ArticleThe Journal of biological chemistry2015
Nedd4 family interacting protein 1 (Ndfip1) is required for ubiquitination and nuclear trafficking of BRCA1-associated ATM activator 1 (BRAT1) during the DNA damage response.
Article in The Journal of biological chemistry, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers, 1 of them a synthesis that pooled it.
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Who cites it
23 citing papers in PubMed, 1 synthesis or guideline pooled it, 33 citations in OpenAlex.
- Clinical characteristics of BRAT1-related disease: a systematic literature review.Acta neurologica Belgica · 2024Pooled it
- BRAT1 - a new therapeutic target for glioblastoma.Cellular and molecular life sciences : CMLS · 2025Article
- The Ubiquitin Ligase Adaptor NDFIP1 Interacts with TRESK and Negatively Regulates the Background KInternational journal of molecular sciences · 2024Article
- Cytoplasmic binding partners of the Integrator endonuclease INTS11 and its paralog CPSF73 are required for their nuclear function.Molecular cell · 2024Article
- Neuronal differentiation requires BRAT1 complex to remove REST from chromatin.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- RNA helicase DDX3 regulates RAD51 localization and DNA damage repair in Ewing sarcoma.iScience · 2024Article
- Involvement of ubiquitination in Alzheimer's disease.Frontiers in neurology · 2024Review
- BRAT1-related disorders: phenotypic spectrum and phenotype-genotype correlations from 97 patients.European journal of human genetics : EJHG · 2023Article
- Compound heterozygous loss-of-function variants in BRAT1 cause lethal neonatal rigidity and multifocal seizure syndrome.Molecular genetics & genomic medicine · 2023Article
- Novel Biallelic Variant in theFrontiers in genetics · 2022Article
- Case report: 7p22.3 deletion and 8q24.3 duplication in a patient with epilepsy and psychomotor delay-Does both possibly act to modulate a candidate gene region for the patient's phenotype?Frontiers in genetics · 2022Article
- The E3 Ubiquitin Ligase NEDD4L Targets OGG1 for Ubiquitylation and Modulates the Cellular DNA Damage Response.Frontiers in cell and developmental biology · 2020Article
- A candidate gene analysis and GWAS for genes associated with maternal nondisjunction of chromosome 21.PLoS genetics · 2019Article
- Ubiquitin Regulation of Trk Receptor Trafficking and Degradation.Molecular neurobiology · 2019Article
- Isobaric Tag-Based Protein Profiling of a Nicotine-Treated Alpha7 Nicotinic Receptor-Null Human Haploid Cell Line.Proteomics · 2018Article
- Lower Expression of Ndfip1 Is Associated With Alzheimer Disease Pathogenesis Through Decreasing DMT1 Degradation and Increasing Iron Influx.Frontiers in aging neuroscience · 2018Article
- Article
- Extracellular vesicles as emerging targets in cancer: Recent development from bench to bedside.Biochimica et biophysica acta. Reviews on cancer · 2017Review
- Engineered Exosomes as Vehicles for Biologically Active Proteins.Molecular therapy : the journal of the American Society of Gene Therapy · 2017Article
- Light of DNA-alkylating agents in castration-resistant prostate cancer cells: a novel mixed EGFR/DNA targeting combi-molecule.American journal of translational research · 2017Article
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 2 countries.
Funding
Abstract
During injury, cells are vulnerable to apoptosis from a variety of stress conditions including DNA damage causing double-stranded breaks. Without repair, these breaks lead to aberrations in DNA replication and transcription, leading to apoptosis. A major response to DNA damage is provided by the protein kinase ATM (ataxia telangiectasia mutated) that is capable of commanding a plethora of signaling networks for DNA repair, cell cycle arrest, and even apoptosis. A key element in the DNA damage response is the mobilization of activating proteins into the cell nucleus to repair damaged DNA. BRAT1 is one of these proteins, and it functions as an activator of ATM by maintaining its phosphorylated status while also keeping other phosphatases at bay. However, it is unknown how BRAT1 is trafficked into the cell nucleus to maintain ATM phosphorylation. Here we demonstrate that Ndfip1-mediated ubiquitination of BRAT1 leads to BRAT1 trafficking into the cell nucleus. Without Ndfip1, BRAT1 failed to translocate to the nucleus. Under genotoxic stress, cells showed increased expression of both Ndfip1 and phosphorylated ATM. Following brain injury, neurons show increased expression of Ndfip1 and nuclear translocation of BRAT1. These results point to Ndfip1 as a sensor protein during cell injury and Ndfip1 up-regulation as a cue for BRAT1 ubiquitination by Nedd4 E3 ligases, followed by nuclear translocation of BRAT1.
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