Research Topics
| MIRIT ALADJEMSummaryAffiliation: National Institutes of Health Country: USA Publications
| Collaborators
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Detail Information
Publications
A formal MIM specification and tools for the common exchange of MIM diagrams: an XML-Based format, an API, and a validation methodAugustin Luna
Laboratory of Molecular Pharmacology, Center for Cancer Research, National Cancer Institute, NIH, Bethesda, MD 20892, USA
BMC Bioinformatics 12:167. 2011..A lack of software tools for the notation restricts wider usage of the notation. Development of software is facilitated by a more detailed specification regarding software requirements than has previously existed for the MIM notation...- The replicon revisited: an old model learns new tricks in metazoan chromosomesMirit I Aladjem
Laboratory of Molecular Pharmacology, DSB, National Cancer Institute, National Institutes of Health, Building 37, Room 5056, 37 Convent Drive, Bethesda, Maryland 20892 4255, USA
EMBO Rep 5:686-91. 2004..Here, we review the properties of metazoan replicators, and discuss the genetic and epigenetic factors that determine where and when DNA replication is initiated... 
The mammalian beta globin origin of DNA replicationMirit I Aladjem
Laboratory of Molecular Pharmacology, National Cancer Institute, Bethesda, MD, USA
Front Biosci 9:2540-7. 2004....- Replication in context: dynamic regulation of DNA replication patterns in metazoansMirit I Aladjem
Laboratory of Molecular Pharmacology, National Cancer Institute, National Institutes of Health, Building 37, Room 5056, 37 Convent Drive, Bethesda, Maryland 20892 4255, USA
Nat Rev Genet 8:588-600. 2007.... - Molecular interaction maps--a diagrammatic graphical language for bioregulatory networksMirit I Aladjem
Laboratory of Molecular Pharmacology, Center for Cancer Research, National Cancer Institute, Bethesda, MD 20892, USA
Sci STKE 2004:pe8. 2004.... 
EMBO Conference on Replication and Segregation of Chromosomes, Geilo, Norway, June 16-20. Replication and segregation of chromosomes in the three domains of life: EMBO conference reports common grounds. Meeting reportMIRIT ALADJEM
Laboratories of Pharmacology, Center for Cancer Research, NCI, NIH, Bethesda, MD 20892 4260, USA
Plasmid 61:89-93. 2009..The organizers Kirsten Skarstad and Erik Boye deserve praise for their skillful organization of the meeting, the highlights of which are discussed below...- The intra-S-phase checkpoint affects both DNA replication initiation and elongation: single-cell and -DNA fiber analysesJennifer A Seiler
Laboratory of Molecular Pharmacology, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20892 4255, USA
Mol Cell Biol 27:5806-18. 2007..Together, our study demonstrates that the intra-S-phase checkpoint is exerted by Chk1 not only upon replication initiation but also upon DNA elongation... - Phosphorylation of histone H2AX and activation of Mre11, Rad50, and Nbs1 in response to replication-dependent DNA double-strand breaks induced by mammalian DNA topoisomerase I cleavage complexesTakahisa Furuta
Laboratory of Molecular Pharmacology, Center for Cancer Research, NCI, National Institutes of Health, Bethesda, Maryland 20892 4255, USA
J Biol Chem 278:20303-12. 2003..These results demonstrate a conserved gammaH2AX response for double-strand breaks induced by replication fork collision. gammaH2AX foci are required for recruiting repair and checkpoint protein complexes to the replication break sites... - Cooperative sequence modules determine replication initiation sites at the human beta-globin locusLixin Wang
Laboratory of Molecular Pharmacology, National Cancer Institute, Bethesda, MD 20892, USA
Hum Mol Genet 15:2613-22. 2006..These data support a combinatorial model for replicator activity and suggest that the initiation of DNA replication requires interaction between at least two distinct sequence modules... - Bloom's syndrome helicase and Mus81 are required to induce transient double-strand DNA breaks in response to DNA replication stressTsutomu Shimura
Laboratory of Molecular Pharmacology, Center for Cancer Research, NCI, NIH, Bethesda, MD 20892 4255, USA
J Mol Biol 375:1152-64. 2008.... - Chromatin challenges during DNA replication: a systems representationKurt W Kohn
Laboratory of Molecular Pharmacology, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892, USA
Mol Biol Cell 19:1-7. 2008..on the complexities of chromatin replication, thereby providing a tool for system-level comprehension of the effects of genetic mutations, altered gene expression, and pharmacologic intervention... - Replication initiation patterns in the beta-globin loci of totipotent and differentiated murine cells: evidence for multiple initiation regionsMirit I Aladjem
Laboratory of Molecular Pharmacology, National Cancer Institute, Bethesda, Maryland 20892 4255, USA
Mol Cell Biol 22:442-52. 2002..As this deletion also did not affect the chromatin structure of the locus, we propose that the sequences determining both chromatin structure and replication initiation lie outside the hypersensitive sites removed by the deletion... 
