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Mecp2 Nuclear Dynamics in Live Neurons Results from Low and High Affinity Chromatin Interactions

https://doi.org/10.2139/ssrn.3376659
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54/54 checkable references clean · checked 2026-08-31

Every reference with a DOI in the deposited reference list resolved to a known work in Crossref or DataCite at the dated check, and none carried a retraction, withdrawal, or removal notice.

8 without a DOI — not checked. A reference deposited without a DOI is never matched by title or guessed at; it stays outside the checked set, and this line discloses that.

The 54 checked references that resolve
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MeCP2 Rett mutations affect large scale chromatin organization
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Rett syndrome is caused by mutations in X-linked MECP2, encoding methyl-CpG-binding protein 2
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Selective Dendritic Alterations in the Cortex of Rett Syndrome
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An AT-Hook Domain in MeCP2 Determines the Clinical Course of Rett Syndrome and Related Disorders
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Effects of Rett Syndrome Mutations of the Methyl-CpG Binding Domain of the Transcriptional Repressor MeCP2 on Selectivity for Association with Methylated DNA
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MeCP2, a Key Contributor to Neurological Disease, Activates and Represses Transcription
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Faculty Opinions recommendation of MeCP2, a key contributor to neurological disease, activates and represses transcription.
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Dynamic and Selective Low-Complexity Domain Interactions Revealed by Live-Cell Single-Molecule Imaging
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The intervening domain from MeCP2 enhances the DNA affinity of the methyl binding domain and provides an independent DNA interaction site
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Mild overexpression of MeCP2 causes a progressive neurological disorder in mice
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<i>Methyl-CpG-binding protein 2</i> ( <i>MECP2</i> ) mutation type is associated with disease severity in Rett syndrome
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MECP2, a multi-talented modulator of chromatin architecture
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MeCP2 Binds Cooperatively to Its Substrate and Competes with Histone H1 for Chromatin Binding Sites
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Unique Physical Properties and Interactions of the Domains of Methylated DNA Binding Protein 2
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Spot-On: robust model-based analysis of single-particle tracking experiments
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Rett-causing mutations reveal two domains critical for MeCP2 function and for toxicity in MECP2 duplication syndrome mice
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Methylated DNA and MeCP2 recruit histone deacetylase to repress transcription
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The Ski Protein Family Is Required for MeCP2-mediated Transcriptional Repression
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Brain Activity Mapping in <i>Mecp2</i> Mutant Mice Reveals Functional Deficits in Forebrain Circuits, Including Key Nodes in the Default Mode Network, that are Reversed with Ketamine Treatment
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Structure of the MeCP2–TBLR1 complex reveals a molecular basis for Rett syndrome and related disorders
resolves10.1242/jcs.016865
Analysis of protein domains and Rett syndrome mutations indicate that multiple regions influence chromatin-binding dynamics of the chromatin-associated protein MECP2 in vivo
resolves10.1016/0092-8674(92)90610-o
Purification, sequence, and cellular localization of a novel chromosomal protein that binds to Methylated DNA
resolves10.1073/pnas.1617802113
Tet proteins influence the balance between neuroectodermal and mesodermal fate choice by inhibiting Wnt signaling
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Live-cell p53 single-molecule binding is modulated by C-terminal acetylation and correlates with transcriptional activity
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Rett syndrome: a complex disorder with simple roots
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Rett syndrome mutations abolish the interaction of MeCP2 with the NCoR/SMRT co-repressor
