Yosef Shiloh

The ataxia-telangiectasia gene product, a constitutively expressed nuclear protein that is not up-regulated following genome damage.

ATM binds to beta-adaptin in cytoplasmic vesicles.

Selective loss of dopaminergic nigro-striatal neurons in brains of Atm-deficient mice.

Defective potassium currents in ataxia telangiectasia fibroblasts.

Rapid ATM-dependent phosphorylation of MDM2 precedes p53 accumulation in response to DNA damage.

Ataxia telangiectasia-mutated phosphorylates Chk2 in vivo and in vitro.

Jun NH2-terminal kinase phosphorylation of p53 on Thr-81 is important for p53 stabilization and transcriptional activities in response to stress.

Elevated Cu/Zn-SOD exacerbates radiation sensitivity and hematopoietic abnormalities of Atm-deficient mice.

ATM-dependent phosphorylation of Mdm2 on serine 395: role in p53 activation by DNA damage.

Accumulation of DNA damage and reduced levels of nicotine adenine dinucleotide in the brains of Atm-deficient mice.

ATM-dependent activation of the gene encoding MAP kinase phosphatase 5 by radiomimetic DNA damage.

Contribution of the Atm protein to maintaining cellular homeostasis evidenced by continuous activation of the AP-1 pathway in Atm-deficient brains.

ATM deficiency and oxidative stress: a new dimension of defective response to DNA damage.

ATM and related protein kinases: safeguarding genome integrity.

ATM: ready, set, go.

Genome-wide in silico identification of transcriptional regulators controlling the cell cycle in human cells.

Requirement of the MRN complex for ATM activation by DNA damage.

PIVOT: protein interacions visualizatiOn tool.

In search of drug treatment for genetic defects in the DNA damage response: the example of ataxia-telangiectasia.

In silico identification of transcriptional regulators associated with c-Myc.

Maintaining integrity.

Phosphorylation of Hdmx mediates its Hdm2- and ATM-dependent degradation in response to DNA damage.

Dissection of a DNA-damage-induced transcriptional network using a combination of microarrays, RNA interference and computational promoter analysis.

ATM-dependent phosphorylation of ATF2 is required for the DNA damage response.

Impaired genomic stability and increased oxidative stress exacerbate different features of Ataxia-telangiectasia.

EXPANDER--an integrative program suite for microarray data analysis.

DNA damage-induced phosphorylation of MdmX at serine 367 activates p53 by targeting MdmX for Mdm2-dependent degradation.

Deciphering transcriptional regulatory elements that encode specific cell cycle phasing by comparative genomics analysis.

Nuclear ataxia-telangiectasia mutated (ATM) mediates the cellular response to DNA double strand breaks in human neuron-like cells.

The ATM-mediated DNA-damage response: taking shape.

Condensin I recruitment and uneven chromatin condensation precede mitotic cell death in response to DNA damage.

Analysis of the ataxia telangiectasia mutated-mediated DNA damage response in murine cerebellar neurons.

Chromatin relaxation in response to DNA double-strand breaks is modulated by a novel ATM- and KAP-1 dependent pathway.

Differential roles of ATM- and Chk2-mediated phosphorylations of Hdmx in response to DNA damage.

ATM-mediated response to DNA double strand breaks in human neurons derived from stem cells.

Programs for cell death: apoptosis is only one way to go.

Ataxia-telangiectasia: mild neurological presentation despite null ATM mutation and severe cellular phenotype.

Functional genomic delineation of TLR-induced transcriptional networks.

MRI evidence of white matter damage in a mouse model of Nijmegen breakage syndrome.

SPIKE--a database, visualization and analysis tool of cellular signaling pathways.

The neurological phenotype of ataxia-telangiectasia: solving a persistent puzzle.

The role of the DNA damage response in neuronal development, organization and maintenance.

WRN is required for ATM activation and the S-phase checkpoint in response to interstrand cross-link-induced DNA double-strand breaks.

The histone H2B-specific ubiquitin ligase RNF20/hBRE1 acts as a putative tumor suppressor through selective regulation of gene expression.

Analysis of the relationships between ATM and the Rad54 paralogs involved in homologous recombination repair.

Activation of ATM depends on chromatin interactions occurring before induction of DNA damage.

