The Potential Role of Krüppel-Like Zinc-Finger Protein Glis3 in Genetic Diseases and Cancers
| Autor: | Eing-Mei Tsai, Ming-Chong Ng, Chien-Chih Chiu, Shyng-Shiou F. Yuan, Chin-Ju Tang, Chun Yen Liu, Han-Lin Chou, Chon-Kit Chou, Yu-Ting Chang |
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| Rok vydání: | 2016 |
| Předmět: |
0301 basic medicine
Immunology Mutant Kruppel-Like Transcription Factors Biology 03 medical and health sciences Mice 0302 clinical medicine Krüppel Neoplasms Polycystic kidney disease medicine Congenital Hypothyroidism Diabetes Mellitus Immunology and Allergy Animals Humans Transcription factor Gene Pancreas Genetics Zinc finger Mice Knockout Gene knockdown Polycystic Kidney Diseases General Medicine medicine.disease Cell biology DNA-Binding Proteins Repressor Proteins 030104 developmental biology 030220 oncology & carcinogenesis Mutation Trans-Activators Beta cell Transcription Factors |
| Zdroj: | Archivum immunologiae et therapiae experimentalis. 65(5) |
| ISSN: | 1661-4917 |
| Popis: | Gli-similar 3 (Glis3) belongs to a Glis subfamily of Kruppel-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. |
| Databáze: | OpenAIRE |
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