ArticleCell cycle (Georgetown, Tex.)2014
ATM controls proper mitotic spindle structure.
Article in Cell cycle (Georgetown, Tex.), 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 38 citations in OpenAlex.
- SASH1 S519N Variant Links Skin Hyperpigmentation and Premature Hair Graying to Dysfunction of Melanocyte Lineage.The Journal of investigative dermatology · 2025Article
- SF3B1 mutation and ATM deletion codrive leukemogenesis via centromeric R-loop dysregulation.The Journal of clinical investigation · 2023Article
- A New Class of Selective ATM Inhibitors as Combination Partners of DNA Double-Strand Break Inducing Cancer Therapies.Molecular cancer therapeutics · 2022Article
- Cancer Cells Haploinsufficient for ATM Are Sensitized to PARP Inhibitors byInternational journal of molecular sciences · 2022Article
- Targeted Mass Spectrometry Enables Quantification of Novel Pharmacodynamic Biomarkers of ATM Kinase Inhibition.Cancers · 2021Article
- The Significance of Targeting Poly (ADP-Ribose) Polymerase-1 in Pancreatic Cancer for Providing a New Therapeutic Paradigm.International journal of molecular sciences · 2021Review
- Deciphering MET-dependent modulation of global cellular responses to DNA damage by quantitative phosphoproteomics.Molecular oncology · 2020Article
- ATM Dysfunction in Pancreatic Adenocarcinoma and Associated Therapeutic Implications.Molecular cancer therapeutics · 2019Review
- Targeting ADP-ribosylation as an antimicrobial strategy.Biochemical pharmacology · 2019Review
- ADP-ribosylation signalling and human disease.Open biology · 2019Review
- RXXPEG motif of MERIT40 is required to maintain spindle structure and function through its interaction with Tankyrase1.Cell biology international · 2019Article
- PARPs in genome stability and signal transduction: implications for cancer therapy.Biochemical Society transactions · 2018Review
- Evidence that PP2A activity is dispensable for spindle assembly checkpoint-dependent control of Cdk1.Oncotarget · 2018Article
- ADP-ribosylation: new facets of an ancient modification.The FEBS journal · 2017Review
- ERCC1 and telomere status in breast tumours treated with neoadjuvant chemotherapy and their association with patient prognosis.The journal of pathology. Clinical research · 2016Article
- ENPP1 processes protein ADP-ribosylation in vitro.The FEBS journal · 2016Article
- Connecting Malfunctioning Glial Cells and Brain Degenerative Disorders.Genomics, proteomics & bioinformatics · 2016Review
- Stalled replication forks within heterochromatin require ATRX for protection.Cell death & disease · 2016Article
- Tankyrases Promote Homologous Recombination and Check Point Activation in Response to DSBs.PLoS genetics · 2016Article
- Tankyrase inhibition impairs directional migration and invasion of lung cancer cells by affecting microtubule dynamics and polarity signals.BMC biology · 2016Article
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The recessive ataxia-telangiectasia (A-T) syndrome is characterized by cerebellar degeneration, immunodeficiency, cancer susceptibility, premature aging, and insulin-resistant diabetes and is caused by loss of function of the ATM kinase, a member of the phosphoinositide 3-kinase-like protein kinases (PIKKs) family. ATM plays a crucial role in the DNA damage response (DDR); however, the complexity of A-T features suggests that ATM may regulate other cellular functions. Here we show that ATM affects proper bipolar mitotic spindle structure independently of DNA damage. In addition, we find that in mitosis ATM forms a complex with the poly(ADP)ribose (PAR) polymerase Tankyrase (TNKS) 1, the spindle pole protein NuMA1, and breast cancer susceptibility protein BRCA1, another crucial DDR player. Our evidence indicates that the complex is required for efficient poly(ADP)ribosylation of NuMA1. We find further that a mutant NuMA1 version, non-phosphorylatable at potential ATM-dependent phosphorylation sites, is poorly PARylated and induces loss of spindle bipolarity. Our findings may help to explain crucial A-T features and provide further mechanistic rationale for TNKS inhibition in cancer therapy.
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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.