Yael Ziv

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.

Defective potassium currents in ataxia telangiectasia fibroblasts.

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

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

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

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.

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

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

AN-7, a butyric acid prodrug, sensitizes cutaneous T-cell lymphoma cell lines to doxorubicin via inhibition of DNA double strand breaks repair.

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.

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

It takes three to the DNA damage response tango.

Auditory Performance in Recovered SARS-COV-2 Patients.

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.