https://transhumanist.ru/index.php?action=history&feed=atom&title=CIZ1CIZ1 - История изменений2026-05-19T01:54:27ZИстория изменений этой страницы в викиMediaWiki 1.43.6https://transhumanist.ru/index.php?title=CIZ1&diff=4121&oldid=prevOdysseusBot: Новая страница: «Cip1-interacting zinc finger protein (CDKN1A-interacting zinc finger protein 1) (Nuclear protein NP94) (Zinc finger protein 356) [LSFR1] [NP94] [ZNF356] ==Public...»2021-04-29T19:01:45Z<p>Новая страница: «Cip1-interacting zinc finger protein (CDKN1A-interacting zinc finger protein 1) (Nuclear protein NP94) (Zinc finger protein 356) [LSFR1] [NP94] [ZNF356] ==Public...»</p>
<p><b>Новая страница</b></p><div>Cip1-interacting zinc finger protein (CDKN1A-interacting zinc finger protein 1) (Nuclear protein NP94) (Zinc finger protein 356) [LSFR1] [NP94] [ZNF356]<br />
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==Publications==<br />
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{{medline-entry<br />
|title=DNA damage and neurodegenerative phenotypes in aged Ciz1 null mice.<br />
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/29154038<br />
|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.<br />
|mesh-terms=* Aging<br />
* Animals<br />
* Apoptosis<br />
* Brain<br />
* Cell Cycle<br />
* Cells, Cultured<br />
* Cognition<br />
* Cognitive Aging<br />
* DNA Damage<br />
* DNA Repair<br />
* Female<br />
* Fibroblasts<br />
* Genes, cdc<br />
* Male<br />
* Mice<br />
* Molecular Targeted Therapy<br />
* NF-kappa B<br />
* Neurodegenerative Diseases<br />
* Nuclear Proteins<br />
* Oxidative Stress<br />
* Phenotype<br />
|keywords=* Aging<br />
* Apoptosis<br />
* CIZ1<br />
* Cell cycle<br />
* DNA damage<br />
|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5877805<br />
}}</div>OdysseusBot