Research Topics
Species | Y ShilohSummaryAffiliation: Tel Aviv University Country: Israel Publications
Research Grants
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Detail Information
Publications
Ataxia-telangiectasia and the Nijmegen breakage syndrome: related disorders but genes apartY Shiloh
Department of Human Genetics, Sackler School of Medicine, Tel Aviv University, Israel
Annu Rev Genet 31:635-62. 1997..The as yet unknown NBS protein may be a component in an ATM-based complex, with a key role in sensing and processing specific DNA damage or intermediates and signaling their presence to the cell cycle machinery...- ATM-mediated response to DNA double strand breaks in human neurons derived from stem cellsSharon Biton
David and Inez Myers Laboratory for Genetic Research, Department of Molecular Genetics and Biochemistry, Sackler School of Medicine, Tel Aviv University, Tel Aviv 69978, Israel
DNA Repair (Amst) 6:128-34. 2007..We present here unique and powerful model systems to further study the ATM-mediated network in neurons... - Inhibition of transforming growth factor-beta1 signaling attenuates ataxia telangiectasia mutated activity in response to genotoxic stressJulia Kirshner
Life Sciences Division, Lawrence Berkeley National Laboratory, Berkeley, California, USA
Cancer Res 66:10861-9. 2006.... 
Differential roles of ATM- and Chk2-mediated phosphorylations of Hdmx in response to DNA damageYaron Pereg
Department of Molecular Genetics and Biochemistry, Sackler School of Medicine, Tel Aviv University, Tel Aviv 69978, Israel
Mol Cell Biol 26:6819-31. 2006..These results demonstrate a sophisticated control by ATM of a target protein, Hdmx, which itself is one of several ATM targets in the ATM-p53 axis of the DNA damage response...- Chromatin relaxation in response to DNA double-strand breaks is modulated by a novel ATM- and KAP-1 dependent pathwayYael Ziv
The David and Inez Myers Laboratory for Genetic Research, Department of Molecular Genetics and Biochemistry, Sackler School of Medicine, Tel Aviv University, Tel Aviv 69978, Israel
Nat Cell Biol 8:870-6. 2006..These results suggest that chromatin relaxation is a fundamental pathway in the DNA-damage response and identify its primary mediators... - Analysis of the ataxia telangiectasia mutated-mediated DNA damage response in murine cerebellar neuronsInbal Dar
Department of Neurobiochemistry, George S. Wise Faculty of Life Sciences, Tel Aviv University, Tel Aviv 69978, Israel
J Neurosci 26:7767-74. 2006..These results support the notion that the cerebellar degeneration in A-T patients results from defective DNA damage response... - Condensin I recruitment and uneven chromatin condensation precede mitotic cell death in response to DNA damageMichael Blank
The David and Inez Myers Laboratory for Genetic Research, Department of Molecular Genetics and Biochemistry, and Interdepartmental Core Facility, Sackler School of Medicine, Tel Aviv University, Tel Aviv 69978, Israel
J Cell Biol 174:195-206. 2006.... - The ATM-mediated DNA-damage response: taking shapeYosef Shiloh
The David and Inez Myers Laboratory for Genetic Research, Department of Molecular Genetics and Biochemistry, Sackler School of Medicine, Tel Aviv University, Tel Aviv 69978, Israel
Trends Biochem Sci 31:402-10. 2006..Genetic, biochemical and structural studies have recently provided insights into the ATM-mediated DSB response, reshaping our view of this signaling pathway while raising new questions... - Nuclear ataxia-telangiectasia mutated (ATM) mediates the cellular response to DNA double strand breaks in human neuron-like cellsSharon Biton
The David and Inez Myers Laboratory for Genetic Research, Department of Molecular Genetics and Biochemistry, Tel Aviv University, Tel Aviv 69978, Israel
J Biol Chem 281:17482-91. 2006..We concluded that nuclear ATM mediates the DSB response in NLCs similarly to in proliferating cells. Attempts to understand the neurodegeneration in A-T should be directed to investigating the DSB response in the nervous system... - Ataxia telangiectasia mutated (ATM) is essential for DNA-PKcs phosphorylations at the Thr-2609 cluster upon DNA double strand breakBenjamin P C Chen
Division of Molecular Radiation Biology, Department of Radiation Oncology, University of Texas Southwestern Medical Center at Dallas, Dallas, Texas 75390, USA
J Biol Chem 282:6582-7. 2007..Finally, our result provides a possible mechanism for the direct involvement of ATM in non-homologous end joining-mediated DSB repair... - ATM and ATR substrate analysis reveals extensive protein networks responsive to DNA damageShuhei Matsuoka
Department of Genetics and Center for Genetics and Genomics, Brigham and Women s Hospital, Howard Hughes Medical Institute, Harvard Medical School, Boston, MA 02115, USA
Science 316:1160-6. 2007..This database paints a much broader landscape for the DDR than was previously appreciated and opens new avenues of investigation into the responses to DNA damage in mammals... - The histone H2B-specific ubiquitin ligase RNF20/hBRE1 acts as a putative tumor suppressor through selective regulation of gene expressionEfrat Shema
Department of Molecular Cell Biology, The Weizmann Institute of Science, Rehovot 76100, Israel
Genes Dev 22:2664-76. 2008..Furthermore, frequent RNF20 promoter hypermethylation was observed in tumors. RNF20 may thus be a putative tumor suppressor, acting through selective regulation of a distinct subset of genes... 
