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Jérôme Déjardin

Bio: Jérôme Déjardin is an academic researcher from Harvard University. The author has contributed to research in topics: Chromatin & Non-histone protein. The author has an hindex of 3, co-authored 4 publications receiving 473 citations.

Papers
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Journal ArticleDOI
09 Jan 2009-Cell
TL;DR: Proteomics of isolated chromatin segments (PICh) is described, identifying and validated several proteins that specifically bind to ALT telomeres, establishing PICh as a useful tool for characterizing chromatin composition.

498 citations

Patent
20 Aug 2008
TL;DR: In this paper, the authors proposed a method for isolating polypeptides and protein complexes that are associated with a target nucleic acid sequence by contacting the sample with at least one oligonucleotide probe that comprises a sequence that is complimentary to and capable of hybridising with a portion of the target NCA sequence.
Abstract: Methods for isolating polypeptides and polypeptide complexes that are associated with a target nucleic acid sequence are provided. The methods comprise the steps of obtaining a sample that comprises a target nucleic acid sequence and one or more polypeptides or proteins associated with that target nucleic acid sequence; contacting the sample with at least one oligonucleotide probe that comprises a sequence that is complimentary to and capable of hybridising with at least a portion of the target nucleic acid sequence, wherein the oligonucleotide probe comprises at least one locked nucleic acid (LNA) nucleotide and wherein the oligonucleotide probe further comprises at least one affinity label (e.g. biotin); allowing the at least one oligonucleotide probe and the target nucleic acid sequence to hybridise with each other so as to form a probe-target hybrid; isolating the probe-target hybrid from the sample by immobilizing the probe-target hybrid through a molecule that binds to the at least one affinity label (e.g. using streptavidin-coated magnetic beads); and eluting the one or more polypeptides that are associated with the target nucleic acid sequence. Probes (e.g. with long spacer) for use in the methods of screening are also provided.

10 citations

Journal ArticleDOI
TL;DR: This work has shown that some microRNAs downregulate large number of target mRNAs, and microarray analysis shows that someMicroRNA expression profiles classify human cancers.
Abstract: 1. Ambros V. The functions of animal microRNAs. Nature 2004 ; 431 : 350-5. 2. Matzke IA, Birchler JA. RNAi-mediated pathways in the nucleus. Nat Rev Genet 2005 ; 6 : 24-35. 3. Lecellier CH, Dunoyer P, Arark K, et al. A cellular microRNA mediates antiviral defense in human cells. Science 2005 ; 308 : 557-60. 4. Kanellopoulou C, Muljo S, Kung AL, et al. Dicerdeficient mouse embryonic stem cells are defective in differentiation and centromeric silencing. Genes Dev 2005 ; 19 : 489-501. 5. Lim LP, Lau NC, Garret-Engele P, et al. Microarray analysis shows that some microRNAs downregulate large number of target mRNAs. Nature 2005 ; 433 : 769-73. 6. Johnson SM, Grosshans H, Shingara J, et al. Ras is regulated by the let-7 microRNA family. Cell 2005 ; 120 : 635-47. 7. He L, Thomson JM, Heman MT, et al. A microRNA polycistron as a potential human oncogene. Nature 2005 ; 435 : 828-33. 8. O’Donnel KA, Wentzel EA, Zeller KI, Dang CV, Mendell JT. c-Myc-regulated microRNAS modulate E2F1 expression. Nature 2005 ; 435 : 839-43. 9. Lu J, Getz G, Miska EA, et al. MicroRNA expression profiles classify human cancers. Nature 2005 ; 435 : 834-8.

1 citations


Cited by
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Journal ArticleDOI
TL;DR: This work has shown how plants are able to integrate the multitude of abiotic and biotic stresses in their natural habitat into their phenotypic plasticity.
Abstract: Plants constantly face a plethora of abiotic and biotic stresses in their natural habitat. Adapting to such changes requires a great degree of phenotypic plasticity that is mainly determined by the plant's genome. We currently do not know how plants are able to integrate the multitude of partly

1,034 citations

Journal ArticleDOI
10 Jul 2009-Cell
TL;DR: The TTAGGG repeat arrays of mammalian telomeres pose a challenge to the DNA replication machinery, giving rise to replication-dependent defects that resemble those of aphidicolin-induced common fragile sites.

887 citations

Journal ArticleDOI
TL;DR: There are nine protein arginine methyltransferases (PRMTs) encoded in mammalian genomes, the protein products of which catalyse three types of ARG modifications: monomethylation and two types of dimethylation as discussed by the authors.
Abstract: There are nine protein arginine methyltransferases (PRMTs) encoded in mammalian genomes, the protein products of which catalyse three types of arginine methylation--monomethylation and two types of dimethylation. Protein arginine methylation is an abundant modification that has been implicated in signal transduction, gene transcription, DNA repair and mRNA splicing, among others. Studies have only recently linked this modification to carcinogenesis and metastasis. Sequencing studies have not generally found alterations to the PRMTs; however, overexpression of these enzymes is often associated with various cancers, which might make some of them viable targets for therapeutic strategies.

853 citations

Journal ArticleDOI
TL;DR: This work has shown that the sequestration of the telomeric sequence into a protective nucleoprotein cap that masks the ends from constitutive exposure to the DNA damage response machinery reduces the risk of genome instability.
Abstract: The natural ends of linear chromosomes require unique genetic and structural adaptations to facilitate the protection of genetic material. This is achieved by the sequestration of the telomeric sequence into a protective nucleoprotein cap that masks the ends from constitutive exposure to the DNA damage response machinery. When telomeres are unmasked, genome instability arises. Balancing capping requirements with telomere replication and the enzymatic processing steps that are obligatory for telomere function is a complex problem. Telomeric proteins and their interacting factors create an environment at chromosome ends that inhibits DNA repair; however, the repair machinery is essential for proper telomere function.

842 citations

Journal ArticleDOI
10 Sep 2009-Nature
TL;DR: These studies identify points in the transcription cycle where RNA polymerase II accumulates after encountering a rate-limiting step and identify key regulatory steps and factors and provide an understanding of the mechanistic generalities, as well as the rich diversities, of gene regulation.
Abstract: In the eukaryotic genome, the thousands of genes that encode messenger RNA are transcribed by a molecular machine called RNA polymerase II. Analysing the distribution and status of RNA polymerase II across a genome has provided crucial insights into the long-standing mysteries of transcription and its regulation. These studies identify points in the transcription cycle where RNA polymerase II accumulates after encountering a rate-limiting step. When coupled with genome-wide mapping of transcription factors, these approaches identify key regulatory steps and factors and, importantly, provide an understanding of the mechanistic generalities, as well as the rich diversities, of gene regulation.

575 citations