Becker, Annette

English

Ludwig-Maximilians-Universität München Dissertationen

Regulation of MeCP2 induced heterochromatin remodeling

Digitale Hochschulschriften der LMU

A mammalian protein with specific demethylase activity for mCpG DNA.

A mouse Mecp2-null mutation causes neurological symptoms that mimic Rett syndrome.

A previously unidentified MECP2 open reading frame defines a new protein isoform relevant to Rett syndrome.

A progressive syndrome of autism, dementia, ataxia, and loss of purposeful hand use in girls: Rett's syndrome: report of 35 cases.

A rapid alkaline extraction procedure for screening recombinant plasmid DANN.

A targeting sequence directs DNA methyltransferase to sites of DNA replication in mammalian nuclei.

A versatile nanotrap for biochemical and functional studies with fluorescent fusion proteins.

a vertebrate DNA binding protein with affinity for methylated DNA.

A WW domain binding region in methyl-CpGbinding protein MeCP2: impact on Rett syndrome.

Abnormalities of social interactions and home-cage behavior in a mouse model of Rett syndrome.

Activation-induced cytidine deaminase deaminates 5-methylcytosine in DNA and is expressed in pluripotent tissues: implications for epigenetic reprogramming.

Active repression of methylated genes by the chromosomal protein MBD1.

ADP-ribosylation of histone H1. Identification of glutamic acid residues 2, 14, and the COOH-terminal lysine residue as modification sites.

ADP-ribosylation of histone H2B. Identification of glutamic acid residue 2 as the modification site.

Analysis of protein domains and Rett syndrome mutations indicate that multiple regions influence chromatin-binding dynamics of the chromatin-associated protein MECP2 in vivo.

Analysis of the NuRD subunits reveals a histone deacetylase core complex and a connection with DNA methylation.

and modulates its heterochromatin association during myogenic differentiation.

are essential for de novo methylation and mammalian development.

Arrangement of centromeres in mouse cells.

ATRX partners with cohesin and MeCP2 and contributes to developmental silencing of imprinted genes in the brain.

b e l o n g s t o t h e s a me molecular pathway of MeCP2 and it is responsible for the early-onset seizure variant of Rett syndrome.

Binding of adenosine diphosphoribosyltransferase to the termini and internal regions of linear DNAs.

Biphasic kinetics of the human DNA repair protein MED1 (MBD4), a mismatch-specific DNA N-glycosylase.

CDKL5/STK9 is m utated in R ett syndrome variant with infantile spasms.

CDKL5/Stk9 kinase inactivation is associated with neuronal developmental disorders.

Cell cycle controlling the silencing and functioning of mammalian activators.

Cell-by-cell dissection of gene expression and chromosomal interactions reveals consequences of nuclear reorganization.

Characterization of a n t i -peptide antibodies directed towards the automodification domain and apoptotic fragment of poly (ADP-ribose) polymerase.

Chromatin compaction by human MeCP2. Assembly of novel secondary chromatin structures in the absence of DNA methylation.

Chromatin deacetylation by an ATP-dependent nucleosome remodelling complex.

Chromosomal and nuclear location of mouse satellite DNA in individual cells.

Chromosomal localization of mouse satellite DNA.

Cloning and expression of human G/T mismatch-specific thymine-DNA glycosylase.

Cloning of human satellite III DNA: different components are on different chromosomes.

Closely related proteins MBD2 and MBD3 play distinctive but interacting roles in mouse development.

complex for PU.1-mediated transcriptional repression.

Components of the DNA methylation system of chromatin control are RNA-binding proteins.

Corepressordependent silencing of chromosomal regions encoding neuronal genes.

CoREST is an integral component of the CoREST- human histone deacetylase complex.

CpG methylation of the cAMP-responsive enhancer/promoter sequence TGACGTCA abolishes specific factor binding as well as transcriptional activation.

CpG-rich islands and the function of DNA methylation.

Deficiency of methyl-CpG binding protein-2 in CNS neurons results in a Rett-like phenotype in mice.

Derepression of BDNF transcription involves calciumdependent phosphorylation of MeCP2.

Dissection of the methyl-CpG binding domain from the chromosomal protein MeCP2.

DNA binding selectivity of MeCP2 due to a requirement for A/T sequences adjacent to methyl-CpG.

DNA demethylation in zebrafish involves the coupling of a deaminase, a glycosylase, and gadd45.

DNA methylation patterns and epigenetic memory.

DNA methylation specifies chromosomal localization of MeCP2.

DNA methylation-related chromatin remodeling in activity-dependent BDNF gene regulation.

DNA methylation, nuclear structure, gene expression and cancer.

Enhanced anxiety and stress-induced corticosterone release are associated with increased Crh expression in a mouse model of Rett syndrome.

Enhanced CpG mutability and tumorigenesis in MBD4-deficient mice.

