Редактирование: PATZ1

POZ-, AT hook-, and zinc finger-containing protein 1 (BTB/POZ domain zinc finger transcription factor) (Protein kinase A RI subunit alpha-associated protein) (Zinc finger and BTB domain-containing protein 19) (Zinc finger protein 278) (Zinc finger sarcoma gene protein) [PATZ] [RIAZ] [ZBTB19] [ZNF278] [ZSG]

==Publications==

{{medline-entry
|title=POZ/BTB and AT-hook-containing zinc finger protein 1 ([[PATZ1]]) inhibits endothelial cell senescence through a p53 dependent pathway.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/22052190
|abstract=Vascular cell senescence, induced by the DNA damage response or inflammatory stress, contributes to age-associated vascular disease. Using complementary DNA microarray technology, we found that the level of POZ/BTB and AT-hook-containing zinc finger protein 1 ([[PATZ1]]) is downregulated during endothelial cell (EC) senescence. [[PATZ1]] may have an important role as a transcriptional repressor in chromatin remodeling and transcription regulation; however, the role of [[PATZ1]] in EC senescence and vascular aging remains unidentified. Knockdown of [[PATZ1]] in young cells accelerated premature EC senescence, which was confirmed by growth arrest, increased p53 protein level and senescence-associated β-galactosidase (SA-β-gal) activity, and repression of EC tube formation. In contrast, overexpression of [[PATZ1]] in senescent cells reversed senescent phenotypes. Cellular senescence induced by [[PATZ1]] knockdown in young cells was rescued by knockdown of p53, but not by knockdown of p16(INK4a). [[PATZ1]] knockdown increased ROS levels, and pretreatment with N-acetylcysteine abolished EC senescence induced by [[PATZ1]] knockdown. Notably, [[PATZ1]] immunoreactivity was lower in ECs of atherosclerotic tissues than those of normal arteries in LDLR(-/-) mice, and immunoreactivity also decreased in ECs of old human arteries. These results suggest that [[PATZ1]] may have an important role in the regulation of EC senescence through an ROS-mediated p53-dependent pathway and contribute to vascular diseases associated with aging.
|mesh-terms=* Aging
* Animals
* Arteries
* Atherosclerosis
* Cell Cycle Checkpoints
* Cellular Senescence
* Cyclin-Dependent Kinase Inhibitor p16
* Endothelial Cells
* Gene Knockdown Techniques
* Humans
* Kruppel-Like Transcription Factors
* Mice
* Mice, Knockout
* Reactive Oxygen Species
* Repressor Proteins
* Tumor Suppressor Protein p53

|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3307983
}}