ATM signaling facilitates repair of DNA double-strand breaks associated with heterochromatinAaron A Goodarzi
Genome Damage and Stability Centre, University of Sussex, East Sussex BN1 9RQ, UK
Mol Cell 31:167-77. 2008..These data suggest that the importance of ATM signaling for DSB repair increases as the heterochromatic component of a genome expands...- The role of the DNA damage response in neuronal development, organization and maintenanceAri Barzilai
Department of Neurobiology, George S Wise Faculty of Life Sciences, Tel Aviv University, Tel Aviv 69978, Israel
DNA Repair (Amst) 7:1010-27. 2008..This review focuses on the DNA damage response in neuronal cells and points to the importance of this elaborate network to the integrity of the nervous system from its early development and throughout the lifetime of the organism... - The neurological phenotype of ataxia-telangiectasia: solving a persistent puzzleSharon Biton
Department of Human Molecular Genetics and Biochemistry, Sackler School of Medicine, Tel Aviv University, Tel Aviv 69978, Israel
DNA Repair (Amst) 7:1028-38. 2008..A-T remains a prototype disease for the study of the DDR's role in CNS development and maintenance... - SPIKE--a database, visualization and analysis tool of cellular signaling pathwaysRan Elkon
The David and Inez Myers Laboratory for Genetic Research, Department of Molecular Genetics and Biochemistry, Sackler School of Medicine, Tel Aviv University, Tel Aviv 69978, Israel
BMC Bioinformatics 9:110. 2008..The assimilation, visualization and interpretation of these data have become a major challenge in biological research, and once met, will greatly boost our ability to understand cell functioning on a systems level... - MRI evidence of white matter damage in a mouse model of Nijmegen breakage syndromeYaniv Assaf
Department of Neurobiochemistry, George S Wise Faculty of Life Sciences, Tel Aviv University, Tel Aviv, Israel
Exp Neurol 209:181-91. 2008..Myelin index and protein levels were significantly reduced in these brains. Our results point to a novel function of Nbs1 in the development and organization of the white matter... - Functional genomic delineation of TLR-induced transcriptional networksRan Elkon
The David and Inez Myers Laboratory for Genetic Research, Department of Molecular Genetics and Biochemistry, Sackler School of Medicine, Tel Aviv University, Tel Aviv 69978, Israel
BMC Genomics 8:394. 2007..We sought global delineation of transcriptional networks induced by TLRs, analyzing four genome-wide expression datasets in mouse and human macrophages stimulated with pathogen-mimetic agents that engage various TLRs... - Ataxia-telangiectasia: mild neurological presentation despite null ATM mutation and severe cellular phenotypeNeora Alterman
The David and Inez Myers Laboratory for Genetic Research, Department of Human Molecular Genetics and Biochemistry, Sackler School of Medicine, Tel Aviv University, Tel Aviv, Israel
Am J Med Genet A 143:1827-34. 2007..This analysis shows that the severity of the neurological component of A-T is determined not only by ATM mutations but also by other influences yet to be found... - DNA damage-induced phosphorylation of MdmX at serine 367 activates p53 by targeting MdmX for Mdm2-dependent degradationKoji Okamoto
Radiobiology Division, National Cancer Center Research Institute, Tsukiji 5 1 1, Chuo Ku, Tokyo 104 0045, Japan
Mol Cell Biol 25:9608-20. 2005..We propose that Mdmx phosphorylation at S367 plays an important role in p53 activation after DNA damage by triggering Mdm2-dependent degradation of Mdmx... - EXPANDER--an integrative program suite for microarray data analysisRon Shamir
School of Computer Science, Sackler Faculty of Exact Sciences, Tel Aviv University, Tel Aviv 69978, Israel
BMC Bioinformatics 6:232. 2005..Of special need are integrative packages that provide biologist users with advanced but yet easy to use, set of algorithms, together covering the whole range of steps in microarray data analysis... - Impaired genomic stability and increased oxidative stress exacerbate different features of Ataxia-telangiectasiaShelly Ziv
Department of Neurobiochemistry, George S Wise Faculty of Life Sciences, Tel Aviv University, Tel Aviv 69978, Israel
Hum Mol Genet 14:2929-43. 2005.... - Genome-wide in silico identification of transcriptional regulators controlling the cell cycle in human cellsRan Elkon