Conditional inactivation of the NBS1 gene in the mouse central nervous system leads to neurodegeneration and disorganization of the visual system.

Optimal function of the DNA repair enzyme TDP1 requires its phosphorylation by ATM and/or DNA-PK.

FBXO31: a new player in the ever-expanding DNA damage response orchestra.

Accelerated carcinogenesis following liver regeneration is associated with chronic inflammation-induced double-strand DNA breaks.

Expander: from expression microarrays to networks and functions.

Involvement of Matrin 3 and SFPQ/NONO in the DNA damage response.

SPIKE: a database of highly curated human signaling pathways.

ATM-dependent and -independent dynamics of the nuclear phosphoproteome after DNA damage.

Astrocyte dysfunction associated with cerebellar attrition in a Nijmegen breakage syndrome animal model.

Investigation of the functional link between ATM and NBS1 in the DNA damage response in the mouse cerebellum.

Requirement of ATM-dependent monoubiquitylation of histone H2B for timely repair of DNA double-strand breaks.

ATM-mediated phosphorylation of polynucleotide kinase/phosphatase is required for effective DNA double-strand break repair.

A role for vascular deficiency in retinal pathology in a mouse model of ataxia-telangiectasia.

Transcriptional modulation induced by ionizing radiation: p53 remains a central player.

RNF20-RNF40: A ubiquitin-driven link between gene expression and the DNA damage response.

Matrin 3 binds and stabilizes mRNA.

Malfunctioning DNA damage response (DDR) leads to the degeneration of nigro-striatal pathway in mouse brain.

Involvement of the nuclear proteasome activator PA28γ in the cellular response to DNA double-strand breaks.

The ATM protein: the importance of being active.

The ATM protein kinase: regulating the cellular response to genotoxic stress, and more.

DNA damage response, bioenergetics, and neurological disease: the challenge of maintaining brain health in an aging human population.

The ATM protein kinase: regulating the cellular response to genotoxic stress, and more.

Parallel profiling of the transcriptome, cistrome, and epigenome in the cellular response to ionizing radiation.

ATM: expanding roles as a chief guardian of genome stability.

The COP9 signalosome is vital for timely repair of DNA double-strand breaks.

Systemic DNA damage responses in aging and diseases.

Genome instability: Linking ageing and brain degeneration.

Ataxia-telangiectasia (A-T): An emerging dimension of premature ageing.

Monitoring the ATM-Mediated DNA Damage Response in the Cerebellum Using Organotypic Cultures.

Nuclear poly(A)-binding protein 1 is an ATM target and essential for DNA double-strand break repair.

The Ubiquitin E3/E4 Ligase UBE4A Adjusts Protein Ubiquitylation and Accumulation at Sites of DNA Damage, Facilitating Double-Strand Break Repair.

Inactive Atm abrogates DSB repair in mouse cerebellum more than does Atm loss, without causing a neurological phenotype.

UBQLN4 Represses Homologous Recombination and Is Overexpressed in Aggressive Tumors.

The EXPANDER Integrated Platform for Transcriptome Analysis.

The Role of E3, E4 Ubiquitin Ligase (UBE4B) in Human Pathologies.

The serendipitous dawn of DNA repair.

The cerebellar degeneration in ataxia-telangiectasia: A case for genome instability.

Phosphoproteomics reveals novel modes of function and inter-relationships among PIKKs in response to genotoxic stress.

Regulation of MRE11A by UBQLN4 leads to cisplatin resistance in patients with esophageal squamous cell carcinoma.

It takes three to the DNA damage response tango.

The hallmarks of aging in Ataxia-Telangiectasia.

UBQLN4 promotes STING proteasomal degradation during cisplatin-induced DNA damage in triple-negative breast cancer.

New hallmarks of ageing: a 2022 Copenhagen ageing meeting summary.

Genomic Amplification of Is a Prognostic and Treatment Resistance Factor.

Ataxia Telangiectasia Mutated Signaling Delays Skin Pigmentation upon UV Exposure by Mediating MITF Function toward DNA Repair Mode.

Accelerated replicative senescence of ataxia-telangiectasia skin fibroblasts is retained at physiologic oxygen levels, with unique and common transcriptional patterns.

ATM germ line pathogenic variants affect outcomes in children with ataxia-telangiectasia and hematological malignancies.