ArticleOpen biology2016
The telomeric protein AKTIP interacts with A- and B-type lamins and is involved in regulation of cellular senescence.
Article in Open biology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 26 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
26 citing papers in PubMed, 31 citations in OpenAlex.
- Sensing centrosome amplification: the interface between centriole duplication and autophagy.Nature communications · 2026Article
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- Acute chromatin decompaction stiffens the nucleus as revealed by nanopillar-induced nuclear deformation in cells.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
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- Correction to: 'The telomeric protein AKTIP interacts with A- and B-type lamins and is involved in regulation of cellular senescence' (2016), by BurlaOpen biology · 2024Article
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- Impact of diffused versus vasculature targeted DNA damage on the heart of mice depleted of telomeric factor Ft1.Aging cell · 2023Article
- Technologies, strategies, and cautions when deconvoluting genome-wide association signals: FTO in focus.Obesity reviews : an official journal of the International Association for the Study of Obesity · 2023Review
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- Combined alteration of lamin and nuclear morphology influences the localization of the tumor-associated factor AKTIP.Journal of experimental & clinical cancer research : CR · 2022Article
- Review
- The functional impact of nuclear reorganization in cellular senescence.Briefings in functional genomics · 2022Review
- Interaction of TLK1 and AKTIP as a Potential Regulator of AKT Activation in Castration-Resistant Prostate Cancer Progression.Pathophysiology : the official journal of the International Society for Pathophysiology · 2021Article
- Progerin impairs 3D genome organization and induces fragile telomeres by limiting the dNTP pools.Scientific reports · 2021Article
- PI(3,4)PProceedings of the National Academy of Sciences of the United States of America · 2021Article
- Interplay of the nuclear envelope with chromatin in physiology and pathology.Nucleus (Austin, Tex.) · 2020Review
- Towards delineating the chain of events that cause premature senescence in the accelerated aging syndrome Hutchinson-Gilford progeria (HGPS).Biochemical Society transactions · 2020Review
- Review
- Telomere elongation through hTERT immortalization leads to chromosome repositioning in control cells and genomic instability in Hutchinson-Gilford progeria syndrome fibroblasts, expressing a novel SUN1 isoform.Genes, chromosomes & cancer · 2019Article
Corrections and comments
- Erratum issued
Authors and funding
15 authors at 7 institutions in 1 country.
Funding
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.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.