Essential role for de novo DNA methyltransferase Dnmt3a in paternal and maternal imprinting.

Expression of MeCP2 in postmitotic neurons rescues Rett syndrome in mice.

Extension of life-span by introduction of telomerase into normal human cells.

F u n c t i o n a l APPENDIX interaction between poly(ADP-Ribose) polymerase 2 (PARP-2) and TRF2: PARP activity negatively regulates TRF2.

FBP WW domains and the Abl SH3 domain bind to a specific class of proline-rich ligands.

FoldIndex: a simple tool to predict whether a given protein sequence is intrinsically unfolded.

Gene silencing quantitatively controls the function of a developmental trans-activator.

Generation of deletion and point mutations with one primer in a single cloning step.

Glycation and glycoxidation of histones by ADP-ribose.

Heterogeneity in residual function of MeCP2 carrying missense mutations in the methyl CpG binding domain.

Higher order structure in a short repeat length chromatin.

HIPK2: a multitalented partner for transcription factors in DNA damage response and development.

HIPK2: a versatile switchboard regulating the transcription machinery and cell death.

Human DNA(cytosine-5) methyltransferase-PCNA complex as a target for p21WAF1.

Identification and characterization of a family of mammalian methyl-CpG binding proteins.

Identification of a mammalian protein that binds specifically to DNA containing methylated CpGs.

Identification of potential active-site residues in the human poly(ADP-ribose) polymerase.

In vitro correction of G.T mispairs to G.C pairs in nuclear extracts from human cells.

Inhibitor and NAD+ binding to poly(ADPribose) polymerase as derived from crystal structures and homology modeling.

Integrated epigenomic analyses of neuronal MeCP2 reveal a role for long-range interaction with active genes.

Interaction between chromatin proteins MECP2 and ATRX is disrupted by mutations that cause inherited mental retardation.

Intrinsic disorder and autonomous domain function in the multifunctional nuclear protein,

Intrinsic protein disorder, amino acid composition, and histone terminal domains.

Involvement of SUMO modification in MBD1- a n d

M b d 4 i n a c t i v a t i o n i n c r e a s e s C r i g h t -arrowT transition mutations and promotes gastrointestinal tumor formation.

mAM facilitates conversion by ESET of dimethyl to trimethyl lysine 9 of histone H3 to cause transcriptional repression.

Mbd1 is r e c r u i t e d t o b o t h methylated and nonmethylated CpGs via distinct DNA binding domains.

MBD2 is a transcriptional repressor belonging to the MeCP1 histone deacetylase complex.

MCAF mediates MBD1-dependent transcriptional repression.

MeCP2 behaves as an elongated monomer that does not stably associate with the Sin3a chromatin remodeling complex.

MeCP2 binding to DNA depends upon hydration at methyl-CpG.

MeCP2 is a transcriptional repressor with abundant binding sites in genomic chromatin.

MECP2 mutation in male patients with nonspecific X-linked mental retardation.

MeCP2 preferentially binds to methylated linker DNA in the absence of the terminal tail of histone H3 and independently of histone acetylation.

MeCP2-chromatin interactions include the formation of chromatosome-like structures and are altered in mutations causing Rett syndrome.

MeCP2, a key contributor to neurological disease, activates and represses transcription.

MED1, a novel human methylCpG-binding endonuclease, interacts with DNA mismatch repair protein MLH1.

Methyl CpG binding proteins: coupling chromatin architecture to gene regulation.

Methyl CpG-binding proteins induce large-scale chromatin reorganization during terminal differentiation.

Methyl-CpG binding domain 1 (MBD1) interacts with the Suv39h1-HP1 heterochromatic complex for DNA methylation-based transcriptional repression.

Methyl-CpG binding protein MBD1 couples histone H3 methylation at lysine 9 by SETDB1 to DNA replication and chromatin assembly.

Methyl-CpG-binding protein 2 is phosphorylated by homeodomain-interacting protein kinase 2 and contributes to apoptosis.

Methyl-CpG-binding protein, MeCP2, is a target molecule for maintenance DNA methyltransferase,

Methylation-induced repression--belts, braces, and chromatin.

Methylation-mediated transcriptional silencing in euchromatin by methylCpG binding protein MBD1 isoforms.

Mice lacking methylCpG binding protein 1 have deficits in adult neurogenesis and hippocampal function.

Mice with truncated MeCP2 recapitulate many Rett syndrome features and display hyperacetylation of histone H3.

Mild overexpression of MeCP2 causes a progressive neurological disorder in mice.

https://edoc.ub.uni-muenchen.de/13128/1/Becker_Annette.pdf

Regulation of MeCP2 induced heterochromatin remodeling

Abstract

Similar works

Full text

Available Versions

Ludwig-Maximilians-Universität München Dissertationen

Digitale Hochschulschriften der LMU