The David and Inez Myers Laboratory for Genetic Research, Department of Human Genetics, Sackler School of Medicine, and School of Computer Science, Tel Aviv University, Tel Aviv 69978, Israel
Genome Res 13:773-80. 2003..The methods presented here are general and can be applied to the analysis of transcriptional networks controlling any biological process... - ATM: ready, set, goYosef Shiloh
The Dovid and Inez Myers Laboratory lor Genetic Research, Department of Human Genetics and Molecular Medicine, Sackler School of Medicine, Tel Aviv University, Tel Aviv 69978, Israel
Cell Cycle 2:116-7. 2003 - ATM and related protein kinases: safeguarding genome integrityYosef Shiloh
The David and Inez Myers Laboratory for Genetic Research, Department of Human Genetics and Molecular Medicine, Sackler School of Medicine, Tel Aviv University, Tel Aviv 69978, Israel
Nat Rev Cancer 3:155-68. 2003..Understanding ATM's mode of action provides new insights into the association between defective responses to DNA damage and cancer, and brings us closer to resolving the issue of cancer predisposition in some A-T carriers... - ATM deficiency and oxidative stress: a new dimension of defective response to DNA damageAri Barzilai
Department of Neurobiochemistry, George S. Wise Faculty of Life Sciences, Tel Aviv University, 69978, Tel Aviv, Israel
DNA Repair (Amst) 1:3-25. 2002..This connection may provide new insights into the phenotypes associated with genetic deficiencies of DNA damage responses, and point to new strategies to alleviate some of their clinical symptoms... - Contribution of the Atm protein to maintaining cellular homeostasis evidenced by continuous activation of the AP-1 pathway in Atm-deficient brainsNir Weizman
Department of Neurobiochemistry, George S Wise Faculty of Life Sciences, Sackler School of Medicine, Tel Aviv University, Tel Aviv 69978 Israel
J Biol Chem 278:6741-7. 2003..Our results further demonstrate that inactivation of the ATM gene results in a state of constant stress... - Ionizing radiation induces ataxia telangiectasia mutated kinase (ATM)-mediated phosphorylation of LKB1/STK11 at Thr-366Gopal P Sapkota
MRC Protein Phosphorylation Unit, MSI WTB complex, University of Dundee, Dow Street, Dundee DD1 5EH, Scotland, U K
Biochem J 368:507-16. 2002..These observations provide the first link between ATM and LKB1 and suggest that ATM could regulate LKB1... - Ubiquitination capabilities in response to neocarzinostatin and H(2)O(2) stress in cell lines from patients with ataxia-telangiectasiaAllen Taylor
JM USDA Human Nutrition Research Center on Aging at Tufts University, Laboratory for Nutrition and Vision Research, 711 Washington Street, Boston, Massachusetts 02111, USA
Oncogene 21:4363-73. 2002..The data also add support to the impression that potentiated ubiquitination response to mild oxidative stress is a generalizable phenomenon... - ATM-dependent activation of the gene encoding MAP kinase phosphatase 5 by radiomimetic DNA damageAnat Bar-Shira
The David and Inez Myers Laboratory for Genetic Research, Department of Human Genetics and Molecular Medicine, Sackler School of Medicine, Tel Aviv University, Tel Aviv 69978, Israel
Oncogene 21:849-55. 2002..Thus, ATM modulates this cycle in response to DSBs. These results further highlight ATM as a link between the DNA damage response and major signaling pathways involved in proliferative and apoptotic processes... - Requirement of the MRN complex for ATM activation by DNA damageTamar Uziel
The David and Inez Myers Laboratory for Genetic Research, Department of Human Genetics and Molecular Medicine, Sackler School of Medicine, Tel Aviv University, Tel Aviv 69978, Israel
EMBO J 22:5612-21. 2003..Collectively, these and previous results assign to components of the MRN complex roles upstream and downstream of ATM in the DNA damage response pathway and explain the clinical resemblance between A-T and A-TLD... - PIVOT: protein interacions visualizatiOn toolNir Orlev
Department of Human Genetics, Faculty of Medicine, Tel Aviv University, Israel
Bioinformatics 20:424-5. 2004..The user can also employ PIVOT to predict unknown interactions among proteins, based on interactions among their homologous proteins in other species... - ATM-mediated phosphorylations inhibit Mdmx/Mdm2 stabilization by HAUSP in favor of p53 activationErik Meulmeester