Depicting combinatorial complexity with the molecular interaction map notationKurt W Kohn
Laboratory of Molecular Pharmacology, Center for Cancer Research, National Cancer Institute, NIH, Bethesda, MD, USA
Mol Syst Biol 2:51. 2006..These comparisons may help cell and systems biologists adopt a graphical language that is unambiguous and generally understood...- Chk2 molecular interaction map and rationale for Chk2 inhibitorsYves Pommier
Laboratory of Molecular Pharmacology, Center for Cancer Research, National Cancer Institute, NIH, Bethesda, Maryland 20892 4255, USA
Clin Cancer Res 12:2657-61. 2006..Visualizing the regulatory circuits underlying cellular signaling may help identify key regulatory reactions and defects that can serve as targets for anticancer drugs... - Molecular interaction maps of bioregulatory networks: a general rubric for systems biologyKurt W Kohn
Laboratory of Molecular Pharmacology, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892, USA
Mol Biol Cell 17:1-13. 2006..Drawing a MIM diagram, adhering to the rules of notation, imposes a logical discipline that sharpens one's understanding of the structure and function of a network... - Network architecture of signaling from uncoupled helicase-polymerase to cell cycle checkpoints and trans-lesion DNA synthesisKurt W Kohn
Laboratory of Molecular Pharmacology, Center for Cancer Research, National Cancer Institute, NIH, Bethesda, MD 20892, USA
Cell Cycle 8:2281-99. 2009..In addition, the network architecture disclosed by the hierarchical map, suggested a speculative model for how molecular crowding and the granular localization of network components in the cell nucleus can facilitate function... - Werner syndrome protein directly binds to the AAA ATPase p97/VCP in an ATP-dependent fashionFred Eliezer Indig
Laboratory of Molecular Gerontology, NIA, NIH, Baltimore MD 21224, USA
J Struct Biol 146:251-9. 2004..Immunohistochemical analysis of various VCP domains and mutated proteins expressed in vitro demonstrated that VCP may contain several hierarchical cellular localization motifs within its domain structure... - Preventing gene silencing with human replicatorsHaiqing Fu
Laboratory of Molecular Pharmacology, NCI, Bethesda, Maryland 20892, USA
Nat Biotechnol 24:572-6. 2006..Inclusion of functional replicators in gene therapy vectors may provide a tool for stabilizing gene expression patterns... - Dynamic alterations of replication timing in mammalian cellsChii Mei Lin
Laboratory of Molecular Pharmacology, Center for Cancer Research, NCI, National Institutes of Health, Bethesda, Maryland 20892-4255, USA
Curr Biol 13:1019-28. 2003..These observations suggest that the timing of DNA replication can be manipulated by changes in DNA sequence, but that the determinants of replication timing are distinct from the sequences that specify replication initiation sites... - DNA-PK is involved in repairing a transient surge of DNA breaks induced by deceleration of DNA replicationTsutomu Shimura
Laboratory of Molecular Pharmacology, Center for Cancer Research, NCI, NIH, Bethesda, MD 20892, USA
J Mol Biol 367:665-80. 2007..These observations suggest that DNA-PK is involved in setting a high threshold for the ATR-Chk1-mediated S-phase checkpoint by promptly repairing DNA breaks that appear immediately following inhibition of DNA replication... - The human beta-globin replication initiation region consists of two modular independent replicatorsLixin Wang
Laboratory of Molecular Pharmacology, Center for Cancer Research, National Cancer Institute, Bethesda, Maryland, USA
Mol Cell Biol 24:3373-86. 2004.... - Inhibition of histone deacetylase in cancer cells slows down replication forks, activates dormant origins, and induces DNA damageChiara Conti
Laboratory of Molecular Pharmacology, National Cancer Institute, NIH, Bethesda, Maryland 20892 4255, USA
Cancer Res 70:4470-80. 2010..Our findings demonstrate that SAHA produces profound alterations in DNA replication that cause DNA damage, establishing a critical link between robust chromatin acetylation and DNA replication in human cancer cells... - The cyclin-dependent kinase inhibitor Dacapo promotes replication licensing during Drosophila endocyclesAmy Hong