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MeCP2 binds to 5hmc enriched within active genes and accessible chromatin in the nervous system
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Multiple Modes of Interaction between the Methylated DNA Binding Protein MeCP2 and Chromatin
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Reviews and comment from nature journals
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Autism and other neuropsychiatric symptoms are prevalent in individuals with <i>MeCP2</i> duplication syndrome
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MeCP2 AT-Hook1 mutations in patients with intellectual disability and/or schizophrenia disrupt DNA binding and chromatin compaction in vitro
resolves10.1016/j.molcel.2010.01.030
Neuronal MeCP2 Is Expressed at Near Histone-Octamer Levels and Globally Alters the Chromatin State
resolves10.1016/j.cell.2017.09.047
Early-Life Gene Expression in Neurons Modulates Lasting Epigenetic States
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Cell-Type-Specific Repression by Methyl-CpG-Binding Protein 2 Is Biased toward Long Genes
resolves10.1101/066464
A Dynamic Mode of Mitotic Bookmarking by Transcription Factors
resolves10.1038/nature24058
Radically truncated MeCP2 rescues Rett syndrome-like neurological defects
resolves10.1093/nar/28.21.4172
Functional consequences of Rett syndrome mutations on human MeCP2
resolves10.7554/elife.05914.007
Figure 5. Binding of proteins extracted from osteoblasts to GST-galectin-8.
resolves10.1126/science.1169786
The Nuclear DNA Base 5-Hydroxymethylcytosine Is Present in Purkinje Neurons and the Brain
resolves10.1101/gr.749203
A Highly Efficient Recombineering-Based Method for Generating Conditional Knockout Mutations
resolves10.1038/nmeth.1233
Dynamic multiple-target tracing to probe spatiotemporal cartography of cell membranes
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resolves10.1083/jcb.201307172
TNF and IL-1 exhibit distinct ubiquitin requirements for inducing NEMO–IKK supramolecular structures
The 8 references without a DOI — listed, not checked
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no DOI — not checkedWhole-genome bisulfite (WGB) sequence of genomic DNA was used to quantify the cytosine modifications (5-methyl-cytosine or 5-hydroxy-methyl-cytosine, 5h+m) in its different sequence context (CG or CH -where H= A, T or C-) in wild type (WT) or Dnmt3a depleted Granule cells (D3a_cKO). (E) A snapshot of the IGV viewer displaying RNA-seq and MeCP2 ChIP-seq in adult cerebellar Granule cells (top) and WGB-seq traces of CG and CH loci in Wild-type or Dnmt3a depleted granule cells (Dnmt3a_cKO). (F) Immunostaining for 5hmC in Tet1 flox/flox ;Tet2 flox/flox ;Tet3 flox/flox GC culture co-transfected with Cre-expressing and DIO-MeCP2-HaloTag constructs. HaloTag positive cells (red) were successfully transfected with the Cre expressing construct and are therefore devoid of 5hmC (purple). (G) Cumulative distribution of diffusion coefficient (D', ?m 2 /s) calculated for individual molecules of MeCP2 in wild type (~25,000 molecules
no DOI — not checkedCells were then washed 4x in PBST, labeled with DAPI and mounted on coverslip for acquisition with confocal microscopy. DNA pull-down assay 293 cells were transfected with a vector expressing MeCP2HaloTag in Nuclear Extraction Buffer containing 0.5mM DTT and protease inhibitor, and incubated on a orbital shaker for 60 minutes at 4 �C. Samples were centrifuged at 16'000 x g for 5 minutes at 4 �C to collect the nuclear protein extract in the supernatant. M280-straptavidin beads (8 mL per sample) were washed once in PBS 0.1% Triton X-100, and then incubated with 200ng of biotinylated DNA probe in 300 mL of PBS, overnight at 4 �C. Then beads were washed 2x in PBS 1% Triton X-100
no DOI — not checkedThe cerebellar nuclear suspension of Pcp2-TRAP animals (carrying Pcp2 BAC transgenic construct carrying IL10a-GFP fusion protein) was supplemented with DyeCycle Violet (Invirogen) to 20 ?M final, as this DNA dye allows for the elimination of multiple nuclei aggregates that are recorded as a single event by the flow cytometer. Purkinje cells were identified by GFP signal and nuclei were sorted with BD FASCAria cell sorter using 405 nm and 488 nm excitation lasers. Ethics Animal experimentation: All animal protocols were carried out in accordance with the US National Institutes of Health Guide for the Care and Use of Laboratory Animals and were approved by The Rockefeller University Institutional Animal Care and Use Committee
no DOI — not checkedSpecies and cell-type properties of classically defined human and rodent neurons and glia
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