| Literature DB >> 28523428 |
Chon-Kit Chou1,2, Chin-Ju Tang2, Han-Lin Chou2, Chun-Yen Liu2, Ming-Chong Ng2, Yu-Ting Chang2, Shyng-Shiou F Yuan3, Eing-Mei Tsai4, Chien-Chih Chiu5,6,7,8.
Abstract
Gli-similar 3 (Glis3) belongs to a Glis subfamily of Krüppel-like zinc-finger transcription factors characterized to regulate a set of downstream targets essential for cellular functions, including pancreatic development, β-cell maturation and maintenance, and insulin production. Examination of the DNA-binding domain of Glis3 reveals that this domain contains a repeated cysteine 2/histidine 2 (Cys2/His2) zinc-finger motif in the central region where the recognized DNA sequence binds. The loss of the production of pancreatic hormones, such as insulin 1 and 2, is linked to the down-regulation of β cells-related genes and promotes the apoptotic death of β cells found in mutant Glis3. Although accumulating studies converge on the Glis3 functioning in β cells, recently, there have been developments in the field of Glis3 using knockdown/mutant mice to better understand the role of Glis3 in diseases. The Glis3 mutant mice have been characterized for their propensity to develop congenital hypothyroidism, polycystic kidney disease, and some types of cancer. In this review, we attempt to comprehensively summarize the knowledge of Glis3, including its structure and general function in cells. We also collected and organized the academic achievements related to the possible mechanisms of Glis3-related diseases.Entities:
Keywords: Cancer; Congenital hypothyroidism; Cys2/His2 zinc-finger domains; Diabetes mellitus; Glis3; Polycystic kidney disease
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Year: 2017 PMID: 28523428 DOI: 10.1007/s00005-017-0470-x
Source DB: PubMed Journal: Arch Immunol Ther Exp (Warsz) ISSN: 0004-069X Impact factor: 4.291