Cell Biology and Metabolism Branch, National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, MD 20892, USA
EMBO J 26:2071-82. 2007..Finally, genetic interaction studies suggest that dap functions to promote replication licensing in a subset of Drosophila mitotic cycles... - Nonclassic functions of human topoisomerase I: genome-wide and pharmacologic analysesZe Hong Miao
Laboratories of Molecular Pharmacology, National Institute of Diabetes and Digestive and Kidney Diseases, NIH, Bethesda, Maryland, USA
Cancer Res 67:8752-61. 2007..The reported cell lines and approaches described in this article provide new tools to perform detailed functional analyses related to Top1 function... - Prevention of transcriptional silencing by a replicator-binding complex consisting of SWI/SNF, MeCP1, and hnRNP C1/C2Liang Huang
Laboratory of Molecular Pharmacology, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20892, USA
Mol Cell Biol 31:3472-84. 2011..These observations suggest that the interaction of LARC complex with replicators plays a role in preventing gene silencing and provides support for a novel, epigenetic mechanism of resistance to methylation inhibitors... - Predicted functions of MdmX in fine-tuning the response of p53 to DNA damageSohyoung Kim
Laboratory of Molecular Pharmacology, National Cancer Institute, National Institute of Health, Bethesda, Maryland, United States of America
PLoS Comput Biol 6:e1000665. 2010..Our study suggests how MdmX may participate in the response of p53 to DNA damage either by increasing dependency of p53 on Mdm2 or by dampening oscillations of p53 activity and presents a model for experimental investigation... - DNA methylation supports intrinsic epigenetic memory in mammalian cellsYong-Qing Feng
Department of Medicine, Division of Hematology, Albert Einstein College of Medicine, Bronx, New York, New York, United States of America
PLoS Genet 2:e65. 2006..We propose that DNA methylation within transgenes serves as an intrinsic epigenetic memory to permanently silence transgenes and prevent their reactivation... - Initiation of DNA replication at the human beta-globin 3' enhancerAlla Buzina
Developmental Biology Program, Hospital for Sick Children Toronto, Ontario, Canada
Nucleic Acids Res 33:4412-24. 2005..We conclude that a mammalian enhancer can cooperate with adjacent sequences to create an efficient replicator module... - The human beta-globin locus control region can silence as well as activate gene expressionYong Qing Feng
Division of Hematology, Department of Medicine, Albert Einstein College of Medicine, 1300 Morris Park Ave, Bronx, NY 10461, USA
Mol Cell Biol 25:3864-74. 2005..We also provide evidence that this novel silencing activity is caused by transcriptional interference triggered by activation of transcription in the flanking sequences by the LCR... - Targeted deletion of the chicken beta-globin regulatory elements reveals a cooperative gene silencing activityJin Wang
Center for Hematologic Malignancies, Oregon Cancer Institute, Department of Medicine, Oregon Health and Science University, Portland, 97239, USA
J Biol Chem 280:23340-8. 2005..Our results using a chromosomal transfer assay demonstrate an identical silencing function for these regulatory elements, which suggests they function as part of a common silencing pathway or complex... - Candidate DNA replication initiation regions at human trinucleotide repeat disease lociTaurai Nenguke
Program in Molecular and Computational Biology, University of Southern California, Los Angeles, CA 90089-1340, USA
Hum Mol Genet 12:1021-8. 2003..Comparison with experimental results from model systems suggests that a complex relationship may exist between instability and the proximity and/or orientation of the repeats with respect to an IR... - Circuit diagrams for biological networksKurt W Kohn
Mol Syst Biol 2:2006.0002. 2006