about
An unmethylated 3' promoter-proximal region is required for efficient transcription initiationhnRNP K coordinates transcriptional silencing by SETDB1 in embryonic stem cellsDistinct roles of KAP1, HP1 and G9a/GLP in silencing of the two-cell-specific retrotransposon MERVL in mouse ES cellsVisRseq: R-based visual framework for analysis of sequencing data.Regulation of DNA methylation turnover at LTR retrotransposons and imprinted loci by the histone methyltransferase Setdb1Retrotransposon-induced heterochromatin spreading in the mouse revealed by insertional polymorphisms.Setdb1 is required for germline development and silencing of H3K9me3-marked endogenous retroviruses in primordial germ cellsAn ultra-low-input native ChIP-seq protocol for genome-wide profiling of rare cell populations.Histone H3K4 demethylation is negatively regulated by histone H3 acetylation in Saccharomyces cerevisiaeSystematic identification of factors for provirus silencing in embryonic stem cellsDynamic and flexible H3K9me3 bridging via HP1β dimerization establishes a plastic state of condensed chromatin.Long Terminal Repeats: From Parasitic Elements to Building Blocks of the Transcriptional Regulatory RepertoireVitamin C induces Tet-dependent DNA demethylation and a blastocyst-like state in ES cells.ChAsE: chromatin analysis and exploration tool.DNA methylation density influences the stability of an epigenetic imprint and Dnmt3a/b-independent de novo methylation.Proviral silencing in embryonic stem cells requires the histone methyltransferase ESET.Targeting of EZH2 to a defined genomic site is sufficient for recruitment of Dnmt3a but not de novo DNA methylation.Targeting silence: the use of site-specific recombination to introduce in vitro methylated DNA into the genome.Activation of Endogenous Retroviruses in Dnmt1(-/-) ESCs Involves Disruption of SETDB1-Mediated Repression by NP95 Binding to Hemimethylated DNA.Kinetics and epigenetics of retroviral silencing in mouse embryonic stem cells defined by deletion of the D4Z4 element.Primate-specific endogenous retrovirus-driven transcription defines naive-like stem cells.ALEA: a toolbox for allele-specific epigenomics analysis.DNA methylation and SETDB1/H3K9me3 regulate predominantly distinct sets of genes, retroelements, and chimeric transcripts in mESCsDetection and isolation of gene-corrected cells in Gaucher disease via a fluorescence-activated cell sorter assay for lysosomal glucocerebrosidase activity.Epigenetic modifier drugs trigger widespread transcription of endogenous retroviruses.H3S10ph broadly marks early-replicating domains in interphase ESCs and shows reciprocal antagonism with H3K9me2.Evidence for Converging DNA Methylation Pathways in Placenta and Cancer.H2A.Z and DNA methylation: irreconcilable differences.Silencing of endogenous retroviruses: when and why do histone marks predominate?Dynamics, stability and inheritance of somatic DNA methylation imprints.Development and application of an integrated allele-specific pipeline for methylomic and epigenomic analysis (MEA).Setdb1 is required for germline development and silencing of H3K9me3-marked endogenous retroviruses in primordial germ cells.Genome-wide mapping of chromatin marks from 1,000 cells to study epigenetic reprogramming in primordial germ cells.LTR retrotransposons transcribed in oocytes drive species-specific and heritable changes in DNA methylationRare treatable neurologic diseasesRNA polymerase II: just stopping byReporters of gene expression: enzymatic assaysOn the role of H3.3 in retroviral silencingSetting the chromatin stage in oocytesSETD2 regulates the maternal epigenome, genomic imprinting and embryonic development
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P50
description
onderzoeker
@nl
researcher
@en
հետազոտող
@hy
name
Matthew C Lorincz
@nl
Matthew C Lorincz
@sl
Matthew C. Lorincz
@en
Matthew C. Lorincz
@es
type
label
Matthew C Lorincz
@nl
Matthew C Lorincz
@sl
Matthew C. Lorincz
@en
Matthew C. Lorincz
@es
prefLabel
Matthew C Lorincz
@nl
Matthew C Lorincz
@sl
Matthew C. Lorincz
@en
Matthew C. Lorincz
@es
P106
P1153
7003383177
P31
P496
0000-0003-0885-0467