmful invaders from causing a domino effect and damaging other cells.<\/p>\n

Wei-Xing-Zong, a professor in the Department of Chemical Biology in the\u00a0Ernest Mario School of Pharmacy\u00a0<\/a>and leader of the study, said the damage occurred because another protein, (TRIM21) \u2013 which should activate the body\u2019s response system to fight off bacteria and virus \u2013 did the opposite in these seriously ill mice and shut the antioxidant protein down, preventing it from doing its job.<\/p>\n

\u201cThe (TRIM21) protein exists naturally in our body; without it, we could easily succumb to other manageable infections,\u201d said Zong. \u201cBut this study has shown us that when we run into severe pathological conditions like heart and liver disease it would be more beneficial to inhibit the TRIM21 protein because it is preventing the cell from protecting itself against damage.\u201d<\/p>\n

In the Rutgers study, Zong and lead author Ji-An Pan, a scientist in his laboratory, looked at liver and heart damage in laboratory mice and found that the mice in which the TRIM21 gene was inactivated suffered little heart or liver damage when put through the same laboratory procedures used to produce tissue damage in mice with the gene.<\/p>\n

\u201cThe hearts and livers of the mice without the TRIM21 gene seemed to be well protected which was opposite of the mice with the gene,\u201d said Zong. \u201cWe believe this evidence is a truly important step to determining how to effectively treat these conditions in humans.\u201d<\/p>\n

Heart disease is the leading cause of death in the United States while one in 10 Americans has some form of liver disease. Rutgers scientists said this study indicates how critical it is to carefully control oxidative stress \u2013 which can also lead to neurodegenerative diseases like Parkinson\u2019s and Alzheimer\u2019s, chronic fatigue syndrome, cancers and gene mutations as well as liver and heart disease \u2013 so that cell or tissue damage doesn\u2019t occur.<\/p>\n

They believe that drugs could be developed that would reduce or stop the activity of the protein that is causing damage and preventing the antioxidant response from occurring.<\/p>\n

\u201cThese exciting new results suggest that drugs that reduce the activity of TRIM21 could be highly effective new tools for the treatment of conditions that are driven by high oxidative stress, including liver and heart disease,\u201d Zong said.<\/p>\n

\n

For media inquiries, contact Robin Lally at 848-932-0557 or rlally@ucm.rutgers.edu<\/p>\n<\/div>\n<\/div>\n<\/div>\n<\/section>\n<\/div>\n<\/div>\n<\/div>\n<\/div>\n<\/div>\n<\/div>\n<\/div>\n<\/div>\n

 <\/p>\n","protected":false},"excerpt":{"rendered":"

Heart and Liver Disease Linked to Antioxidant Shutdown By Robin Lally A protein that should help fight infection and keep us healthy may be targeted for treating devastating illnesses like … Read More<\/a><\/p>\n","protected":false},"author":3273,"featured_media":0,"comment_status":"closed","ping_status":"closed","sticky":false,"template":"","format":"standard","meta":{"_acf_changed":false,"footnotes":""},"categories":[10],"tags":[],"class_list":["post-477","post","type-post","status-publish","format-standard","hentry","category-research-discoveries"],"acf":[],"yoast_head":"\nRutgers Scientists Identify a Defective Protein Causing Damage and Serious Illness - Wei-Xing Zong Laboratory<\/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:\/\/sites.rutgers.edu\/wei-xing-zong\/rutgers-scientists-identify-a-defective-protein-causing-damage-and-serious-illness\/\" \/>\n<meta property=\"og:locale\" content=\"en_US\" \/>\n<meta property=\"og:type\" content=\"article\" \/>\n<meta property=\"og:title\" content=\"Rutgers Scientists Identify a Defective Protein Causing Damage and Serious Illness - 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Clinical data also indicate a strong correlation between defective ammonia clearance and liver cancer. We are studying the hypothesis that defective ammonia clearance is a risk factor and plays a major role in liver cancer development. To do this, we will modulate the expression of several ammonia-clearance enzymes and test the effect in mouse liver cancer models. We will also study how oncogenes such as beta-catenin regulate the expression of these enzymes including glutamine synthetase and urea cycle enzymes. 2. Novel tumor suppressors in B-cell lymphoma We study several novel potential tumor suppressor genes in B-cell lymphoma. Via a CRISPR\/Cas9 screen in an interleukin 3 (IL3)-dependent pro-B cell line Ba\/F3, we have identified a number of genes whose deletion promotes B-cell oncogenic transformation. We are currently focusing on three genes that are localized to human chromosome 6q, namely OSTM1, ZBTB24, and SLC35A1. 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