ArticleDNA repair2018
Inactive Atm abrogates DSB repair in mouse cerebellum more than does Atm loss, without causing a neurological phenotype.
Article in DNA repair, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
What it found
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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.
The trial behind it
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Who cites it
14 citing papers in PubMed, 21 citations in OpenAlex.
- ATM-kinase deficiency triggers early multi-compartment remodeling of the cerebellar microenvironment.Acta neuropathologica communications · 2026Article
- Double jeopardy: howFrontiers in cell and developmental biology · 2026Review
- ATM deficiency drives phenotypic diversity and Purkinje cell degeneration in a macaque model of ataxia-telangiectasia.Cell reports. Medicine · 2025Article
- The cGAS-STING, p38 MAPK, and p53 pathways link genome instability to accelerated cellular senescence in ATM-deficient murine lung fibroblasts.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- A-T neurodegeneration and DNA damage-induced transcriptional stress.DNA repair · 2024Review
- Ataxia-telangiectasia mutated plays an important role in cerebellar integrity and functionality.Neural regeneration research · 2023Review
- Ataxia-associated DNA repair genes protect theFrontiers in neural circuits · 2023Article
- Review
- Persistent DNA damage associated with ATM kinase deficiency promotes microglial dysfunction.Nucleic acids research · 2022Article
- A novel, ataxic mouse model of ataxia telangiectasia caused by a clinically relevant nonsense mutation.eLife · 2021Article
- Review
- The Cancer-Associated ATM R3008H Mutation Reveals the Link between ATM Activation and Its Exchange.Cancer research · 2021Article
- The Essential DNA Damage Response Complex MRN Is Dispensable for the Survival and Function of Purkinje Neurons.Frontiers in aging neuroscience · 2021Article
- A Critical Role for ISGylation, Ubiquitination and, SUMOylation in Brain Damage: Implications for Neuroprotection.Neurochemical research · 2020Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 3 institutions in 3 countries.
Funding
Abstract
The genome instability syndrome, ataxia-telangiectasia (A-T) is caused by null mutations in the ATM gene, that lead to complete loss or inactivation of the gene's product, the ATM protein kinase. ATM is the primary mobilizer of the cellular response to DNA double-strand breaks (DSBs) - a broad signaling network in which many components are ATM targets. The major clinical feature of A-T is cerebellar atrophy, characterized by relentless loss of Purkinje and granule cells. In Atm-knockout (Atm-KO) mice, complete loss of Atm leads to a very mild neurological phenotype, suggesting that Atm loss is not sufficient to markedly abrogate cerebellar structure and function in this organism. Expression of inactive ("kinase-dead") Atm (Atm
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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.