The Potential Role of Krüppel-Like Zinc-Finger Protein Glis3 in Genetic Diseases and Cancers.
Chon-Kit ChouChin-Ju TangHan-Lin ChouChun-Yen LiuMing-Chong NgYu-Ting ChangShyng-Shiou F YuanEing-Mei TsaiChien-Chih ChiuPublished in: Archivum immunologiae et therapiae experimentalis (2017)
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.
Keyphrases
- induced apoptosis
- cell cycle arrest
- dna binding
- type diabetes
- transcription factor
- cell death
- endoplasmic reticulum stress
- oxidative stress
- stem cells
- gene expression
- signaling pathway
- wild type
- dna methylation
- adipose tissue
- weight loss
- glycemic control
- medical students
- papillary thyroid
- smoking cessation
- replacement therapy
- circulating tumor
- nucleic acid
- living cells