Редактирование: CIZ1 (раздел)

==Publications==

{{medline-entry
|title=DNA damage and neurodegenerative phenotypes in aged Ciz1 null mice.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/29154038
|abstract=Cell-cycle dysfunction and faulty DNA repair are closely intertwined pathobiological processes that may contribute to several neurodegenerative disorders. [[CDKN1A]] interacting zinc finger protein 1 ([[CIZ1]]) plays a critical role in DNA replication and cell-cycle progression at the G1/S checkpoint. Germline or somatic variants in [[CIZ1]] have been linked to several neural and extra-neural diseases. Recently, we showed that germline knockout of Ciz1 is associated with motor and hematological abnormalities in young adult mice. However, the effects of [[CIZ1]] deficiency in much older mice may be more relevant to understanding age-related declines in cognitive and motor functioning and age-related neurologic disorders such as isolated dystonia and Alzheimer disease. Mouse embryonic fibroblasts from Ciz1  mice showed abnormal sensitivity to the effects of γ-irradiation with persistent DNA breaks, aberrant cell-cycle progression, and apoptosis. Aged (18-month-old) Ciz1  mice exhibited marked deficits in motor and cognitive functioning, and, in brain tissues, overt DNA damage, NF-κB upregulation, oxidative stress, vascular dysfunction, inflammation, and cell death. These findings indicate that the deleterious effects of [[CIZ1]] deficiency become more pronounced with aging and suggest that defects of cell-cycle control and associated DNA repair pathways in postmitotic neurons could contribute to global neurologic decline in elderly human populations. Accordingly, the G1/S cell-cycle checkpoint and associated DNA repair pathways may be targets for the prevention and treatment of age-related neurodegenerative processes.
|mesh-terms=* Aging
* Animals
* Apoptosis
* Brain
* Cell Cycle
* Cells, Cultured
* Cognition
* Cognitive Aging
* DNA Damage
* DNA Repair
* Female
* Fibroblasts
* Genes, cdc
* Male
* Mice
* Molecular Targeted Therapy
* NF-kappa B
* Neurodegenerative Diseases
* Nuclear Proteins
* Oxidative Stress
* Phenotype
|keywords=* Aging
* Apoptosis
* CIZ1
* Cell cycle
* DNA damage
|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5877805
}}