Редактирование: AKTIP (раздел)

==Publications==

{{medline-entry
|title=Mice with reduced expression of the telomere-associated protein Ft1 develop p53-sensitive progeroid traits.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/29635765
|abstract=Human [[AKTIP]] and mouse Ft1 are orthologous ubiquitin E2 variant proteins involved in telomere maintenance and DNA replication. [[AKTIP]] also interacts with A- and B-type lamins. These features suggest that Ft1 may be implicated in aging regulatory pathways. Here, we show that cells derived from hypomorph Ft1 mutant (Ft1  ) mice exhibit telomeric defects and that Ft1  animals develop progeroid traits, including impaired growth, skeletal and skin defects, abnormal heart tissue, and sterility. We also demonstrate a genetic interaction between Ft1 and p53. The analysis of mice carrying mutations in both Ft1 and p53 (Ft1  ; p53  and Ft1  ; p53  ) showed that reduction in p53 rescues the progeroid traits of Ft1 mutants, suggesting that they are at least in part caused by a p53-dependent DNA damage response. Conversely, Ft1 reduction alters lymphomagenesis in p53 mutant mice. These results identify Ft1 as a new player in the aging process and open the way to the analysis of its interactions with other progeria genes using the mouse model.
|mesh-terms=* Animals
* Apoptosis Regulatory Proteins
* Cells, Cultured
* Gene Expression Profiling
* Mice
* Mice, Inbred C57BL
* Mutation
* Progeria
* Proteins
* Tumor Suppressor Protein p53
|keywords=* AKTIP
* DNA damage
* aging
* lamins
* progeria
* telomeres
|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6052474
}}
{{medline-entry
|title=The telomeric protein [[AKTIP]] interacts with A- and B-type lamins and is involved in regulation of cellular senescence.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/27512140
|abstract=[[AKTIP]] is a shelterin-interacting protein required for replication of telomeric DNA. Here, we show that [[AKTIP]] biochemically interacts with A- and B-type lamins and affects lamin A, but not lamin C or B, expression. In interphase cells, [[AKTIP]] localizes at the nuclear rim and in discrete regions of the nucleoplasm just like lamins. Double immunostaining revealed that [[AKTIP]] partially co-localizes with lamin B1 and lamin A/C in interphase cells, and that proper [[AKTIP]] localization requires functional lamin A. In mitotic cells, [[AKTIP]] is enriched at the spindle poles and at the midbody of late telophase cells similar to lamin B1. [[AKTIP]]-depleted cells show senescence-associated markers and recapitulate several aspects of the progeroid phenotype. Collectively, our results indicate that [[AKTIP]] is a new player in lamin-related processes, including those that govern nuclear architecture, telomere homeostasis and cellular senescence.
|mesh-terms=* Adaptor Proteins, Signal Transducing
* Apoptosis Regulatory Proteins
* Cells, Cultured
* Cellular Senescence
* Gene Expression Regulation
* Gene Knockdown Techniques
* HeLa Cells
* Humans
* Lamin Type A
* Lamin Type B
* Mitosis
* Nuclear Envelope
* Telomere
* Telomere Homeostasis
|keywords=* cell senescence
* lamin
* laminopathies
* nuclear lamina
* progeria
* telomeres
|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5008010
}}