- DNA damage and transcriptional regulation in iPSC-derived neurons from Ataxia Telangiectasiapatients.
- Epstein-Barr Virus (EBV)-Related Lymphoproliferative Disorders in Ataxia Telangiectasia: Does ATM Regulate EBV Life Cycle?
- Excess growth hormone suppresses DNA damage repair in epithelial cells.
- Functional classification of ATM variants in Ataxia-Telangiectasia patients.
- Genotype-phenotype correlations in ataxia telangiectasia patients with ATM c.3576G>A and c.8147T>C mutations.
- Identification of aberrantly methylated differentially expressed genes in breast cancer by integrated bioinformatics analysis.
- Increased susceptibility of airway epithelial cells from ataxia-telangiectasia to S. pneumoniae infection due to oxidative damage and impaired innate immunity.
- Microglial Self-Recognition STINGs in A-T Neurodegeneration.
- Multifaceted roles of ATM in autophagy: From nonselective autophagy to selective autophagy.
- NMR- and MD simulation-based structural characterization of the membrane-associating FATC domain of ataxia telangiectasia mutated.
- Odalisque's position as a geste antagoniste in a variant phenotype of Ataxia‐Telangiectasia
- Rational Design of 5-(4-(Isopropylsulfonyl)phenyl)-3-(3-(4-((methylamino)methyl)phenyl)isoxazol-5-yl)pyrazin-2-amine (VX-970, M6620): Optimization of Intra- and Intermolecular Polar Interactions of a New Ataxia Telangiectasia Mutated and Rad3-Related (ATR) Kinase Inhibitor.
- Sense and sensibility: ATM oxygen stress signaling manages brain cell energetics.
- SMRT compounds abrogate cellular phenotypes of ataxia telangiectasia in neural derivatives of patient-specific hiPSCs
- The Cerebellar Cognitive Affective/Schmahmann Syndrome: a Task Force Paper.
- Three new cases of Ataxia-Telangiectasia-Like Disorder: no impairment of the ATM pathway, but S-phase checkpoint defect.
- Two novel variants in the ATM gene causing ataxia-telangiectasia, including a duplication of 90 kb: Utility of targeted next-generation sequencing in detection of copy number variation.
- Verification and rectification of cell type-specific splicing of a Seckel syndrome-associated ATR mutation using iPS cell model.
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