DEF6 expression and regulation in cancer, chronic inflammatory diseases and autoimmune diseases: A review

Def6 protein has been highly associated with autoimmune diseases and become one of risk gene in systemic lupus erythematosus (SLE) disease. Def6 deficiency is spontaneously affecting the development of systemic autoimmune disorder in mice as well as in human. Def6 or IRF-4- binding proteins (IBP) th...

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Bibliographic Details
Published in:Journal of International Dental and Medical Research
Main Author: Purwaningsih N.M.S.; Heah K.G.; Zhu H.-J.; Rosdy M.N.M.; Omar E.
Format: Article
Language:English
Published: University of Dicle 2020
Online Access:https://www.scopus.com/inward/record.uri?eid=2-s2.0-85085116659&partnerID=40&md5=b8d57972d1679d74a6ca50a08dd6d5fa
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Summary:Def6 protein has been highly associated with autoimmune diseases and become one of risk gene in systemic lupus erythematosus (SLE) disease. Def6 deficiency is spontaneously affecting the development of systemic autoimmune disorder in mice as well as in human. Def6 or IRF-4- binding proteins (IBP) that mostly found among lymph node and thymus are associated with cell survival and cell proliferation. Def6 protein as a novel biomarker has many important functions and roles in human immune system. Def6 is believed to be a potential therapeutic pharmacological target or/and potential drug for some malignancy diseases and pathological disorders. Current studies reveal Def6 expression and regulations not only are found in autoimmune diseases but also in human cancer and chronic inflammatory diseases. High expression of Def6 is correlated with invasive tumours and malignant stage of various cancers. This review article sums up Def6 expression and regulation in some diseases stated above. Collectively, this review article provides novel studies concerning Def6 as a protein, its correlation with other genes, its mechanism and its expression in some diseases, particularly in cancer, autoimmune diseases and chronic inflammatory diseases. © 2019 University of Dicle.
ISSN:1309100X