Department of Molecular and Cell Biology, Leiden University Medical Center, Leiden, The Netherlands
Cell Cycle 4:1166-70. 2005..Further insight into the mechanism by which ATM switches the interactions between HAUSP, Mdmx, Mdm2 and p53, to favor p53 activation may offer new tools for therapeutic intervention in the p53 pathway for cancer treatment... - ATM-dependent phosphorylation of ATF2 is required for the DNA damage responseAnindita Bhoumik
Signal Transduction Program, The Burnham Institute, La Jolla, California 92037, USA
Mol Cell 18:577-87. 2005..ATF2 requires neither JNK/p38 nor its DNA binding domain for recruitment to IRIF and the S phase checkpoint. Our findings identify a role for ATF2 in the DNA damage response that is uncoupled from its transcriptional activity... - Dissection of a DNA-damage-induced transcriptional network using a combination of microarrays, RNA interference and computational promoter analysisRan Elkon
The David and Inez Myers Laboratory for Genetic Research, Department of Human Genetics, Sackler School of Medicine, Tel Aviv University, Tel Aviv, 69978, Israel
Genome Biol 6:R43. 2005.... - Phosphorylation of Hdmx mediates its Hdm2- and ATM-dependent degradation in response to DNA damageYaron Pereg
The David and Inez Myers Laboratory for Genetic Research, Department of Human Genetics and Molecular Medicine, Sackler School of Medicine, Tel Aviv University, Tel Aviv 69978, Israel
Proc Natl Acad Sci U S A 102:5056-61. 2005..These results demonstrate a sophisticated mechanism whereby ATM fine-tunes the optimal activation of p53 by simultaneously modifying each player in the process... - Maintaining integrityYosef Shiloh
The David and Inez Myers Laboratory for Genetic Research, Department of Human Genetics and Molecular Medicine, Sackler School of Medicine, Tel Aviv University, Tel Aviv 69978, Israel
Nat Cell Biol 6:923-8. 2004..Current progress in this rapidly expanding field was the subject of an EMBO workshop, Maintenance of Genomic Integrity, that took place in June 2004 in Galway, Ireland. Top.. - In search of drug treatment for genetic defects in the DNA damage response: the example of ataxia-telangiectasiaYosef Shiloh
Department of Human Genetics and Molecular Medicine, Sackler School of Medicine, Tel Aviv University, Tel Aviv 69978, Israel
Semin Cancer Biol 14:295-305. 2004..This article describes a high throughput strategy for drug screening for A-T that is based on the above principles. A similar strategy can potentially be applied to drug screening for other genetic disorders... - Accumulation of DNA damage and reduced levels of nicotine adenine dinucleotide in the brains of Atm-deficient miceNora Stern
Department of Neurobiochemistry, George S Wise Faculty of Life Sciences, Sackler School of Medicine, Tel Aviv University, Tel Aviv 69978, Israel
J Biol Chem 277:602-8. 2002..Taken together, our findings support the hypothesis that absence of functional ATM results in continuous stress, which may be an important cause of the degeneration of cerebellar neurons in A-T... - In silico identification of transcriptional regulators associated with c-MycRan Elkon
The David and Inez Myers Laboratory for Genetic Research, Department of Human Genetics, Sackler School of Medicine, Tel Aviv University, Israel
Nucleic Acids Res 32:4955-61. 2004..The approach applied here is general and demonstrates how computational analysis of functional genomics experiments can identify novel modules in complex networks of transcriptional regulation... - Deciphering transcriptional regulatory elements that encode specific cell cycle phasing by comparative genomics analysisChaim Linhart
School of Computer Science, Tel Aviv University, Tel Aviv, Israel
Cell Cycle 4:1788-97. 2005..Our results reveal novel modules that determine specific cell cycle phasing, and identify their respective putative target genes with remarkably high specificity...
Research Grants
- ATAXIA TELANGIECTASIA--FROM GENE BACK TO PHENOTYPEYosef Shiloh; Fiscal Year: 1999....
- ATAXIA-TELANGIECTASIS: FROM GENE BACK TO PHENOTYPEYosef Shiloh; Fiscal Year: 2005..Since Ataxia-telangiectasia is a multisystem disease, understanding its physiological basis is expected to have broad ramifications in various areas of medicine. ..